start-ver=1.4
cd-journal=joma
no-vol=38
cd-vols=
no-issue=4
article-no=
start-page=e70187
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=2026 4
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Type III CD38 is present in the membrane of neurosecretory vesicles and has a cytosol-facing catalytic domain in primate oxytocin neurons
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=CD38, an ADP-ribosyl cyclase that generates cyclic ADP-ribose (cADPR), is essential for Ca2+-dependent oxytocin release. However, its subcellular localisation and membrane topology within oxytocin neurones have remained unclear. We investigated the distribution and orientation of CD38 in oxytocin-producing neurones of Japanese macaques (Macaca fuscata) using immunoelectron microscopy combined with biochemical isolation of neurosecretory vesicles (NSVs). CD38 immunoreactivity was selectively detected on oxytocin-containing NSVs in axon terminals in the posterior pituitary and dendrites of the supraoptic nucleus, whereas vasopressin vesicles and the plasma membrane lacked detectable labelling. Cryo-electron microscopy confirmed the structural integrity of purified NSV fractions, and Western blotting verified the presence of CD38 protein within these fractions. Permeabilisation-dependent immunogold labelling further demonstrated that the NSV membrane localisation of CD38 and that the N-terminal region of CD38 is oriented toward the vesicle lumen, consistent with a type III membrane topology in which the catalytic domain faces the cytosol. This arrangement positions the active site near cytosolic NAD+, enabling localised cADPR production adjacent to Ca2+-mobilising channels that support regulated exocytosis. These findings identify, in primate oxytocin neurones, a previously unrecognised, vesicle-associated pool of CD38 with a cytosol-facing catalytic domain and provide a structural framework for understanding how intracellular type III CD38 contributes to neuropeptide release.
en-copyright=
kn-copyright=

en-aut-name=MiyamotoTatsuki
en-aut-sei=Miyamoto
en-aut-mei=Tatsuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MatsushimaAkari
en-aut-sei=Matsushima
en-aut-mei=Akari
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OtuboAkito
en-aut-sei=Otubo
en-aut-mei=Akito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SongChihong
en-aut-sei=Song
en-aut-mei=Chihong
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MurataKazuyoshi
en-aut-sei=Murata
en-aut-mei=Kazuyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OtiTakumi
en-aut-sei=Oti
en-aut-mei=Takumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SakamotoHirotaka
en-aut-sei=Sakamoto
en-aut-mei=Hirotaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Department of Biology, Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Biology, Faculty of Science, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Biology, Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=4
en-affil=Exploratory Research Center on Life and Living Systems (ExCELLS), National Institutes of Natural Sciences
kn-affil=

affil-num=5
en-affil=Exploratory Research Center on Life and Living Systems (ExCELLS), National Institutes of Natural Sciences
kn-affil=

affil-num=6
en-affil=Department of Biology, Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Biology, Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=
en-keyword=CD38
kn-keyword=CD38
en-keyword=cyclic ADP-ribose
kn-keyword=cyclic ADP-ribose
en-keyword=membrane topology
kn-keyword=membrane topology
en-keyword=neurosecretory vesicles
kn-keyword=neurosecretory vesicles
en-keyword=oxytocin
kn-keyword=oxytocin
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=20260429
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=CDPKs as Ca2+ signaling decoders in guard cell signaling
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Stomatal movements are essential for balancing photosynthetic carbon dioxide uptake with water conservation and defense against pathogens. These processes are controlled by complex signaling networks in guard cells, in which calcium ions (Ca2+) act as a ubiquitous second messenger. Although stimulus-specific Ca2+ signatures have been well documented, how these signals are decoded into distinct physiological responses remains a central question in plant biology. Increasing evidence highlights calcium-dependent protein kinases (CDPKs) as key signal decoders in guard cell signaling. This mini-review summarizes recent advances in our understanding of how CDPKs perceive and translate Ca2+ fluctuations into stomatal responses. We focus on the roles of CDPKs in signaling pathways triggered by diverse stimuli, including phytohormones such as abscisic acid ABA, jasmonates, and salicylic acid, as well as biotic cues such as microbe- or pathogen-associated molecular patterns (MAMPs/PAMPs) and pathogen infection. We also discuss how gaseous signals and metabolic cues are integrated into CDPK-mediated pathways. In addition to their established role as downstream decoders of Ca2+ signals, emerging studies suggest that CDPKs can act upstream of Ca2+ oscillations and may also function through Ca2+-independent mechanisms. Together, these findings highlight the context-dependent and integrative roles of CDPKs in regulating stomatal behavior, contributing to plant fitness under fluctuating environmental conditions.
en-copyright=
kn-copyright=

en-aut-name=MoriIzumi C.
en-aut-sei=Mori
en-aut-mei=Izumi C.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=
en-keyword=Ca2+ signaling
kn-keyword=Ca2+ signaling
en-keyword=CDPK
kn-keyword=CDPK
en-keyword=Signal decoding
kn-keyword=Signal decoding
en-keyword=Stomata
kn-keyword=Stomata
END

start-ver=1.4
cd-journal=joma
no-vol=29
cd-vols=
no-issue=5
article-no=
start-page=115667
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=202605
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Wnt3-mediated fibrosis and carcinogenesis of lung squamous cell carcinoma in idiopathic pulmonary fibrosis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Idiopathic pulmonary fibrosis (IPF) increases the risk of lung squamous cell carcinoma (LUSC), yet its molecular pathogenesis remains unclear. We conducted multi-omics analysis, including single-cell RNA sequencing and digital spatial profiling, on LUSC specimens from seven patients with usual interstitial pneumonia (UIP). In UIP lung tissue, metaplastic basal cells arising from the transdifferentiation of alveolar type 2 (AT2) cells were increased. LUSC tumors arising within UIP exhibited molecular profiles and trajectory dynamics suggesting derivation from these metaplastic basal cells. Both UIP-affected tissue and associated tumors showed activation of Wnt signaling, particularly WNT3 expression. Additionally, enrichment of the nuclear factor erythroid 2-related factor 2 (NRF2)-linked antioxidant response was observed in LUSC within UIP. Targeting Wnt/β-catenin signaling restored the sensitivity of these stress-adapted cancer cell lines to oxidative damage. These findings suggest that LUSC within UIP originates from AT2-derived metaplastic basal cells and involves aberrant Wnt3 activation, linking fibrosis to carcinogenesis and highlighting a potential therapeutic strategy.
en-copyright=
kn-copyright=

en-aut-name=MatsuokaAtsushi
en-aut-sei=Matsuoka
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ShienKazuhiko
en-aut-sei=Shien
en-aut-mei=Kazuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TomidaShuta
en-aut-sei=Tomida
en-aut-mei=Shuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OhkiMasayoshi
en-aut-sei=Ohki
en-aut-mei=Masayoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TorigoeHidejiro
en-aut-sei=Torigoe
en-aut-mei=Hidejiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=HisamatsuKazuya
en-aut-sei=Hisamatsu
en-aut-mei=Kazuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=FujiwaraRyota
en-aut-sei=Fujiwara
en-aut-mei=Ryota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=IshimuraKosei
en-aut-sei=Ishimura
en-aut-mei=Kosei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MoriShunsuke
en-aut-sei=Mori
en-aut-mei=Shunsuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=FujiiRyunosuke
en-aut-sei=Fujii
en-aut-mei=Ryunosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=MimataAsuka
en-aut-sei=Mimata
en-aut-mei=Asuka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=OkadaKazuhiro
en-aut-sei=Okada
en-aut-mei=Kazuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=YoshichikaRyo
en-aut-sei=Yoshichika
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=YoshikawaMao
en-aut-sei=Yoshikawa
en-aut-mei=Mao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=FukumotoYuma
en-aut-sei=Fukumoto
en-aut-mei=Yuma
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=YamamotoHaruchika
en-aut-sei=Yamamoto
en-aut-mei=Haruchika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=NakajimaKumi
en-aut-sei=Nakajima
en-aut-mei=Kumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=TanakaShin
en-aut-sei=Tanaka
en-aut-mei=Shin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=SuzawaKen
en-aut-sei=Suzawa
en-aut-mei=Ken
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=MiyoshiKentaroh
en-aut-sei=Miyoshi
en-aut-mei=Kentaroh
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

en-aut-name=OkazakiMikio
en-aut-sei=Okazaki
en-aut-mei=Mikio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=21
ORCID=

en-aut-name=SugimotoSeiichiro
en-aut-sei=Sugimoto
en-aut-mei=Seiichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=22
ORCID=

en-aut-name=InoueHirofumi
en-aut-sei=Inoue
en-aut-mei=Hirofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=23
ORCID=

en-aut-name=EnnishiDaisuke
en-aut-sei=Ennishi
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=24
ORCID=

en-aut-name=ToyookaShinichi
en-aut-sei=Toyooka
en-aut-mei=Shinichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=25
ORCID=

affil-num=1
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Center for Comprehensive Genomic Medicine, Okayama University Hospital
kn-affil=

affil-num=4
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=12
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=13
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=14
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=15
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=16
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=17
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=18
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=19
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=20
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=21
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=22
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=23
en-affil=Center for Comprehensive Genomic Medicine, Okayama University Hospital
kn-affil=

affil-num=24
en-affil=Center for Comprehensive Genomic Medicine, Okayama University Hospital
kn-affil=

affil-num=25
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Oncology
kn-keyword=Oncology
en-keyword=Respiratory medicine
kn-keyword=Respiratory medicine
en-keyword=Pathology
kn-keyword=Pathology
en-keyword=Precision medicine
kn-keyword=Precision medicine
en-keyword=Target identification
kn-keyword=Target identification
en-keyword=Systems biology
kn-keyword=Systems biology
en-keyword=Cancer
kn-keyword=Cancer
en-keyword=Omics
kn-keyword=Omics
en-keyword=Transcriptomics
kn-keyword=Transcriptomics
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=20260427
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Clinical anatomy of the superior labial branch of infraorbital nerve
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The infraorbital nerve (ION), a branch of the maxillary division of the trigeminal nerve, provides sensory innervation to the midface via its terminal divisions. Among these, the superior labial branch (SLb) supplies the upper lip and adjacent mucosa, regions frequently involved in oral, maxillofacial, and cosmetic procedures. Despite its clinical importance, the anatomy of the SLb has received relatively limited attention compared with other ION branches. This review synthesizes current evidence on the SLb’s course, branching patterns, innervation, morphometry, and variations, with emphasis on its relevance to surgical practice. Anatomical studies demonstrate that the SLb is the largest terminal division of the ION, often exhibiting medial and lateral subdivisions that anastomose with neighboring nerves. Its distribution predominantly follows a vertical orientation, supplying both cutaneous and mucosal structures of the upper lip. Variability in origin, branching, and accessory foramina underscores the need for careful surgical planning. Injury to the SLb is a recognized complication of Le Fort I osteotomy, midfacial trauma, and periapical procedures, potentially leading to long-term sensory disturbances. A comprehensive understanding of the SLb enhances intraoperative nerve preservation and may reduce postoperative morbidity, highlighting its significance for clinicians operating in the midfacial region.
en-copyright=
kn-copyright=

en-aut-name=TakakuraHiroaki
en-aut-sei=Takakura
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TanaiAiri
en-aut-sei=Tanai
en-aut-mei=Airi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KunisadaYuki
en-aut-sei=Kunisada
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KikutaShogo
en-aut-sei=Kikuta
en-aut-mei=Shogo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KitagawaNorio
en-aut-sei=Kitagawa
en-aut-mei=Norio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=IbaragiSoichiro
en-aut-sei=Ibaragi
en-aut-mei=Soichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=HurMi-Sun
en-aut-sei=Hur
en-aut-mei=Mi-Sun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=AslamRizwan
en-aut-sei=Aslam
en-aut-mei=Rizwan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TubbsR. Shane
en-aut-sei=Tubbs
en-aut-mei=R. Shane
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=IwanagaJoe
en-aut-sei=Iwanaga
en-aut-mei=Joe
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of Oral and Maxillofacial Surgery, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Oral and Maxillofacial Surgery, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Oral and Maxillofacial Surgery, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Dental and Oral Medical Center, Kurume University School of Medicine
kn-affil=

affil-num=5
en-affil=Department of Oral and Maxillofacial Anatomy, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo
kn-affil=

affil-num=6
en-affil=Department of Oral and Maxillofacial Surgery, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Anatomy, Daegu Catholic University School of Medicine
kn-affil=

affil-num=8
en-affil=Department of Otolaryngology, Tulane University School of Medicine
kn-affil=

affil-num=9
en-affil=Department of Neurosurgery, Tulane Center for Clinical Neurosciences, Tulane University School of Medicine
kn-affil=

affil-num=10
en-affil=Dental and Oral Medical Center, Kurume University School of Medicine
kn-affil=
en-keyword=Anatomy
kn-keyword=Anatomy
en-keyword=Cadaver
kn-keyword=Cadaver
en-keyword=Trigeminal nerve
kn-keyword=Trigeminal nerve
en-keyword=Oral and maxillofacial
kn-keyword=Oral and maxillofacial
en-keyword=Histology
kn-keyword=Histology
END

start-ver=1.4
cd-journal=joma
no-vol=9
cd-vols=
no-issue=1
article-no=
start-page=146
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=20260205
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Structural study of monomeric and dimeric photosystem I-LHCI supercomplexes from a bryophyte
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Photosystem I (PSI) is one of the two photosystems conserved from cyanobacteria to vascular plants, and associates with multiple light-harvesting complexes (LHCs) that capture and transfer solar energy. Liverworts such as Marchantia polymorpha occupy an early evolutionary position among land plants and faced major challenges during terrestrial adaptation, including desiccation, strong light, and UV radiation. We reveal the cryo-electron microscopic structures of PSI-LHCI monomer and homodimer from the liverwort M. polymorpha at resolutions of 1.94 and 2.52 Å, respectively. The high-resolution map allows identification of the cofactors of the monomer and reveal differences between the liverwort and moss, another clade of bryophytes. The PSI-LHCI monomer-monomer is stabilized by PsaG and PsaH interactions on the stromal side, which causes the bending and twisting of the homodimer. PsaM interacts with PsaB tightly, indicating a key role of PsaM in mediating the dimerization.
en-copyright=
kn-copyright=

en-aut-name=TsaiPi-Cheng
en-aut-sei=Tsai
en-aut-mei=Pi-Cheng
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=La RoccaRomain
en-aut-sei=La Rocca
en-aut-mei=Romain
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MotoseHiroyasu
en-aut-sei=Motose
en-aut-mei=Hiroyasu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ShenJian-Ren
en-aut-sei=Shen
en-aut-mei=Jian-Ren
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=AkitaFusamichi
en-aut-sei=Akita
en-aut-mei=Fusamichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Research Institute for Interdisciplinary Science, Advanced Research Field, Okayama University
kn-affil=

affil-num=2
en-affil=Research Institute for Interdisciplinary Science, Advanced Research Field, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Biology, Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=4
en-affil=Research Institute for Interdisciplinary Science, Advanced Research Field, Okayama University
kn-affil=

affil-num=5
en-affil=Research Institute for Interdisciplinary Science, Advanced Research Field, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=123
cd-vols=
no-issue=17
article-no=
start-page=e2536813123
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=20260422
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A magnesium efflux transporter required for seed development and eating quality in rice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=As a staple food for half the world’s population, rice is an important dietary source of magnesium (Mg), an essential mineral for human health. Enhanced Mg accumulation in rice grains has also been linked to eating quality. However, the mechanisms underlying Mg transport to the grains remains poorly understood. Here, we report that OsMGR2, a member belonging to Magnesium Release (MGR) family, is required for Mg accumulation in rice grains. OsMGR2 encodes a plasma membrane-localized transporter that mediates Mg efflux. OsMGR2 is constitutively and highly expressed in the stele tissues of roots, the phloem region of both enlarged and diffused vascular bundles in nodes, and the ovular vascular trace of caryopses. Knockout of this gene results in decreased root-to-shoot translocation and altered distribution of Mg to different organs; less Mg is allocated to the second newest leaf with high Mg requirement for active photosynthesis. The osmgr2 mutants exhibit decreased Mg accumulation in the grain, which are smaller, lighter, and shriveled, but show increased accumulation in the husk. The eating quality of the mutant grains is significantly decreased compared with the wild-type rice. These results indicate that OsMGR2 plays multiple roles within the rice; facilitating the root-to-shoot Mg translocation, mediating phloem-to-xylem Mg transfer at nodes for preferential distribution to the most active leaf, and exporting Mg from maternal vascular tissues of the caryopsis to the grains, processes essential for grain development and eating quality in rice.
en-copyright=
kn-copyright=

en-aut-name=HuangSheng
en-aut-sei=Huang
en-aut-mei=Sheng
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HoriKiyosumi
en-aut-sei=Hori
en-aut-mei=Kiyosumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YamajiNaoki
en-aut-sei=Yamaji
en-aut-mei=Naoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YoshiokaYuma
en-aut-sei=Yoshioka
en-aut-mei=Yuma
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NingMin
en-aut-sei=Ning
en-aut-mei=Min
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NagayaYu
en-aut-sei=Nagaya
en-aut-mei=Yu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MiyajiTakaaki
en-aut-sei=Miyaji
en-aut-mei=Takaaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=Mitani-UenoNamiki
en-aut-sei=Mitani-Ueno
en-aut-mei=Namiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=InoueShin-ichiro
en-aut-sei=Inoue
en-aut-mei=Shin-ichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=KimJune-Sik
en-aut-sei=Kim
en-aut-mei=June-Sik
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=KashinoMiho
en-aut-sei=Kashino
en-aut-mei=Miho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=MaJian Feng
en-aut-sei=Ma
en-aut-mei=Jian Feng
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

affil-num=1
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=2
en-affil=National Institute of Crop Science, National Agriculture Research Organization
kn-affil=

affil-num=3
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=4
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=6
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Regulatory Biology, Saitama University
kn-affil=

affil-num=10
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=11
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=12
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=
en-keyword=magnesium
kn-keyword=magnesium
en-keyword=rice
kn-keyword=rice
en-keyword=transporter
kn-keyword=transporter
END

start-ver=1.4
cd-journal=joma
no-vol=29
cd-vols=
no-issue=4
article-no=
start-page=115341
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=202604
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Human iPSC cardiomyocyte patch transplantation modifies extracellular matrix and fibroblast behavior after myocardial infarction
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Myocardial infarction (MI) followed by chronic heart failure is the main cause of mortality of heart diseases. Although reparative cell transplantation therapies with pluripotent stem cell-derived cardiomyocytes (CMs) represent a promising therapeutic strategy, molecular mechanisms of the therapy remain elusive. Here, we show that transplantation of the human induced pluripotent stem cell (hiPSC)-derived CM patch onto the damaged heart after MI increases the ratio of collagen type I against collagen type III to modulate alignment of the collagen fibers at the infarcted zone. As a result, tissue elasticity of the heart is improved, and fibrosis at the remote zone is reduced. Mechanistically, we find that hiPSC-derived CM patches secrete TGF-β1, directly inducing collagen type I production in fibroblasts but not collagen type III. Our results suggest the direct effect of the transplanted CM patch on the cardiac fibroblasts to improve elasticity of the damaged heart, resulting in functional recovery after MI.
en-copyright=
kn-copyright=

en-aut-name=TorigataKosuke
en-aut-sei=Torigata
en-aut-mei=Kosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MatsuuraRyohei
en-aut-sei=Matsuura
en-aut-mei=Ryohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NagatomoFumiya
en-aut-sei=Nagatomo
en-aut-mei=Fumiya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ThihaMoe
en-aut-sei=Thiha
en-aut-mei=Moe
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HikitaTakao
en-aut-sei=Hikita
en-aut-mei=Takao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=IseokaHiroko
en-aut-sei=Iseoka
en-aut-mei=Hiroko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TakagiHiromitsu
en-aut-sei=Takagi
en-aut-mei=Hiromitsu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KoshimizuUichi
en-aut-sei=Koshimizu
en-aut-mei=Uichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=SakakimaHiroki
en-aut-sei=Sakakima
en-aut-mei=Hiroki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=IzumiSatoshi
en-aut-sei=Izumi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=HatanoAsuka
en-aut-sei=Hatano
en-aut-mei=Asuka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=BraunThomas
en-aut-sei=Braun
en-aut-mei=Thomas
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=SawaYoshiki
en-aut-sei=Sawa
en-aut-mei=Yoshiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=MiyagawaShigeru
en-aut-sei=Miyagawa
en-aut-mei=Shigeru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=NakayamaMasanori
en-aut-sei=Nakayama
en-aut-mei=Masanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

affil-num=1
en-affil=Cuorips Inc.
kn-affil=

affil-num=2
en-affil=Max Planck Institute for Heart and Lung Research, Laboratory for Cell Polarity and Organogenesis
kn-affil=

affil-num=3
en-affil=Department of Mechanical Engineering, School of Engineering, The University of Tokyo
kn-affil=

affil-num=4
en-affil=Department of Pathophysiology and Drug Discovery, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences Okayama University
kn-affil=

affil-num=5
en-affil=Department of Pathophysiology and Drug Discovery, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences Okayama University
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Surgery, Osaka University Graduate School of Medicine
kn-affil=

affil-num=7
en-affil=Daiichi Sankyo Co., Ltd.
kn-affil=

affil-num=8
en-affil=Daiichi Sankyo Co., Ltd.
kn-affil=

affil-num=9
en-affil=Department of Mechanical Engineering, School of Engineering, The University of Tokyo
kn-affil=

affil-num=10
en-affil=Department of Mechanical Engineering, School of Engineering, The University of Tokyo
kn-affil=

affil-num=11
en-affil=Department of Mechanical Engineering, School of Engineering, The University of Tokyo
kn-affil=

affil-num=12
en-affil=MaxPlanck Institute for Heart and Lung Research, Department of Cardiac Development and Remodeling
kn-affil=

affil-num=13
en-affil=Department of Cardiovascular Surgery, Osaka University Graduate School of Medicine
kn-affil=

affil-num=14
en-affil=Department of Cardiovascular Surgery, Osaka University Graduate School of Medicine
kn-affil=

affil-num=15
en-affil=Department of Pathophysiology and Drug Discovery, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences Okayama University
kn-affil=
en-keyword=cell biology
kn-keyword=cell biology
en-keyword=fibrosis
kn-keyword=fibrosis
en-keyword=stem cell research
kn-keyword=stem cell research
END

start-ver=1.4
cd-journal=joma
no-vol=80
cd-vols=
no-issue=2
article-no=
start-page=85
end-page=97
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=202604
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Effects of Nonsurgical Periodontal Treatment on Bacterial and Clinical Parameters in Down Syndrome Patients Based on 16S rRNA Gene Amplicon Sequencing
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Individuals with Down syndrome (DS) are more susceptible to periodontal disease; however, microbial changes following treatment remain insufficiently understood. This study evaluated the effects of nonsurgical periodontal therapy on clinical outcomes and oral microbiome dynamics in 6 patients with DS using 16S rRNA gene amplicon sequencing. Bacterial diversity, composition, network structure, and predicted functional pathways were analyzed using dental plaque samples. Bleeding on probing decreased significantly (p=0.047) after treatment, with a trend toward reduction in periodontal inflamed surface area (p=0.05). The abundance of Fusobacteria at the class level decreased significantly after treatment. The abundance of Mogibacterium timidum was higher in the pretreatment group than in the posttreatment group. M. timidum was positively correlated with Treponema denticola and associated with multiple bacterial taxa in the network during pretreatment. Predicted functional pathways related to aromatic compound degradation were more abundant in posttreatment samples than in pretreatment samples. An increase in the abundance of Fusobacterium and the positive correlation between T. denticola and M. timidum, together with their associations with other periodontal pathogens before treatment, may contribute to the development of periodontitis in individuals with DS. Nonsurgical periodontal therapy produces measurable clinical improvement and promotes microbial shifts in patients with DS.
en-copyright=
kn-copyright=

en-aut-name=ShibaTakahiko
en-aut-sei=Shiba
en-aut-mei=Takahiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakamoriMitsuhito
en-aut-sei=Takamori
en-aut-mei=Mitsuhito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KatagiriSayaka
en-aut-sei=Katagiri
en-aut-mei=Sayaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KobayashiRyota
en-aut-sei=Kobayashi
en-aut-mei=Ryota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KawauchiAki
en-aut-sei=Kawauchi
en-aut-mei=Aki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OhsugiYujin
en-aut-sei=Ohsugi
en-aut-mei=Yujin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=LinPeiya
en-aut-sei=Lin
en-aut-mei=Peiya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=EkuniDaisuke
en-aut-sei=Ekuni
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=EgusaMasahiko
en-aut-sei=Egusa
en-aut-mei=Masahiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=IwataTakanori
en-aut-sei=Iwata
en-aut-mei=Takanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=MaedaShigeru
en-aut-sei=Maeda
en-aut-mei=Shigeru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

affil-num=1
en-affil=Department of Periodontology, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo
kn-affil=

affil-num=2
en-affil=Department of Oral Physiology, Graduate School of Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Oral Biology, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo
kn-affil=

affil-num=4
en-affil=Department of Periodontology, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo
kn-affil=

affil-num=5
en-affil=Department of Dental Anesthesiology, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo
kn-affil=

affil-num=6
en-affil=Department of Oral Biology, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo
kn-affil=

affil-num=7
en-affil=Department of Oral Biology, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo
kn-affil=

affil-num=8
en-affil=Department of Preventive Dentistry, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=The center for Special Needs Dentistry, Medical Development Field, Okayama University
kn-affil=

affil-num=10
en-affil=Department of Periodontology, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo
kn-affil=

affil-num=11
en-affil=Department of Dental Anesthesiology, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo
kn-affil=
en-keyword=Down Syndrome
kn-keyword=Down Syndrome
en-keyword=16S rRNA Gene Amplicon Sequencing
kn-keyword=16S rRNA Gene Amplicon Sequencing
en-keyword=periodontitis
kn-keyword=periodontitis
en-keyword=nonsurgical periodontal treatment
kn-keyword=nonsurgical periodontal treatment
en-keyword=oral microbiome
kn-keyword=oral microbiome
END

start-ver=1.4
cd-journal=joma
no-vol=367
cd-vols=
no-issue=
article-no=
start-page=199714
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=202605
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Virome of the fungi associated with mushroom dry bubble disease
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Dry bubble disease, attributed to the filamentous fungus Lecanicillium fungicola (Cordycipitaceae) results in huge yield losses in mushroom (Agaricus bisporus) cultivation worldwide. The possibilities for controlling the disease using commercial fungicides are highly limited, and therefore, there is an increasing demand for novel, alternative means of pest management. Our research objective was the comprehensive examination of viruses in the causal agents of dry bubble disease, which may open up an avenue for its virocontrol in the future. Out of 57 fungal isolates obtained from dry bubble-affected A. bisporus crops in various countries, 47 (82%) were confirmed by ITS (Internal Transcribed Spacer) sequence analysis as L. fungicola. In addition, different members of the genera Akanthomyces and Simplicillium (7 and 3 isolates, respectively), yet unknown to cause dry bubble symptoms, have also been detected. Cellulose column chromatography revealed the presence of double-stranded (ds) RNA in seven L. fungicola and three Akanthomyces sp. isolates, suggesting viral infection. The ten dsRNA-positive and eight randomly selected dsRNA-negative fungal strains were subjected to rRNA-depletion high-throughput RNA-sequencing analysis. The presence of seven new viruses representing four new species in the established families, Partitiviridae, Polymycoviridae, Botourmiaviridae and the narna-like virus group, and three previously established/proposed species in the families Chrysoviridae and “Mycovirgaviridae” were confirmed. The impact of the detected and identified viruses on their host fungi, and their potential applicability for virocontrol purposes will be examined in the future. This study provides the first detailed report on viruses of mushroom pathogenic fungi.
en-copyright=
kn-copyright=

en-aut-name=HatvaniLóránt
en-aut-sei=Hatvani
en-aut-mei=Lóránt
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HisanoSakae
en-aut-sei=Hisano
en-aut-mei=Sakae
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KondoHideki
en-aut-sei=Kondo
en-aut-mei=Hideki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SugaharaHitomi
en-aut-sei=Sugahara
en-aut-mei=Hitomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TelengechPaul
en-aut-sei=Telengech
en-aut-mei=Paul
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ShahiSabitree
en-aut-sei=Shahi
en-aut-mei=Sabitree
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=IbiangSarah Remi
en-aut-sei=Ibiang
en-aut-mei=Sarah Remi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KocsubéSándor
en-aut-sei=Kocsubé
en-aut-mei=Sándor
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KartaliTünde
en-aut-sei=Kartali
en-aut-mei=Tünde
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=FitzpatrickDavid A.
en-aut-sei=Fitzpatrick
en-aut-mei=David A.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=GroganHelen
en-aut-sei=Grogan
en-aut-mei=Helen
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=SuzukiNobuhiro
en-aut-sei=Suzuki
en-aut-mei=Nobuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

affil-num=1
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=2
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=3
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=4
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=5
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=6
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=7
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Biotechnology and Microbiology, Faculty of Science and Informatics, University of Szeged
kn-affil=

affil-num=9
en-affil=Department of Biotechnology and Microbiology, Faculty of Science and Informatics, University of Szeged
kn-affil=

affil-num=10
en-affil=Genome Evolution Laboratory, Department of Biology, Maynooth University
kn-affil=

affil-num=11
en-affil=Teagasc Food Research Center, Horticulture Development Department
kn-affil=

affil-num=12
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=
en-keyword=Lecanicillium fungicola
kn-keyword=Lecanicillium fungicola
en-keyword=Agaricus bisporus
kn-keyword=Agaricus bisporus
en-keyword=Akanthomyces
kn-keyword=Akanthomyces
en-keyword=Simplicillium
kn-keyword=Simplicillium
en-keyword=dsRNA
kn-keyword=dsRNA
en-keyword=Myovirus
kn-keyword=Myovirus
en-keyword=Fungal virus
kn-keyword=Fungal virus
en-keyword=Mycovirgaviridae
kn-keyword=Mycovirgaviridae
en-keyword=Partitiviridae
kn-keyword=Partitiviridae
en-keyword=Polymycoviridae
kn-keyword=Polymycoviridae
en-keyword=Botourmiaviridae
kn-keyword=Botourmiaviridae
en-keyword=Splipalmiviridae
kn-keyword=Splipalmiviridae
en-keyword=Narna-like virus
kn-keyword=Narna-like virus
END

start-ver=1.4
cd-journal=joma
no-vol=380
cd-vols=
no-issue=
article-no=
start-page=114924
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=202604
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Constitutive activation of MC1R in the large-billed crow (Corvus macrorhynchos) and its potential role in black plumage
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Melanin-based plumage coloration in birds is largely regulated by the melanocortin 1 receptor (MC1R), a G protein–coupled receptor that promotes eumelanin synthesis via cAMP signaling. In domestic chickens, constitutively activating mutations such as the MC1R^E (E92K) allele cause melanistic phenotypes, demonstrating that persistent MC1R activation can drive generalized darkening. However, to our knowledge, no experimental study has directly demonstrated constitutive MC1R activation in wild birds exhibiting uniformly black plumage. We investigated the sequence and signaling properties of MC1R from the Large-billed Crow (Corvus macrorhynchos), a species with strongly eumelanin-dominant plumage. Crow MC1R exhibited elevated basal cAMP signaling and minimal responsiveness to α-melanocyte-stimulating hormone (α-MSH) in both stable Chinese hamster ovary (CHO-K1) cells and transient CRE-luciferase assays in HEK293T cells, demonstrating ligand-independent activation comparable to that observed in the melanizing chicken MC1R^E (E92K) allele. Comparative sequence analysis identified multiple substitutions conserved across Corvus species. Among these, E12K and E18K were functionally evaluated based on prior associations with melanism in other birds. Although E12K modestly increased basal signaling in chicken MC1R, E18K alone or in combination with E12K did not reproduce crow-level constitutive activity, and reciprocal substitutions in crow MC1R failed to abolish ligand-independent activation. These findings demonstrate that crow MC1R possesses constitutive activity and suggest that this phenotype reflects lineage-specific modifications rather than a single activating substitution. Our results provide experimental evidence that constitutive MC1R activation is a plausible molecular mechanism that may contribute to the black plumage in the Large-billed Crow, although a direct causal relationship remains to be established.
en-copyright=
kn-copyright=

en-aut-name=NakanoSaya
en-aut-sei=Nakano
en-aut-mei=Saya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TashiroYuichi
en-aut-sei=Tashiro
en-aut-mei=Yuichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=FukuchiHibiki
en-aut-sei=Fukuchi
en-aut-mei=Hibiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=AizawaSayaka
en-aut-sei=Aizawa
en-aut-mei=Sayaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TakeuchiSakae
en-aut-sei=Takeuchi
en-aut-mei=Sakae
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=4
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=5
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=
en-keyword=MC1R
kn-keyword=MC1R
en-keyword=Constitutive activation
kn-keyword=Constitutive activation
en-keyword=Ligand-independent signaling
kn-keyword=Ligand-independent signaling
en-keyword=Melanism
kn-keyword=Melanism
en-keyword=Plumage coloration
kn-keyword=Plumage coloration
en-keyword=Corvus macrorhynchos
kn-keyword=Corvus macrorhynchos
END

start-ver=1.4
cd-journal=joma
no-vol=29
cd-vols=
no-issue=4
article-no=
start-page=115137
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=202604
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Multifaceted role of POU5F1P1 in regulating its parental stem cell gene, POU5F1
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The human-specific retrogene POU5F1P1 (OCT4-Pseudogene1; OCT4-PG1), derived from stem cell factor POU5F1 (OCT4A), is predicted to encode an OCT4A-like protein; however, its function remains unclear. This study investigated OCT4-PG1 expression, translational control, and its role in endometrial cancer and stem cell regulation. Quantitative analyses revealed that elevated OCT4A, but not OCT4-PG1, expression correlated with clinical risk factors associated with poor prognosis in patients with endometrial cancer. OCT4-PG1 is under strong translational suppression mediated by its untranslated region and does not function as a protein under normal conditions. Instead, it acts as a non-coding RNA that suppresses OCT4A translation. Structural analyses showed that a single amino acid deletion (Gln259) destabilizes the OCT4-PG1 protein, thereby preventing its tumorigenic and transcriptional functions. Nevertheless, OCT4-PG1 forms heterodimers with OCT4A or SOX2, enhancing the regulatory activity of OCT4A. These findings highlight the regulatory role of pseudogenes in cancer and stem cell biology, with implications for therapies targeting OCT4A-related pathways.
en-copyright=
kn-copyright=

en-aut-name=IrieKyohei
en-aut-sei=Irie
en-aut-mei=Kyohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KosakaMitsuko
en-aut-sei=Kosaka
en-aut-mei=Mitsuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MizunoNobuhiko
en-aut-sei=Mizuno
en-aut-mei=Nobuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OmaeRyo
en-aut-sei=Omae
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NakataniYoshimasa
en-aut-sei=Nakatani
en-aut-mei=Yoshimasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OoSandi Myat Noe
en-aut-sei=Oo
en-aut-mei=Sandi Myat Noe
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MasuyamaHisashi
en-aut-sei=Masuyama
en-aut-mei=Hisashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KawaguchiAyano
en-aut-sei=Kawaguchi
en-aut-mei=Ayano
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Human Morphology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Human Morphology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Human Morphology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Human Morphology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Human Morphology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Human Morphology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Obstetrics and Gynecology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Human Morphology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=2
article-no=
start-page=bio062463
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=20260215
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Gap junction-mediated signaling coordinates Rhodopsin coupling for Drosophila color vision
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The Drosophila compound eye is composed of approximately 800 ommatidia, and every ommatidium contains eight photoreceptor cells, six outer cells (R1-R6) and two inner cells (R7 and R8), and accessory cells (cone and pigment cells). The expression of rhodopsin genes in R7 and R8 is highly coordinated through an instructive signal from R7 to R8. The activity of the homeodomain protein Defective proventriculus in R1 is also required to transmit this instructive signal, suggesting that cell–cell communication between R7, R1, and R8 is important to generate the pattern of Rh expression in R7/R8 (Rhodopsin coupling). As cell junctions play crucial roles in maintaining the structural and functional integrity of tissues, we tested whether cell junction proteins are involved in the interactions between photoreceptor cells. Here, we demonstrate that gap junction proteins innexin 2 and innexin 7 in accessory cells are necessary for transmitting signals from R7 to R8. In addition, Notch-mediated accessory cell development and Rhodopsin coupling in R7/R8 are highly correlated. Our results provide evidence that functional coupling of two different neurons, R7 and R8, is established through gap junction-mediated signaling from adjacent accessory cells.
en-copyright=
kn-copyright=

en-aut-name=ZhangXuanshuo
en-aut-sei=Zhang
en-aut-mei=Xuanshuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ShinjoRyoki
en-aut-sei=Shinjo
en-aut-mei=Ryoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KitamataManabu
en-aut-sei=Kitamata
en-aut-mei=Manabu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OtsuneShinichi
en-aut-sei=Otsune
en-aut-mei=Shinichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NakagoshiHideki
en-aut-sei=Nakagoshi
en-aut-mei=Hideki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Division of Biological Sciences, Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Division of Biological Sciences, Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=3
en-affil=Division of Health Science, Advanced Comprehensive Research Organization, Teikyo University
kn-affil=

affil-num=4
en-affil=Division of Biological Sciences, Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=5
en-affil=Division of Biological Sciences, Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=
en-keyword=Drosophila
kn-keyword=Drosophila
en-keyword=Eye
kn-keyword=Eye
en-keyword=Gap junction
kn-keyword=Gap junction
en-keyword=Innexin
kn-keyword=Innexin
en-keyword=Opsin
kn-keyword=Opsin
END

start-ver=1.4
cd-journal=joma
no-vol=49
cd-vols=
no-issue=2
article-no=
start-page=364
end-page=370
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=20260221
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Functional Transport Properties of Human Zinc Transporter 1: Kinetics and pH-Dependency
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Intracellular zinc (Zn2+) homeostasis is essential for physiological and pathological processes and is strictly regulated by Zn2+ transporters. Zinc transporter 1 (ZnT1) is a ubiquitously expressed plasma membrane-localized Zn transporter that exports Zn2+ from the cytoplasm to the extracellular space. However, the functional transport properties regarding kinetics and driving forces of ZnT1 remain debatable. In this study, we established a cell-free proteoliposome assay system and demonstrated that ZnT1 transports Zn2+ with high affinity in pH-dependent and pH-independent manners. The Km and Vmax of pH-dependent Zn2+ transport were 0.40 μM and 15.13 nmol/min/mg protein, and those of pH-independent Zn2+ transport were 0.52 μM and 8.88 nmol/min/mg protein (low concentrations of Zn2+), 3.02 μM and 17.59 nmol/min/mg protein (high concentrations of Zn2+), respectively, suggesting biphasic kinetic components of Zn2+ transport. Even without pH gradient formation, ZnT1 exhibits potent Zn2+ transport activity. In pH dependency, Zn2+ transport activity was higher at an inside pH of 6.0 than at 6.5–7.5 for proteoliposomes, despite the same ΔpH of 0.5–1.5. The Zn2+ transport activity decreased at an outside pH of 8.0, despite an increase in ΔpH. Although previous studies have proposed that ZnT1-mediated Zn2+ transport activity is driven by a calcium (Ca2+) gradient and not by a pH gradient, Ca2+ does not enhance Zn2+ transport activity in the presence or absence of a pH gradient. These results strongly suggest that ZnT1 protein transports Zn2+ optimally at a specific pH and exports excess intracellular Zn2+ even without ΔpH.
en-copyright=
kn-copyright=

en-aut-name=YoshiokaYuma
en-aut-sei=Yoshioka
en-aut-mei=Yuma
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MiyajiTakaaki
en-aut-sei=Miyaji
en-aut-mei=Takaaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

affil-num=1
en-affil=Department of Molecular Membrane Biology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Molecular Membrane Biology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=zinc transporter 1
kn-keyword=zinc transporter 1
en-keyword=SLC30A1
kn-keyword=SLC30A1
en-keyword=zinc
kn-keyword=zinc
en-keyword=pH
kn-keyword=pH
en-keyword=proteoliposome
kn-keyword=proteoliposome
END

start-ver=1.4
cd-journal=joma
no-vol=27
cd-vols=
no-issue=2
article-no=
start-page=831
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=20260114
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Porphyromonas gingivalis Vesicles Control Osteoclast–Macrophage Lineage Fate
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Porphyromonas gingivalis (Pg), a keystone pathogen of chronic periodontitis, releases outer membrane vesicles (OMVs) that act as nanoscale vehicles to disseminate virulence factors within periodontal tissues and systemically beyond the oral cavity. Although Pg-OMVs are increasingly recognized as critical mediators of host–pathogen interactions, their effects on the differentiation and function of monocyte–macrophage/osteoclast lineage cells remain unclear. Here, we examined the impact of Pg-OMVs on the differentiation of RAW264.7 monocyte/macrophage-like cells into osteoclasts (OC) and/or macrophages (MΦ) in the presence of receptor activator of nuclear factor-κB ligand (RANKL). OMVs were isolated from Pg W83 and applied to RANKL-primed RAW264.7 cells using three distinct stimulation schedules: (1) simultaneous treatment with Pg-OMVs and RANKL at Day 0; (2) RANKL priming at Day 0 followed by Pg-OMV stimulation at Day 1; and (3) RANKL priming at Day 0 followed by Pg-OMV stimulation at Day 3. In all schedules, cells were cultured for 7 days from the initial RANKL exposure. Remarkably, simultaneous exposure to Pg-OMVs and RANKL (Schedule 1) markedly suppressed osteoclastogenesis (OC-genesis) while promoting M1 macrophage polarization. In contrast, delayed Pg-OMV stimulation of RANKL-primed cells (Schedules 2 and 3) significantly enhanced OC-genesis while reducing M1 polarization. These schedule-dependent effects were consistent with altered expression of osteoclastogenic markers, including dc-stamp, oc-stamp, nfatc1, and acp5. Importantly, a monoclonal antibody against OC-STAMP counteracted the Pg-OMV-induced upregulation of OC-genesis in Schedules 2 and 3. Furthermore, levels of Pg-OMV phagocytosis were inversely correlated with osteoclast formation. Finally, co-stimulation with RANKL and Pg-OMVs (Schedule 1) enhanced macrophage migratory capacity, whereas delayed stimulation with Pg-OMVs (Schedules 2 and 3) did not. Collectively, these findings indicate that Pg-OMVs exert stage-specific effects on the OC/MΦ lineage: stimulation at early stages of RANKL priming suppresses OC-genesis and promotes M1 polarization, whereas stimulation at later stages enhances OC-genesis without inducing M1 differentiation. Thus, Pg-OMVs may critically influence the fate of the OC/MΦ unit in periodontal lesions, contributing to disease progression and tissue destruction.
en-copyright=
kn-copyright=

en-aut-name=LeonElizabeth
en-aut-sei=Leon
en-aut-mei=Elizabeth
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakamuraShin
en-aut-sei=Nakamura
en-aut-mei=Shin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ShindoSatoru
en-aut-sei=Shindo
en-aut-mei=Satoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=PastoreMaria Rita
en-aut-sei=Pastore
en-aut-mei=Maria Rita
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KumagaiTomoki
en-aut-sei=Kumagai
en-aut-mei=Tomoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=HeidariAlireza
en-aut-sei=Heidari
en-aut-mei=Alireza
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=AbdolahiniaElaheh Dalir
en-aut-sei=Abdolahinia
en-aut-mei=Elaheh Dalir
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=UedaTomoya
en-aut-sei=Ueda
en-aut-mei=Tomoya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MemidaTakumi
en-aut-sei=Memida
en-aut-mei=Takumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=Duran-PinedoAna
en-aut-sei=Duran-Pinedo
en-aut-mei=Ana
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=Frias-LopezJorge
en-aut-sei=Frias-Lopez
en-aut-mei=Jorge
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=HanXiaozhe
en-aut-sei=Han
en-aut-mei=Xiaozhe
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=ChenXin
en-aut-sei=Chen
en-aut-mei=Xin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=HuangShengyuan
en-aut-sei=Huang
en-aut-mei=Shengyuan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=CaoGuoqin
en-aut-sei=Cao
en-aut-mei=Guoqin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=RuizSunniva
en-aut-sei=Ruiz
en-aut-mei=Sunniva
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=PotempaJan
en-aut-sei=Potempa
en-aut-mei=Jan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=KawaiToshihisa
en-aut-sei=Kawai
en-aut-mei=Toshihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

affil-num=1
en-affil=Department of Oral Science and Translational Research, College of Dental Medicine, Nova Southeastern University
kn-affil=

affil-num=2
en-affil=Department of Periodontics and Endodontics, Division of Dentistry, Okayama University Hospital
kn-affil=

affil-num=3
en-affil=Department of Oral Science and Translational Research, College of Dental Medicine, Nova Southeastern University
kn-affil=

affil-num=4
en-affil=Department of Oral Science and Translational Research, College of Dental Medicine, Nova Southeastern University
kn-affil=

affil-num=5
en-affil=Department of Oral Science and Translational Research, College of Dental Medicine, Nova Southeastern University
kn-affil=

affil-num=6
en-affil=Department of Oral Science and Translational Research, College of Dental Medicine, Nova Southeastern University
kn-affil=

affil-num=7
en-affil=Department of Oral Science and Translational Research, College of Dental Medicine, Nova Southeastern University
kn-affil=

affil-num=8
en-affil=Department of Oral Science and Translational Research, College of Dental Medicine, Nova Southeastern University
kn-affil=

affil-num=9
en-affil=Department of Oral Science and Translational Research, College of Dental Medicine, Nova Southeastern University
kn-affil=

affil-num=10
en-affil=Department of Oral Biology, College of Dentistry, University of Florida
kn-affil=

affil-num=11
en-affil=Department of Oral Biology, College of Dentistry, University of Florida
kn-affil=

affil-num=12
en-affil=Department of Oral Science and Translational Research, College of Dental Medicine, Nova Southeastern University
kn-affil=

affil-num=13
en-affil=Department of Oral Science and Translational Research, College of Dental Medicine, Nova Southeastern University
kn-affil=

affil-num=14
en-affil=Department of Oral Science and Translational Research, College of Dental Medicine, Nova Southeastern University
kn-affil=

affil-num=15
en-affil=Department of Oral Science and Translational Research, College of Dental Medicine, Nova Southeastern University
kn-affil=

affil-num=16
en-affil=Department of Oral Science and Translational Research, College of Dental Medicine, Nova Southeastern University
kn-affil=

affil-num=17
en-affil=Department of Oral Immunology and Infectious Diseases, School of Dentistry, University of Louisville
kn-affil=

affil-num=18
en-affil=Department of Oral Science and Translational Research, College of Dental Medicine, Nova Southeastern University, Fort Lauderdale, FL 33314, USA
kn-affil=
en-keyword=Porphyromonas gingivalis
kn-keyword=Porphyromonas gingivalis
en-keyword=outer membrane vesicle
kn-keyword=outer membrane vesicle
en-keyword=periodontitis pathogenesis
kn-keyword=periodontitis pathogenesis
en-keyword=macrophage polarization
kn-keyword=macrophage polarization
en-keyword=osteoclastogenesis
kn-keyword=osteoclastogenesis
en-keyword=OC/MΦ unit
kn-keyword=OC/MΦ unit
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=20260318
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Suppression of salt-enhanced apoplastic flow by salicylic acid in rice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Salinity enhances apoplastic flow, resulting in an increment of Na+ uptake and a lower K+/Na+ ratio. Salicylic acid (SA) plays an important role in improving salinity tolerance in plants. The effect of exogenous SA on apoplastic flow in salt-treated rice seedlings was studied using an apoplastic tracer, 8-hydroxy-1,3,6-pyrenetrisulphonic acid (PTS) in light. Application of NaCl at 25 mM to the hydroponic solution significantly increased PTS uptake, while 25 mM NaCl did not affect seedling growth. Application of 25 mM NaNO3 increased PTS uptake to the same degree. Salinity significantly increased sodium (Na+) content but had no significant effect on potassium (K+) content, resulting in a lower K+/Na+ ratio. The application of SA at 0.05 mM and 0.1 mM to the hydroponic solution reduced Na-enhanced PTS uptake. Salicylic acid at 0.05 mM and 0.1 mM significantly reduced Na+ content and slightly increased K+ content in the shoots of rice seedlings, resulting in a higher K+/Na+ ratio. However, SA at up to 0.1 mM did not increase SA contents in shoots under salt stress. These results suggest that exogenous SA reduces Na+ uptake by suppressing Na+-enhanced apoplastic flow in rice seedlings. These findings provide insight into modulation of Na+ transport pathways from roots to shoots by SA and may allow us to utilize brackish water for rice cultivation and to improve salt-tolerant rice through suppression of salt-enhanced apoplastic flow by chemicals such as salicylic acid.
en-copyright=
kn-copyright=

en-aut-name=GalibMd. Asadulla Al
en-aut-sei=Galib
en-aut-mei=Md. Asadulla Al
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ZhaoMaoxiang
en-aut-sei=Zhao
en-aut-mei=Maoxiang
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NakamuraToshiyuki
en-aut-sei=Nakamura
en-aut-mei=Toshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NakamuraYoshimasa
en-aut-sei=Nakamura
en-aut-mei=Yoshimasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HiraiYoshihiko
en-aut-sei=Hirai
en-aut-mei=Yoshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NakashimaYoshitaka
en-aut-sei=Nakashima
en-aut-mei=Yoshitaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MunemasaShintaro
en-aut-sei=Munemasa
en-aut-mei=Shintaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MoriIzumi C.
en-aut-sei=Mori
en-aut-mei=Izumi C.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MurataYoshiyuki
en-aut-sei=Murata
en-aut-mei=Yoshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=4
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=5
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=6
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=7
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=8
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=9
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
en-keyword=Apoplastic flow
kn-keyword=Apoplastic flow
en-keyword=Salicylic acid
kn-keyword=Salicylic acid
en-keyword=Rice
kn-keyword=Rice
en-keyword=Salinity
kn-keyword=Salinity
en-keyword=Trisodium-8-hydroxy-1,3,6-pyrenetrisulphonic acid
kn-keyword=Trisodium-8-hydroxy-1,3,6-pyrenetrisulphonic acid
END

start-ver=1.4
cd-journal=joma
no-vol=135
cd-vols=
no-issue=
article-no=
start-page=103134
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=202605
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Regulation of brain-specific kinases 1 and 2 (BRSK1/2) by Ca2+/calmodulin
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=We conducted a genome-wide calmodulin (CaM) interaction screening of 462 GST-fused human protein kinases to identify novel CaM-dependent protein kinases (CaMKs). In addition to known CaMKs, including myosin light chain kinases, CaMK2γ, and death-associated kinase 2, we identified the brain-specific protein kinase 2 (BRSK2, also known as SAD-A) as a novel CaM interactant. Proximity biotinylation and CaM–sepharose chromatography assays revealed that rat BRSK isoforms (BRSK1/2) interact with CaM in a Ca2+-dependent manner in vitro. We found that CaM suppresses the activation-loop phosphorylation of BRSK1 (at Thr189) and BRSK2 (at Thr175) by liver kinase B1 (LKB1), an activating kinase, in a Ca2+-dependent manner (IC50 of ∼7 µM), thereby inhibiting BRSK activation. LKB1-catalyzed phosphorylation of the catalytic domain mutant of BRSK1 (residues 1–294) at Thr189 was suppressed by the addition of Ca2+/CaM, consistent with direct CaM binding of the kinase domain, as well as wild-type BRSK1. We confirmed that the LKB1 activity was not directly suppressed by Ca2+/CaM, supporting the hypothesis that the direct interaction of Ca2+/CaM with the kinase domain blocks the phosphorylation/activation of BRSK1/2 by LKB1. The kinase activity and PP2Cα-catalyzed dephosphorylation of LKB1-phosphorylated BRSK1 were not altered by Ca2+/CaM, although it was demonstrated to bind to Ca2+/CaM like that of unphosphorylated BRSK1. This unrecognized mechanism of BRSK1/2 regulation, involving the direct role of Ca2+/CaM binding, which inhibits phosphorylation/activation by LKB1, may open a new Ca2+ signal transduction pathway in neurons.
en-copyright=
kn-copyright=

en-aut-name=WashidaNaoyuki
en-aut-sei=Washida
en-aut-mei=Naoyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KataokaMoe
en-aut-sei=Kataoka
en-aut-mei=Moe
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=BrunAnna R.
en-aut-sei=Brun
en-aut-mei=Anna R.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TakezakiUryu
en-aut-sei=Takezaki
en-aut-mei=Uryu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HijikawaKo
en-aut-sei=Hijikawa
en-aut-mei=Ko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YamauchiHaruki
en-aut-sei=Yamauchi
en-aut-mei=Haruki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=OhtsukaSatomi
en-aut-sei=Ohtsuka
en-aut-mei=Satomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MagariMasaki
en-aut-sei=Magari
en-aut-mei=Masaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MorishitaRyo
en-aut-sei=Morishita
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=TokumitsuHiroshi
en-aut-sei=Tokumitsu
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=
kn-affil=

affil-num=2
en-affil=Department of Applied Chemistry and Biotechnology, Faculty of Engineering, Okayama University
kn-affil=

affil-num=3
en-affil=Applied Cell Biology, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=4
en-affil=Applied Cell Biology, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Applied Chemistry and Biotechnology, Faculty of Engineering, Okayama University
kn-affil=

affil-num=6
en-affil=Applied Cell Biology, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=7
en-affil=Applied Cell Biology, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=8
en-affil=Applied Cell Biology, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=9
en-affil=CellFree Sciences Co., Ltd.
kn-affil=

affil-num=10
en-affil=Applied Cell Biology, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
en-keyword=BRSK1
kn-keyword=BRSK1
en-keyword=BRSK2
kn-keyword=BRSK2
en-keyword=calmodulin
kn-keyword=calmodulin
en-keyword=LKB1
kn-keyword=LKB1
en-keyword=phosphorylation
kn-keyword=phosphorylation
en-keyword=Ca2+
kn-keyword=Ca2+
en-keyword=CaM-dependent protein kinase
kn-keyword=CaM-dependent protein kinase
END

start-ver=1.4
cd-journal=joma
no-vol=6
cd-vols=
no-issue=3
article-no=
start-page=e202500639
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=202603
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=PPy‐Coated Wire Actuators for the Micromechanostimulation of Cells: Fabrication and Characterization
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Cellular mechanotransduction signals play a crucial role in physiological and pathological conditions, including skeletal disorders. Although various systems exist to mechanically stimulate cultured cells, most are constrained by incubator incompatibility, limited physiological relevance, nonuniform stimulation, or complexity. The objective of this article is to develop and validate a compact, incubator-compatible tool capable of delivering localized and physiologically relevant mechanical stimulation to small cell populations. Here, we introduce a polypyrrole-based wire-shaped microactuator designed to induce localized mechanical stress to adjacent cells. These wire-shaped microactuators are biocompatible, easy-to-use, and compact for use within standard in vitro cell culture systems. Using a noncontact optical method, we characterize the actuation of polypyrrole-coated wires in an aqueous NaDBS electrolyte, showing radial expansion of 1.5–8 µm depending on the deposited polypyrrole film thickness, comparable to cellular dimensions. Next, the actuation is confirmed to be robust and stable to use in cell culture media at physiological temperature. To evaluate biological relevance, osteoblastic KUSA-A1 cells are mechanically stimulated inside the incubator and transcriptomic changes are assessed. Mechanical stimulation resulted in upregulation of genes previously associated with mechanotransduction, including Fos and Fosb. Additionally, several uncharacterized long noncoding RNAs are differentially expressed, suggesting potential novel players in the mechanotransduction pathway.
en-copyright=
kn-copyright=

en-aut-name=Ortega‐SantosAmaia B.
en-aut-sei=Ortega‐Santos
en-aut-mei=Amaia B.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HayanoSatoru
en-aut-sei=Hayano
en-aut-mei=Satoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HaraEmilio Satoshi
en-aut-sei=Hara
en-aut-mei=Emilio Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MartínezJose G.
en-aut-sei=Martínez
en-aut-mei=Jose G.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KamiokaHiroshi
en-aut-sei=Kamioka
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=JagerEdwin W. H.
en-aut-sei=Jager
en-aut-mei=Edwin W. H.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Sensor and Actuator Systems, Department of Physics Chemistry and Biology (IFM), Linköping University
kn-affil=

affil-num=2
en-affil=Department of Orthodontics, Okayama University Hospital
kn-affil=

affil-num=3
en-affil=Advanced Research Center for Oral and Craniofacial Sciences Dental School, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Sensor and Actuator Systems, Department of Physics Chemistry and Biology (IFM), Linköping University
kn-affil=

affil-num=5
en-affil=Department of Orthodontics, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Sensor and Actuator Systems, Department of Physics Chemistry and Biology (IFM), Linköping University
kn-affil=
en-keyword=conducting polymers
kn-keyword=conducting polymers
en-keyword=mechanotransduction
kn-keyword=mechanotransduction
en-keyword=osteoblasts
kn-keyword=osteoblasts
en-keyword=polypyrrole
kn-keyword=polypyrrole
en-keyword=RNA sequencing
kn-keyword=RNA sequencing
en-keyword=soft-microactuators
kn-keyword=soft-microactuators
END

start-ver=1.4
cd-journal=joma
no-vol=19
cd-vols=
no-issue=2
article-no=
start-page=dmm052605
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=20260201
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A genetic model of congenital intestinal atresia implicates Mypt1 in epithelial organisation
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Congenital intestinal atresia (IA) is a birth defect characterised by the absence or closure of part of the intestine. Although genetic factors are implicated, mechanistic understanding has been hindered by the lack of suitable animal models. Here, we describe a medaka (Oryzias latipes) mutant, generated by N-ethyl-N-nitrosourea (ENU) mutagenesis, that develops IA during embryogenesis. Positional cloning identified a nonsense mutation in mypt1, encoding myosin phosphatase target subunit 1. Mutant embryos exhibited ectopic accumulation of F-actin and phosphorylated myosin regulatory light chain (Mrlc) in the intestinal epithelium, consistent with disrupted actomyosin regulation. These cytoskeletal abnormalities were accompanied by epithelial disorganisation, without notable alterations in cell proliferation, motility or apoptosis. Inhibition of myh11a, encoding smooth muscle (SM) myosin heavy chain, ameliorated the IA phenotype, whereas blebbistatin treatment completely rescued the defect, suggesting a non-contractile role prior to SM maturation. Together, these findings demonstrate that mypt1 loss disrupts intestinal morphogenesis through actomyosin dysregulation. Given the recent clinical identification of IA associated with MYPT1 variants, this medaka model offers a valuable platform to investigate the developmental and molecular basis of MYPT1-associated IA in humans.
en-copyright=
kn-copyright=

en-aut-name=KobayashiDaisuke
en-aut-sei=Kobayashi
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=UrasakiAkihiro
en-aut-sei=Urasaki
en-aut-mei=Akihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KimuraTetsuaki
en-aut-sei=Kimura
en-aut-mei=Tetsuaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=AnsaiSatoshi
en-aut-sei=Ansai
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MatsuoKazuhiko
en-aut-sei=Matsuo
en-aut-mei=Kazuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YokoiHayato
en-aut-sei=Yokoi
en-aut-mei=Hayato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TakashimaShigeo
en-aut-sei=Takashima
en-aut-mei=Shigeo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KitagawaTadao
en-aut-sei=Kitagawa
en-aut-mei=Tadao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KageTakahiro
en-aut-sei=Kage
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=NaritaTakanori
en-aut-sei=Narita
en-aut-mei=Takanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=JindoTomoko
en-aut-sei=Jindo
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=KinoshitaMasato
en-aut-sei=Kinoshita
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=NaruseKiyoshi
en-aut-sei=Naruse
en-aut-mei=Kiyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=NakajimaYoshiro
en-aut-sei=Nakajima
en-aut-mei=Yoshiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=ShigetaMasaki
en-aut-sei=Shigeta
en-aut-mei=Masaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=SakakiShinichiro
en-aut-sei=Sakaki
en-aut-mei=Shinichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=InoueSatoshi
en-aut-sei=Inoue
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=SabaRie
en-aut-sei=Saba
en-aut-mei=Rie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=YamadaKei
en-aut-sei=Yamada
en-aut-mei=Kei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=YokoyamaTakahiko
en-aut-sei=Yokoyama
en-aut-mei=Takahiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

en-aut-name=IshikawaYuji
en-aut-sei=Ishikawa
en-aut-mei=Yuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=21
ORCID=

en-aut-name=ArakiKazuo
en-aut-sei=Araki
en-aut-mei=Kazuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=22
ORCID=

en-aut-name=SagaYumiko
en-aut-sei=Saga
en-aut-mei=Yumiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=23
ORCID=

en-aut-name=TakedaHiroyuki
en-aut-sei=Takeda
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=24
ORCID=

en-aut-name=YashiroKenta
en-aut-sei=Yashiro
en-aut-mei=Kenta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=25
ORCID=

affil-num=1
en-affil=Department of Anatomy and Developmental Biology, Kyoto Prefectural University of Medicine
kn-affil=

affil-num=2
en-affil=Department of Anatomy and Developmental Biology, Kyoto Prefectural University of Medicine
kn-affil=

affil-num=3
en-affil=Medical Genome Center, Research Institute, National Center for Geriatrics and Gerontology
kn-affil=

affil-num=4
en-affil=Ushimado Marine Institute, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Anatomy and Developmental Biology, Kyoto Prefectural University of Medicine
kn-affil=

affil-num=6
en-affil=Graduate School of Agricultural Science, Tohoku University
kn-affil=

affil-num=7
en-affil=Institute for Glyco-core Research (iGCORE)/Life Science Research Centre, Gifu University
kn-affil=

affil-num=8
en-affil=Program in Environmental Management, Graduate School of Agriculture, Kindai University
kn-affil=

affil-num=9
en-affil=Department of Biological Sciences, Graduate School of Science, The University of Tokyo
kn-affil=

affil-num=10
en-affil=Laboratory of Molecular Biology, Department of Veterinary Medicine, College of Bioresource Sciences, Nihon University
kn-affil=

affil-num=11
en-affil=Department of Biological Sciences, Graduate School of Science, The University of Tokyo
kn-affil=

affil-num=12
en-affil=Department of Applied Biosciences, Graduate School of Agriculture, Kyoto University
kn-affil=

affil-num=13
en-affil=Laboratory of Bioresources, National Institute for Basic Biology
kn-affil=

affil-num=14
en-affil=Department of Anatomy and Developmental Biology, Kyoto Prefectural University of Medicine
kn-affil=

affil-num=15
en-affil=Department of Anatomy and Developmental Biology, Kyoto Prefectural University of Medicine
kn-affil=

affil-num=16
en-affil=Department of Anatomy and Developmental Biology, Kyoto Prefectural University of Medicine
kn-affil=

affil-num=17
en-affil=Department of Anatomy and Developmental Biology, Kyoto Prefectural University of Medicine
kn-affil=

affil-num=18
en-affil=Department of Radiology, Kyoto Prefectural University of Medicine
kn-affil=

affil-num=19
en-affil=Department of Radiology, Kyoto Prefectural University of Medicine
kn-affil=

affil-num=20
en-affil=Department of Anatomy and Developmental Biology, Kyoto Prefectural University of Medicine
kn-affil=

affil-num=21
en-affil=Research Centre for Radiation Protection, National Institute of Radiological Sciences
kn-affil=

affil-num=22
en-affil=Research Center for Aquatic Breeding, National Research Institute of Aquaculture, Fisheries Research Agency
kn-affil=

affil-num=23
en-affil=Department of Biological Sciences, Graduate School of Science, The University of Tokyo
kn-affil=

affil-num=24
en-affil=Department of Biological Sciences, Graduate School of Science, The University of Tokyo
kn-affil=

affil-num=25
en-affil=Department of Anatomy and Developmental Biology, Kyoto Prefectural University of Medicine
kn-affil=
en-keyword=Intestinal atresia
kn-keyword=Intestinal atresia
en-keyword=Mypt1
kn-keyword=Mypt1
en-keyword=Disease model
kn-keyword=Disease model
en-keyword=Actomyosin regulation
kn-keyword=Actomyosin regulation
en-keyword=Intestinal development
kn-keyword=Intestinal development
END

start-ver=1.4
cd-journal=joma
no-vol=24
cd-vols=
no-issue=1
article-no=
start-page=146
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=20260115
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=MMP-3 cleavage of Lamin A induces pro-migratory nuclear deformity, nucleophagy, and their autophagic secretion with extracellular vesicles in metastatic cancer
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Matrix metalloproteinases (MMPs) are a family of zinc-dependent proteinases that cleave a plethora of substrates, including components of the extracellular matrix and cell-surface-associated proteins, as well as intracellular targets. MMPs have also been found in extracellular vesicles (EVs), such as exosomes. MMP-3 promotes tumor growth, epithelial-to-mesenchymal transition, genome instability, migration, invasion, and metastasis of cancer cells, and nuclear MMP-3 controls gene transcription. Intranuclear proteolysis by MMPs may significantly alter cancer progression. However, the nuclear substrates of MMP-3 have not been well investigated. In this study, we performed proteomic analyses to identify the nuclear substrates and EV proteins regulated by MMP-3. While rabidly metastatic colon cancer (LuM1) three-dimensionally cultured tumoroids secreted EVs containing 30 protein types, including Lamin A (LMNA), MMP-3, fibronectin (FN1), HSPA8 (Hsc70), β-actin (ACTB), and vimentin (VIM), CRISPR/Cas9-based knockout of MMP-3 reduced the secretion of these proteins in EVs. Notably, EV-bound cleaved Lamin secretion was confirmed by immunoelectron microscopy. Also, MMP-3 formed proteolytic dimers via its hemopexin-like repeat domains in nuclei. Many nuclear MMP-3-binding proteins, including Lamin A/C, histones, topoisomerases, and hnRNPs, were screened by co-immunoprecipitation followed by proteomics. Proteolytic MMP-3 overexpression generated a C-terminal 30-kDa fragment of Lamin A, whose cleavage site was defined via structural analysis. MMP-3 digestion of Lamin A induced nuclear deformity (atypia) required for cell migration in confined space. The cleaved Lamin A and MMP-3 were transported with autophagosomes (LC3B+), nucleophagosomes, and amphisomes (CD63 + LC3B+) and co-secreted with EVs. Proteolytic MMP-3 also induced nuclear speckles of Lamin A, suggesting their roles in transcription and splicing. Clinical analysis revealed that high expressions of MMP3 and LMNA were significantly seen in head and neck squamous cell carcinoma (HNSC) than in the other 16 cancer types, and predicted poor prognosis of patients suffering from HNSC, pancreatic, rectum and lung adenocarcinomas at specific stages. Immunohistochemistry revealed that nuclear MMP-3 and cleaved Lamin were significantly higher expressed in stage IV metastatic HNSC cases than in stage I non-metastatic cases. Taken together, MMP3-cleavage of Lamin A induces nuclear deformity, nucleophagy, and their autophagic co-secretion with EVs in metastatic cancer. Also, high expression of MMP-3 and secretion of Lamin A can predict poor prognosis in multiple cancer types at specific stages.
en-copyright=
kn-copyright=

en-aut-name=EguchiTakanori
en-aut-sei=Eguchi
en-aut-mei=Takanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TahaEman A.
en-aut-sei=Taha
en-aut-mei=Eman A.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NakanoKeisuke
en-aut-sei=Nakano
en-aut-mei=Keisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TiwariVikas
en-aut-sei=Tiwari
en-aut-mei=Vikas
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TakebeKatsuki
en-aut-sei=Takebe
en-aut-mei=Katsuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=InoueTomohiro
en-aut-sei=Inoue
en-aut-mei=Tomohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=XingLizi
en-aut-sei=Xing
en-aut-mei=Lizi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=SogawaChiharu
en-aut-sei=Sogawa
en-aut-mei=Chiharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=OkamotoKuniaki
en-aut-sei=Okamoto
en-aut-mei=Kuniaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=CalderwoodStuart K.
en-aut-sei=Calderwood
en-aut-mei=Stuart K.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of Dental Pharmacology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Biochemistry, Faculty of Science, Ain Shams University
kn-affil=

affil-num=3
en-affil=Department of Oral Pathology and Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Council of Scientific & Industrial Research-Indian Institute of Toxicological Research
kn-affil=

affil-num=5
en-affil=Department of Dental Pharmacology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Dental Pharmacology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Dental Pharmacology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Food and Health Sciences, Faculty of Environmental Studies, Hiroshima Institute of Technology
kn-affil=

affil-num=9
en-affil=Department of Dental Pharmacology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=10
en-affil=Division of Molecular and Cellular Biology, Department of Radiation Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School
kn-affil=
en-keyword=Lamin A (LMNA)
kn-keyword=Lamin A (LMNA)
en-keyword=Matrix metalloprotease (MMP)
kn-keyword=Matrix metalloprotease (MMP)
en-keyword=Proteolysis
kn-keyword=Proteolysis
en-keyword=Extracellular vesicle (EV)
kn-keyword=Extracellular vesicle (EV)
en-keyword=Exosome
kn-keyword=Exosome
en-keyword=Autophagy
kn-keyword=Autophagy
en-keyword=Amphisome
kn-keyword=Amphisome
en-keyword=Proteome
kn-keyword=Proteome
en-keyword=Nuclear deformity
kn-keyword=Nuclear deformity
en-keyword=Migration
kn-keyword=Migration
en-keyword=Metastatic cancer
kn-keyword=Metastatic cancer
en-keyword=Head and neck squamous cell carcinoma
kn-keyword=Head and neck squamous cell carcinoma
en-keyword=Colorectal cancer
kn-keyword=Colorectal cancer
END

start-ver=1.4
cd-journal=joma
no-vol=165
cd-vols=
no-issue=
article-no=
start-page=105344
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202503
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Local immune response induced by intra-fin antigen injection in Japanese medaka (Oryzias latipes) is a useful model for immunological studies
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Teleost fishes play a pivotal role in advancing our understanding of immune system evolution because they retain the ancient characteristics of vertebrate immunity, encompassing both innate and adaptive immune systems. Among these, innate immunity plays a critical role in fish as the first line of defense, coordinating rapid responses to pathogen infections. However, the lack of fish-specific immunological methodologies has limited progress in elucidating fish immune mechanisms. To better understand how the innate immune response develops and resolves in fish, detailed observation and integrative analysis of leukocytes at multiple time points is necessary. In the present study, an intra-fin injection method for observing local immune responses in Japanese medaka (Oryzias latipes) was tested and optimized to analyze the progression of zymosan-induced innate immune responses. Zymosan-injected medaka showed a rapid immune response characterized by leukocyte recruitment and phagocytosis. Using TG(FmpxP:mCherry) transgenic medaka with mCherry fluorescence driven by myeloperoxidase (mpx) promoter, granulocyte chemotaxis towards the site of zymosan entry was successfully visualized. The rapid increase in tumor necrosis factor α (tnfa), interleukin-1β (il1b), interleukin-6 (il6), and CXC motif chemokine ligand 8 (cxcl8) expressions in zymosan-injected anal fins provided a molecular basis for the visualized tissue-specific cellular response. Our study underscores the dynamic orchestration of immune components during the innate immune response in Japanese medaka and highlights their potential as a promising model for immunological research.
en-copyright=
kn-copyright=

en-aut-name=RyuTsukasa
en-aut-sei=Ryu
en-aut-mei=Tsukasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YoshinoMizuki
en-aut-sei=Yoshino
en-aut-mei=Mizuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TseWilliam Ka Fai
en-aut-sei=Tse
en-aut-mei=William Ka Fai
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=AnsaiSatoshi
en-aut-sei=Ansai
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=IguchiTaisen
en-aut-sei=Iguchi
en-aut-mei=Taisen
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KumarAnu
en-aut-sei=Kumar
en-aut-mei=Anu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SomamotoTomonori
en-aut-sei=Somamoto
en-aut-mei=Tomonori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NakaoMiki
en-aut-sei=Nakao
en-aut-mei=Miki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=OginoYukiko
en-aut-sei=Ogino
en-aut-mei=Yukiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Graduate School of Bioresource and Bioenvironmental Sciences, Laboratory of Marine Biochemistry, Kyushu University
kn-affil=

affil-num=2
en-affil=Graduate School of Bioresource and Bioenvironmental Sciences, Laboratory of Marine Biology, Kyushu University
kn-affil=

affil-num=3
en-affil=Graduate School of Bioresource and Bioenvironmental Sciences, Laboratory of Developmental Disorders and Toxicology, Kyushu University
kn-affil=

affil-num=4
en-affil=Ushimado Marine Institute, Faculty of Science, Okayama University
kn-affil=

affil-num=5
en-affil=Graduate School of Nanobioscience, Yokohama City University
kn-affil=

affil-num=6
en-affil=Commonwealth Scientific and Industrial Research Organisation, CSIRO Environment
kn-affil=

affil-num=7
en-affil=Graduate School of Bioresource and Bioenvironmental Sciences, Laboratory of Marine Biochemistry, Kyushu University
kn-affil=

affil-num=8
en-affil=Graduate School of Bioresource and Bioenvironmental Sciences, Laboratory of Marine Biochemistry, Kyushu University
kn-affil=

affil-num=9
en-affil=Center for Promotion of International Education and Research, Faculty of Agriculture, Kyushu University
kn-affil=
en-keyword=Chemotaxis
kn-keyword=Chemotaxis
en-keyword=Local immunity
kn-keyword=Local immunity
en-keyword=Inflammation
kn-keyword=Inflammation
en-keyword=Innate immunity
kn-keyword=Innate immunity
en-keyword=Phagocytosis
kn-keyword=Phagocytosis
en-keyword=Zymosan
kn-keyword=Zymosan
END

start-ver=1.4
cd-journal=joma
no-vol=16
cd-vols=
no-issue=1
article-no=
start-page=888
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20251215
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=TRPV2 in muscle satellite cells is crucial for skeletal muscle remodelling
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Skeletal muscle remodelling relies on muscle stem cells (MuSCs) for regeneration after injury and hypertrophy in response to mechanical loading. However, the mechanisms that trigger MuSC activation and proliferation remain unclear. Transient receptor potential vanilloid 2 (TRPV2) ion channels respond to insulin-like growth factor-1 and mechanical stimuli to regulate the biological characteristics of various cells. Using a temporally inducible MuSC-specific conditional knockout (cKO) mouse, we show that TRPV2 regulates MuSC function and is essential for muscle remodelling. In cultured myofibre, MuSCs express TRPV2 and exhibit Ca2+ responses to the TRPV2 agonists 2-aminoethoxydiphenyl borate and probenecid, which are abolished upon TRPV2 deletion. TRPV2-deficient MuSCs exhibit reduced paired box 7 (Pax7) expression and impaired proliferation, suggesting TRPV2 is a factor that regulates the early stage of MuSC function. Myotube formation in MuSCs was enhanced by overexpression of TRPV2 and suppressed by TRPV2 deficiency, suggesting that TRPV2 is a factor that promotes myogenesis. Muscle-administered cardiotoxin promoted muscle regeneration and resulted in the appearance of numerous Pax7-positive MuSCs between myofibres. MuSC-specific TRPV2 cKO mice exhibit substantially impaired muscle regeneration after cardiotoxin-induced injury, drastically reducing Pax7-positive MuSCs between myofibres. In floxed mice, mechanical loading via synergist ablation induces hypertrophy and greatly increases the number of myonuclei per myofibre. In contrast, MuSC-specific TRPV2 cKO mice show no changes in myofibre thickness or nuclear number, either at baseline or after mechanical loading. Mechanical loading of floxed mice increased TRPV2+/Pax7+ double-positive MuSCs, but MuSC-specific TRPV2 cKO mice showed no change. Additionally, MuSCs exhibit Ca2+ responses to hypo-osmotic stimuli, which are suppressed by TRPV2 inhibitors and TRPV2 deletion, suggesting that MuSCs exhibit TRPV2-dependent mechanical responses. These results establish TRPV2 as a critical regulator of MuSC-mediated muscle remodelling, an important finding that may lead to therapeutic strategies for muscle repair and adaptation.
en-copyright=
kn-copyright=

en-aut-name=ChenYanzhu
en-aut-sei=Chen
en-aut-mei=Yanzhu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KatanosakaKimiaki
en-aut-sei=Katanosaka
en-aut-mei=Kimiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ShibuyaMakoto
en-aut-sei=Shibuya
en-aut-mei=Makoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=DongYubing
en-aut-sei=Dong
en-aut-mei=Yubing
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ZhangLidan
en-aut-sei=Zhang
en-aut-mei=Lidan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KanagawaMotoi
en-aut-sei=Kanagawa
en-aut-mei=Motoi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=FukadaSo-ichiro
en-aut-sei=Fukada
en-aut-mei=So-ichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NaruseKeiji
en-aut-sei=Naruse
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KatanosakaYuki
en-aut-sei=Katanosaka
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Biomedical Sciences, College of Life and Health Sciences, Chubu University
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Laboratory of Stem Cell Regeneration and Adaptation, Graduate School of Pharmaceutical Sciences, The University of Osaka
kn-affil=

affil-num=6
en-affil=Department of Cell Biology and Molecular Medicine, Ehime University Graduate School of Medicine
kn-affil=

affil-num=7
en-affil=Laboratory of Stem Cell Regeneration and Adaptation, Graduate School of Pharmaceutical Sciences, The University of Osaka
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=5
cd-vols=
no-issue=1
article-no=
start-page=pgaf393
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20251222
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Chloroplast heat shock protein cpHsc70-1 interacts with thylakoid membrane remodeling protein VIPP1 C-terminal tail and controls VIPP1 oligomer assembly
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Oxygenic photosynthetic organisms depend on the thylakoid membranes (TMs) for light-driven energy conversion. Recent studies on TM homeostasis (thylakostasis) have highlighted the essential role of the TM remodeling protein vesicle-inducing protein in plastid 1 (VIPP1). As a member of the endosomal sorting complexes required for transport-III (ESCRT-III)/phage shock protein A (PspA)/VIPP1 superfamily, VIPP1 forms large ring- and filament-like homo-oligomeric structures that exhibit a membrane remodeling activity. The oligomerization status was proposed to be modulated by the intrinsically disordered C-terminal tail (Vc), whereas its functional role remained unclear. Notably, this Vc region is conserved not only in photosynthetic VIPP1 but also in the PspA proteins of extremophilic species, implicating its role in membrane stress responses. To investigate the role of the Vc region in VIPP1 assembly, we performed coimmunoprecipitation assays in Arabidopsis chloroplasts and identified chloroplast-localized HSP70 proteins (cpHsc70) as major interactors. Among the two isoforms, cpHsc70-1 was found to be specifically required for modulating VIPP1 oligomeric assembly and dynamics in response to heat stress. Genetic analyses revealed that cpHsc70-1 facilitates the disassembly of VIPP1 oligomers, similarly to Vps4 ATPase in ESCRT-III; loss of either the Vc region or cpHsc70-1-impaired VIPP1 disassembly, resulting in more static oligomeric structures. Furthermore, cpHsc70-1 exhibited a broader role in chloroplast proteostasis, as the cphsc70-1 mutant showed impaired accumulation of green fluorescent protein (GFP)-fusion proteins. Together, our findings uncover a crucial crosstalk between proteostasis and thylakostasis in chloroplasts, coordinated by cpHsc70-1 and VIPP1 in response to membrane stress.
en-copyright=
kn-copyright=

en-aut-name=LiDi
en-aut-sei=Li
en-aut-mei=Di
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=GachieSarah Wanjiru
en-aut-sei=Gachie
en-aut-mei=Sarah Wanjiru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OzawaShin-ichiro
en-aut-sei=Ozawa
en-aut-mei=Shin-ichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ScholzMartin
en-aut-sei=Scholz
en-aut-mei=Martin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HipplerMichael
en-aut-sei=Hippler
en-aut-mei=Michael
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SakamotoWataru
en-aut-sei=Sakamoto
en-aut-mei=Wataru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=2
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=3
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=4
en-affil=Institute of Plant Biology and Biotechnology, University of Münster
kn-affil=

affil-num=5
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=6
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=
en-keyword=Arabidopsis thaliana
kn-keyword=Arabidopsis thaliana
en-keyword=chloroplast
kn-keyword=chloroplast
en-keyword=heat shock protein
kn-keyword=heat shock protein
en-keyword=photosynthesis
kn-keyword=photosynthesis
en-keyword=thylakoid membrane remodeling
kn-keyword=thylakoid membrane remodeling
END

start-ver=1.4
cd-journal=joma
no-vol=28
cd-vols=
no-issue=9
article-no=
start-page=113274
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202509
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Extensive urine production in euryhaline red stingray for adaptation to hypoosmotic environments
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Maintaining water balance is a prerequisite for all organisms. Euryhaline elasmobranchs face the severest water-influx potential in fresh water (FW), as they retain high concentrations of urea even in hypotonic environments. To elucidate how they overcome this osmotic challenge, we assessed urine output in conscious euryhaline red stingrays (Hemitrygon akajei). Following acclimation to 5% diluted seawater, the stingrays increased urinary output by 87-fold—the greatest change observed in vertebrates—partly due to 6.8-fold increase in glomerular filtration rate (GFR). In the nephron, expressions of Aquaporin-1 (Aqp1), Aqp3, and Aqp15 were strongly downregulated in FW, indicating that tubular diuresis bridges the gap between GFR and final urine volume. Meanwhile, FW-acclimation upregulated Aqp1 and Aqp4 in the distinct bundle structure, which promotes urea reabsorption. Euryhaline elasmobranchs resolve the huge osmotic challenge of FW by excreting massive amounts of water and retaining osmolytes including urea through coordinated regulation of GFR and Aqp expressions.
en-copyright=
kn-copyright=

en-aut-name=AburataniNaotaka
en-aut-sei=Aburatani
en-aut-mei=Naotaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakagiWataru
en-aut-sei=Takagi
en-aut-mei=Wataru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=WongMarty Kwok-Shing
en-aut-sei=Wong
en-aut-mei=Marty Kwok-Shing
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OgawaNobuhiro
en-aut-sei=Ogawa
en-aut-mei=Nobuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KurakuShigehiro
en-aut-sei=Kuraku
en-aut-mei=Shigehiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SatoMana
en-aut-sei=Sato
en-aut-mei=Mana
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SaitoKazuhiro
en-aut-sei=Saito
en-aut-mei=Kazuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=GodoWaichiro
en-aut-sei=Godo
en-aut-mei=Waichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=SakamotoTatsuya
en-aut-sei=Sakamoto
en-aut-mei=Tatsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=HyodoSusumu
en-aut-sei=Hyodo
en-aut-mei=Susumu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Atmosphere and Ocean Research Institute, The University of Tokyo
kn-affil=

affil-num=2
en-affil=Atmosphere and Ocean Research Institute, The University of Tokyo
kn-affil=

affil-num=3
en-affil=Atmosphere and Ocean Research Institute, The University of Tokyo
kn-affil=

affil-num=4
en-affil=Atmosphere and Ocean Research Institute, The University of Tokyo
kn-affil=

affil-num=5
en-affil=Department of Genomics and Evolutionary Biology, National Institute of Genetics
kn-affil=

affil-num=6
en-affil=Department of Genomics and Evolutionary Biology, National Institute of Genetics
kn-affil=

affil-num=7
en-affil=Ushimado Marine Institute, Faculty of Science, Okayama University
kn-affil=

affil-num=8
en-affil=Ushimado Marine Institute, Faculty of Science, Okayama University
kn-affil=

affil-num=9
en-affil=Ushimado Marine Institute, Faculty of Science, Okayama University
kn-affil=

affil-num=10
en-affil=Atmosphere and Ocean Research Institute, The University of Tokyo
kn-affil=
en-keyword=Zoology
kn-keyword=Zoology
en-keyword=Biochemistry
kn-keyword=Biochemistry
en-keyword=Animal Physiology
kn-keyword=Animal Physiology
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=5
article-no=
start-page=372
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=20260224
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Alpha-Ketoglutarate Drives an Osteogenic and Extracellular Matrix Gene Program in Periodontal Ligament Fibroblasts via Selective Reduction of H3K27me3
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Periodontal disease damages the tissues that support teeth and can ultimately lead to tooth loss, yet effective treatments to regenerate these tissues are still limited. Recent studies have shown that substances produced during normal cellular metabolism can influence how genes are regulated, but their role in periodontal regeneration has not been fully clarified. In this study, we investigated whether alpha-ketoglutarate, a naturally occurring metabolite involved in energy production, could promote periodontal tissue regeneration. We found that alpha-ketoglutarate enhanced bone-related and extracellular matrix-related gene expression in human periodontal ligament cells by reducing a repressive gene-regulatory signal that normally suppresses these genes. Importantly, alpha-ketoglutarate did not broadly alter chromatin accessibility, indicating that its effects were mediated through selective gene regulation. Furthermore, oral administration of alpha-ketoglutarate promoted alveolar bone regeneration and collagen-rich tissue formation in a mouse model of periodontal disease. Because alpha-ketoglutarate is a naturally occurring molecule in the body, these findings suggest that metabolite-based regulation of gene activity may represent a promising and safe approach for periodontal tissue regeneration.
en-copyright=
kn-copyright=

en-aut-name=HasegawaRyu
en-aut-sei=Hasegawa
en-aut-mei=Ryu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SuzukiShigeki
en-aut-sei=Suzuki
en-aut-mei=Shigeki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=FahrezaRahmad Rifqi
en-aut-sei=Fahreza
en-aut-mei=Rahmad Rifqi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TsaiShin-Ho
en-aut-sei=Tsai
en-aut-mei=Shin-Ho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=DaidoujiYoshino
en-aut-sei=Daidouji
en-aut-mei=Yoshino
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OmoriMasato
en-aut-sei=Omori
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KajikawaTetsuhiro
en-aut-sei=Kajikawa
en-aut-mei=Tetsuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YamadaSatoru
en-aut-sei=Yamada
en-aut-mei=Satoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Periodontology and Endodontology, Tohoku University Graduate School of Dentistry
kn-affil=

affil-num=2
en-affil=Department of Operative Dentistry, Okayama University Graduate School, Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Periodontology and Endodontology, Tohoku University Graduate School of Dentistry
kn-affil=

affil-num=4
en-affil=Department of Operative Dentistry, Okayama University Graduate School, Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Periodontology and Endodontology, Tohoku University Graduate School of Dentistry
kn-affil=

affil-num=6
en-affil=Department of Periodontology and Endodontology, Tohoku University Graduate School of Dentistry
kn-affil=

affil-num=7
en-affil=Department of Periodontology and Endodontology, Tohoku University Graduate School of Dentistry
kn-affil=

affil-num=8
en-affil=Department of Periodontology and Endodontology, Tohoku University Graduate School of Dentistry
kn-affil=
en-keyword=alpha-ketoglutarate
kn-keyword=alpha-ketoglutarate
en-keyword=periodontal ligament
kn-keyword=periodontal ligament
en-keyword=extracellular matrix
kn-keyword=extracellular matrix
en-keyword=epigenetic regulation
kn-keyword=epigenetic regulation
en-keyword=H3K27me3
kn-keyword=H3K27me3
END

start-ver=1.4
cd-journal=joma
no-vol=14
cd-vols=
no-issue=1
article-no=
start-page=9
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=20260212
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The Influence of Fluidic Flow Stress on the Development of the Secondary Palate
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Craniofacial development is orchestrated by a finely regulated interplay of numerous genes and signaling pathways. Palatogenesis proceeds through a complex, stepwise process, in which endogenous mechanical stresses within tissues have been implicated. However, the impact of exogenous fluidic flow mechanical stress derived from maternal movement on palatal development remains unclear. In this study, we investigated the effect of exogenous fluidic flow mechanical stress on palatal morphogenesis, focusing on the horizontal outgrowth of palatal shelves after elevation. Palatal tissues dissected from mouse embryos were subjected to organ culture with or without mechanical loading (loaded and unloaded groups, respectively). Stress magnitude was quantified by calculating wave energy, and morphometric and molecular analyses were performed. Compared with the unloaded group, palatal shelves in the loaded group showed significant increases in thickness and volume, accompanied by enhanced cell proliferation, nuclear translocation of YAP and β-catenin, and upregulation of the osteogenic markers Osterix and Osteocalcin. No significant difference in apoptosis was observed. These findings indicate that exogenous mechanical stress promotes cell proliferation and osteogenic differentiation through the Hippo and WNT/β-catenin pathways in palate explants. Our results suggest that moderate maternal movement-induced mechanical stress contributes to normal palatogenesis, providing new insights into the mechanisms underlying cleft palate.
en-copyright=
kn-copyright=

en-aut-name=NagataMasayo
en-aut-sei=Nagata
en-aut-mei=Masayo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HayanoSatoru
en-aut-sei=Hayano
en-aut-mei=Satoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=WangZiyi
en-aut-sei=Wang
en-aut-mei=Ziyi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KosamiTakahiro
en-aut-sei=Kosami
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KamiokaHiroshi
en-aut-sei=Kamioka
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Department of Orthodontics, Okayama University Hospital
kn-affil=

affil-num=2
en-affil=Department of Orthodontics, Okayama University Hospital
kn-affil=

affil-num=3
en-affil=Department of Molecular Biology and Biochemistry, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Orthodontics, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Orthodontics, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=mechanical stress
kn-keyword=mechanical stress
en-keyword=palatal development
kn-keyword=palatal development
en-keyword=β-catenin
kn-keyword=β-catenin
en-keyword=YAP
kn-keyword=YAP
END

start-ver=1.4
cd-journal=joma
no-vol=68
cd-vols=
no-issue=1
article-no=
start-page=100731
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=202602
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Insights into the taste of organic acids via TAS1Rs
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Objectives: Organic acids contribute significantly to the flavor of fermented foods by imparting sourness. Although mice generally avoid sour taste, previous studies have reported greater consumption of l-lactic acid than its d-enantiomer, suggesting enantiomer-specific recognition. This behavior is hypothesized to involve TAS1Rs, which consists of sweet/umami receptors. However, it remains unclear whether TAS1Rs additionally contribute to the recognition of other chiral organic acids. This study aimed to evaluate the role of TAS1Rs, particularly TAS1R3, in the modulation of enantiomer-dependent behavioral responses to organic acids in mice.<br>
Methods: Behavioral responses were evaluated using 48-h and 1-h 2-bottle tests. Binding of organic acids to TAS1Rs was investigated by differential scanning fluorimetry (DSF) with the ligand-binding domain (LBD) of medaka Tas1r2a/Tas1r3.<br>
Results: Wild-type mice consumed more d-malic acid than l-malic acid in the 48-h test, whereas Tas1r3-KO mice showed no such difference. This pattern was not observed in the short-term 1-h test, which minimized the contribution of post-ingestion and learned effects. DSF analysis revealed no binding of any of the tested organic acids to the LBD of medaka Tas1r2a/Tas1r3.<br>
Conclusions: Organic acids may elicit TAS1R3-dependent post-ingestion signals that contribute to enantiomer-selective consumption in mice. Electrostatic interactions and hydrogen-bonding networks within the orthosteric pocket of TAS1Rs may account for the differences in binding affinity to the LBD of medaka Tas1r2a/Tas1r3 between organic acids and L-alanine, a known ligand.
en-copyright=
kn-copyright=

en-aut-name=YamaseYuko
en-aut-sei=Yamase
en-aut-mei=Yuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakebeKatsuki
en-aut-sei=Takebe
en-aut-mei=Katsuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HorieKengo
en-aut-sei=Horie
en-aut-mei=Kengo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MitohYoshihiro
en-aut-sei=Mitoh
en-aut-mei=Yoshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YamashitaAtsuko
en-aut-sei=Yamashita
en-aut-mei=Atsuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YoshidaRyusuke
en-aut-sei=Yoshida
en-aut-mei=Ryusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Department of Dental Anesthesiology and Special Care Dentistry, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Oral Physiology, Graduate School of Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Oral Physiology, Graduate School of Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Institute for Protein Research, The University of Osaka
kn-affil=

affil-num=6
en-affil=Department of Oral Physiology, Graduate School of Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Taste detection
kn-keyword=Taste detection
en-keyword=Organic acid preference
kn-keyword=Organic acid preference
en-keyword=G-protein coupled receptor (GPCR)
kn-keyword=G-protein coupled receptor (GPCR)
en-keyword=Knockout mice
kn-keyword=Knockout mice
en-keyword=Surface electrostatic potential
kn-keyword=Surface electrostatic potential
END

start-ver=1.4
cd-journal=joma
no-vol=65
cd-vols=
no-issue=4
article-no=
start-page=300
end-page=309
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=20130222
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Synthesis of biopterin and related pterin glycosides
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Certain pterins having a hydroxyalkyl side chain at C-6 have been found as glycosidic forms in certain prokaryotes, such as 2′-O-(α-D-glucopyranosyl)biopterin from various kinds of cyanobacteria, and limipterin from a green sulfur photosynthetic bacterium. Synthetic studies on glycosides of biopterin and related pterins have been made in view of the structural proof as well as for closer examination of their biological activities and functions. The syntheses of these natural pterin glycosides have effectively been achieved, mostly through appropriately protected N2-(N,N-dimethylaminomethylene)-3-[2-(4-nitrophenyl)ethyl]pterin derivatives as glycosyl acceptors, and are reviewed here. © 2013 IUBMB Life 65(4):300–309, 2013.
en-copyright=
kn-copyright=

en-aut-name=HanayaTadashi
en-aut-sei=Hanaya
en-aut-mei=Tadashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YamamotoHiroshi
en-aut-sei=Yamamoto
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

affil-num=1
en-affil=Department of Chemistry, Faculty of Science, Okayama University
kn-affil=

affil-num=2
en-affil=School of Pharmacy, Shujitsu University
kn-affil=
en-keyword=pteridine
kn-keyword=pteridine
en-keyword=pterin glycoside
kn-keyword=pterin glycoside
en-keyword=biopterin
kn-keyword=biopterin
en-keyword=ciliapterin
kn-keyword=ciliapterin
en-keyword=neopterin
kn-keyword=neopterin
en-keyword=limipterin
kn-keyword=limipterin
en-keyword=tepidopterin
kn-keyword=tepidopterin
en-keyword=asperopterin-A
kn-keyword=asperopterin-A
en-keyword=protecting group
kn-keyword=protecting group
en-keyword=glycosylation
kn-keyword=glycosylation
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=20260120
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=SPRED2 suppresses the stemness of hepatocellular carcinoma through the p53/miR-506-3p/KLF4 pathway
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Objective: We previously reported that endogenous Sprouty-related, EVH1 domain-containing protein 2 (SPRED2), an inhibitor of the Ras/Raf/ERK-MAPK pathway, controls hepatocellular carcinoma (HCC) cell stemness by downregulating the expression of pluripotency factors, such as Nanog, c-Myc, and KLF4, in an ERK-dependent fashion. However, the exact mechanisms by which SPRED2 regulates HCC cell stemness have not been established.<br>
Methods: Three human HCC cell lines [HepG2 (parental and SPRED2-deficient), HLE, and Hep3B] were used. Cells were transfected to downregulate or overexpress proteins. Western blot and RT-qPCR were used to evaluate the level of protein and mRNA expression. Co-immunoprecipitation and ChIP-qPCR were used to examine protein-protein interactions and the activation of gene transcription. Clinical HCC tissues were also used to validate in vitro data.<br>
Results: KLF4 was identified as the major pluripotency factor responsible for SPRED2-mediated downregulation of HCC cell stemness and KLF4 expression was regulated by miR-506-3p. SPRED2 formed a protein complex with the tumor suppressor (p53) and upregulated miR-506 gene transcription by binding to the promoter region, resulting in subsequent downregulation of KLF4 mRNA expression. There was a negative correlation between KLF4 expression and miR-506-3p and a positive correlation between miR-506-3p expression and SPRED2 in human HCC samples, highlighting the relevance of the study findings.<br>
Conclusions: The current study revealed a novel SPRED2/p53/miR-506-3p/KLF4 axis through which SPRED2 contributes to the suppression of HCC cell stemness and provides a potential new target to prevent HCC progression.
en-copyright=
kn-copyright=

en-aut-name=GaoTong
en-aut-sei=Gao
en-aut-mei=Tong
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ItoSachio
en-aut-sei=Ito
en-aut-mei=Sachio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=Moh-Moh-AungAye
en-aut-sei=Moh-Moh-Aung
en-aut-mei=Aye
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=WangTianyi
en-aut-sei=Wang
en-aut-mei=Tianyi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=FujisawaMasayoshi
en-aut-sei=Fujisawa
en-aut-mei=Masayoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OharaToshiaki
en-aut-sei=Ohara
en-aut-mei=Toshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YoshimuraTeizo
en-aut-sei=Yoshimura
en-aut-mei=Teizo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MatsukawaAkihiro
en-aut-sei=Matsukawa
en-aut-mei=Akihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Pathology and Experimental Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Pathophysiology and Drug Discovery, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Pathology and Experimental Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Pathology and Experimental Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Pathology and Experimental Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Pathology and Experimental Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Pathology and Experimental Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Pathology and Experimental Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=SPRED2
kn-keyword=SPRED2
en-keyword=p53
kn-keyword=p53
en-keyword=KLF4
kn-keyword=KLF4
en-keyword=miR-506-3p
kn-keyword=miR-506-3p
en-keyword=stemness
kn-keyword=stemness
END

start-ver=1.4
cd-journal=joma
no-vol=45
cd-vols=
no-issue=1
article-no=
start-page=116781
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=202601
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Immunopeptidomics combined with full-length transcriptomics uncovers diverse neoantigens
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Neoantigens are crucial for antitumor immunity and immune checkpoint inhibitor (ICI) efficacy by triggering strong immune responses. However, conventional methods for identifying neoantigens, such as whole-exon sequencing and short-read RNA sequencing (RNA-seq), appear to be insufficient, and the tumor mutational burden cannot sufficiently predict ICI efficacy. In this study, we employed a proteogenomic approach using long-read RNA-seq with Pacific Biosciences Single-Molecule Real-Time Sequencing technology to analyze full-length transcripts in combination with the human leukocyte antigen ligandome. As a result, many neoantigen candidates were identified, which were unregistered in a comprehensive database, including those from non-coding regions. Additionally, we validated the responses of specific T cell receptors (TCRs) to these candidates and identified several pairs of TCRs and neoantigens. These findings highlight the presence of more diverse neoantigens than expected that cannot be identified by conventional methods.
en-copyright=
kn-copyright=

en-aut-name=IshinoTakamasa
en-aut-sei=Ishino
en-aut-mei=Takamasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
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en-aut-name=WatanabeTomofumi
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en-aut-name=TokitaSerina
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en-aut-name=UedaYouki
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en-aut-name=KawaseKatsushige
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en-aut-name=TakanoYuka
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en-aut-name=ThuYin Min
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en-aut-name=SuzukiYuta
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en-aut-name=OwaChie
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en-aut-name=InozumeTakashi
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en-aut-name=Honobe-TabuchiAkiko
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en-aut-name=OhnumaTakehiro
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en-aut-name=MatsuzawaTakamitsu
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en-aut-name=KawaharaYu
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en-aut-name=YamashitaKazuo
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en-aut-name=LinJason
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en-aut-name=NishikawaHiroyoshi
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en-aut-name=ArakiMotoo
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en-aut-name=MorishitaShinichi
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en-aut-name=SuzukiYutaka
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en-aut-name=ManoHiroyuki
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en-aut-name=TorigoeToshihiko
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en-aut-name=KanasekiTakayuki
en-aut-sei=Kanaseki
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aut-affil-num=32
ORCID=

en-aut-name=KawazuMasahito
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en-aut-name=TogashiYosuke
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kn-aut-sei=
kn-aut-mei=
aut-affil-num=34
ORCID=

affil-num=1
en-affil=Department of Tumor Microenvironment, Okayama University, Graduate School of Medicine Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Tumor Microenvironment, Okayama University, Graduate School of Medicine Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Division of Cancer Immunology, Graduate School of Medical and Dental Sciences, Niigata University
kn-affil=

affil-num=4
en-affil=Department of Tumor Microenvironment, Okayama University, Graduate School of Medicine Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Division of Cell Therapy, Chiba Cancer Center Research Institute
kn-affil=

affil-num=6
en-affil=Department of Tumor Microenvironment, Okayama University, Graduate School of Medicine Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Tumor Microenvironment, Okayama University, Graduate School of Medicine Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Computational Biology and Medical Sciences, The University of Tokyo
kn-affil=

affil-num=9
en-affil=Department of Computational Biology and Medical Sciences, The University of Tokyo
kn-affil=

affil-num=10
en-affil=Department of Dermatology, Chiba University Graduate School of Medicine
kn-affil=

affil-num=11
en-affil=Department of Tumor Microenvironment, Okayama University, Graduate School of Medicine Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=12
en-affil=Department of Tumor Microenvironment, Okayama University, Graduate School of Medicine Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=13
en-affil=Department of Immunology, Nagoya University Graduate School of Medicine
kn-affil=

affil-num=14
en-affil=Division of Cellular Signaling, National Cancer Center Research Institute
kn-affil=

affil-num=15
en-affil=Division of Cellular Signaling, National Cancer Center Research Institute
kn-affil=

affil-num=16
en-affil=Department of Dermatology, University of Yamanashi
kn-affil=

affil-num=17
en-affil=Department of Dermatology, University of Yamanashi
kn-affil=

affil-num=18
en-affil=Department of Dermatology, Kumamoto Kenhoku Hospital
kn-affil=

affil-num=19
en-affil=Department of Dermatology, Chiba University Graduate School of Medicine
kn-affil=

affil-num=20
en-affil=Department of Dermatology, Chiba University Graduate School of Medicine
kn-affil=

affil-num=21
en-affil=KOTAI Biotechnologies, Inc
kn-affil=

affil-num=22
en-affil=Division of Cell Therapy, Chiba Cancer Center Research Institute
kn-affil=

affil-num=23
en-affil=Division of Systems Biology, Nagoya University Graduate School of Medicine
kn-affil=

affil-num=24
en-affil=Department of Immunology, Nagoya University Graduate School of Medicine
kn-affil=

affil-num=25
en-affil=Department of Urology, Okayama University, Graduate School of Medicine Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=26
en-affil=Department of Gastroenterology, Graduate School of Medicine, Chiba University
kn-affil=

affil-num=27
en-affil=Division of Systems Biology, Nagoya University Graduate School of Medicine
kn-affil=

affil-num=28
en-affil=Department of Computational Biology and Medical Sciences, The University of Tokyo
kn-affil=

affil-num=29
en-affil=Department of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo
kn-affil=

affil-num=30
en-affil=Division of Cellular Signaling, National Cancer Center Research Institute
kn-affil=

affil-num=31
en-affil=
kn-affil=

affil-num=32
en-affil=Division of Cancer Immunology, Graduate School of Medical and Dental Sciences, Niigata University
kn-affil=

affil-num=33
en-affil=Division of Cell Therapy, Chiba Cancer Center Research Institute
kn-affil=

affil-num=34
en-affil=Department of Tumor Microenvironment, Okayama University, Graduate School of Medicine Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=cancer immunology
kn-keyword=cancer immunology
en-keyword=neoantigen
kn-keyword=neoantigen
en-keyword=long-read RNA sequencing
kn-keyword=long-read RNA sequencing
en-keyword=HLA ligandome
kn-keyword=HLA ligandome
en-keyword=single-cell RNA sequencing
kn-keyword=single-cell RNA sequencing
en-keyword=single-cell TCR sequencing
kn-keyword=single-cell TCR sequencing
en-keyword=exhausted T cell
kn-keyword=exhausted T cell
END

start-ver=1.4
cd-journal=joma
no-vol=74
cd-vols=
no-issue=11
article-no=
start-page=1023
end-page=1032
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=2025
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Bioconversion and Metabolic Fate of the n-1 Polyunsaturated Fatty Acids, 6,9,12,15- Hexadecatetraenoic (C16:4 n-1) and 8,11,14,17- Octadecatetraenoic (C18:4 n-1) Acids, in HepG2 Cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Fish oil contains not only major fatty acids with double bonds at the n-3, n-6, n-7, and n-9 positions but also those with a double bond at the n-1 position, such as 6,9,12,15-hexadecatetraenoic acid (C16:4 n-1; HDTA). However, intracellular bioconversion and metabolic fate of n-1 polyunsaturated fatty acids (PUFA) remain unclear. Therefore, in this study, we aimed to assess the intracellular bioconversion and metabolic fate of HDTA and its metabolite, 8,11,14,17- octadecatetraenoic acid (C18:4 n-1; ODTA), using HepG2 cells. Based on the results of cell viability and cytotoxicity assays for HDTA and ODTA, the concentration of each fatty acid supplemented in the experiments was set at 10 μM. HepG2 cell culture with HDTA revealed C20:4 n-1 as a new HDTA metabolite, along with previously reported ODTA. Our findings suggest that the HDTA taken up by HepG2 cells undergoes elongation to form ODTA and C20:4 n-1. Following supplementation with HDTA, ODTA, and 5,8,11,14,17-eicosapentaenoic acid (C20:5 n-3; EPA), fatty acids disappeared from the culture medium within 24 h. Notably, the total relative level of HDTA and its metabolites, including ODTA and C20:4 n-1 in HDTA- and ODTA-supplemented cells were significantly lower than the total relative level of EPA and its metabolites, including 7,10,13,16,19-docosapentaenoic acid (C22:5 n-3), C24:6 n-3, and 4,7,10,13,16,19-docosahexaenoic acid (C22:6 n-3) in the EPA-supplemented cells. Except for a portion that was intracellularly elongated, most HDTA was taken up by HepG2 cells and may undergo rapid fatty acid β-oxidation. However, RNA-sequencing and real-time polymerase chain reaction analysis revealed no significant changes in fatty acid β-oxidation–related gene expression levels in HDTA-supplemented cells. Collectively, these results provide novel insights into the intracellular bioconversion mechanisms and metabolic fate of HDTA and ODTA in HepG2 cells, suggesting that the metabolic fate of n-1 PUFA is distinct from that of common PUFA.
en-copyright=
kn-copyright=

en-aut-name=SugimotoKoki
en-aut-sei=Sugimoto
en-aut-mei=Koki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NishiguchiHideto
en-aut-sei=Nishiguchi
en-aut-mei=Hideto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HosomiRyota
en-aut-sei=Hosomi
en-aut-mei=Ryota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TanizakiToshifumi
en-aut-sei=Tanizaki
en-aut-mei=Toshifumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TsushimaTadahiro
en-aut-sei=Tsushima
en-aut-mei=Tadahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=BabaNaomichi
en-aut-sei=Baba
en-aut-mei=Naomichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MisawaYoshihisa
en-aut-sei=Misawa
en-aut-mei=Yoshihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=WangZiyi
en-aut-sei=Wang
en-aut-mei=Ziyi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=OnoMitsuaki
en-aut-sei=Ono
en-aut-mei=Mitsuaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=MurakamiYuki
en-aut-sei=Murakami
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=KandaSeiji
en-aut-sei=Kanda
en-aut-mei=Seiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=FukunagaKenji
en-aut-sei=Fukunaga
en-aut-mei=Kenji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

affil-num=1
en-affil=Faculty of Food and Nutritional Sciences, Toyo University
kn-affil=

affil-num=2
en-affil=Faculty of Chemistry, Materials, and Bioengineering, Kansai University
kn-affil=

affil-num=3
en-affil=Faculty of Chemistry, Materials, and Bioengineering, Kansai University
kn-affil=

affil-num=4
en-affil=Bizen Chemical Co., Ltd.
kn-affil=

affil-num=5
en-affil=Bizen Chemical Co., Ltd.
kn-affil=

affil-num=6
en-affil=Bizen Chemical Co., Ltd.
kn-affil=

affil-num=7
en-affil=Bizen Chemical Co., Ltd.
kn-affil=

affil-num=8
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Oral Rehabilitation and Regenerative Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Hygiene and Public Health, Kansai Medical University
kn-affil=

affil-num=11
en-affil=Department of Hygiene and Public Health, Kansai Medical University
kn-affil=

affil-num=12
en-affil=Faculty of Chemistry, Materials, and Bioengineering, Kansai University
kn-affil=
en-keyword=n-1 polyunsaturated fatty acids
kn-keyword=n-1 polyunsaturated fatty acids
en-keyword=hexadecatetraenoic acid
kn-keyword=hexadecatetraenoic acid
en-keyword=octadecatetraenoic acid
kn-keyword=octadecatetraenoic acid
en-keyword=HepG2
kn-keyword=HepG2
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=1
article-no=
start-page=29639
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250813
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Single cell spatial transcriptomics links Wnt signaling disruption to extracellular matrix development in a cleft palate model
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Despite advances in understanding the morphological disruptions that lead to defects in palate formation, the precise perturbations within the signaling microenvironment of palatal clefts remain poorly understood. To explore in greater depth the genomic basis of palatal clefts, we designed and implemented the first single cell spatial RNA-sequencing study in a cleft palate model, utilizing the Pax9−/− murine model at multiple developmental timepoints, which exhibits a consistent cleft palate defect. Visium HD, an emerging platform for true single-cell resolution spatially resolved transcriptomics, was employed using custom bins of 2 × 2 μm spatial gene expression data. Validation of spatial gene expression was then validated using custom designed Xenium In Situ mRNA spatial profiling and RNAscope Multiplex assays. Functional enrichment analysis revealed a palate cell-specific perturbation in Wnt signaling effector function in tandem with disrupted expression of extracellular matrix genes in developing mesenchyme. As a key step toward laying the framework for identifying key molecular targets these data can be used for translational studies aimed at developing effective therapies for human palatal clefts.
en-copyright=
kn-copyright=

en-aut-name=PiñaJeremie Oliver
en-aut-sei=Piña
en-aut-mei=Jeremie Oliver
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=RajuResmi
en-aut-sei=Raju
en-aut-mei=Resmi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=StipanoEvan
en-aut-sei=Stipano
en-aut-mei=Evan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MyoAye Chan
en-aut-sei=Myo
en-aut-mei=Aye Chan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=WangZiyi
en-aut-sei=Wang
en-aut-mei=Ziyi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OnoMitsuaki
en-aut-sei=Ono
en-aut-mei=Mitsuaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=ChattarajParna
en-aut-sei=Chattaraj
en-aut-mei=Parna
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=FurukawaMasae
en-aut-sei=Furukawa
en-aut-mei=Masae
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=D’SouzaRena N.
en-aut-sei=D’Souza
en-aut-mei=Rena N.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Section on Craniofacial Genetic Disorders, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health (NIH)
kn-affil=

affil-num=2
en-affil=Section on Craniofacial Genetic Disorders, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health (NIH)
kn-affil=

affil-num=3
en-affil=Section on Craniofacial Genetic Disorders, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health (NIH)
kn-affil=

affil-num=4
en-affil=Section on Craniofacial Genetic Disorders, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health (NIH)
kn-affil=

affil-num=5
en-affil=Graduate School of Medicine Dentistry and Pharmaceutical Sciences, Department of Molecular Biology and Biochemistry, Okayama University
kn-affil=

affil-num=6
en-affil=Graduate School of Medicine Dentistry and Pharmaceutical Sciences, Department of Molecular Biology and Biochemistry, Okayama University
kn-affil=

affil-num=7
en-affil=Section on Craniofacial Genetic Disorders, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health (NIH)
kn-affil=

affil-num=8
en-affil=Section on Craniofacial Genetic Disorders, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health (NIH)
kn-affil=

affil-num=9
en-affil=Section on Craniofacial Genetic Disorders, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health (NIH)
kn-affil=
en-keyword=Spatial biology
kn-keyword=Spatial biology
en-keyword=Cleft palate
kn-keyword=Cleft palate
en-keyword=Genomics
kn-keyword=Genomics
en-keyword=Single cell
kn-keyword=Single cell
en-keyword=Gene expression
kn-keyword=Gene expression
en-keyword=Profiling
kn-keyword=Profiling
en-keyword=Extracellular matrix
kn-keyword=Extracellular matrix
en-keyword=Wnt
kn-keyword=Wnt
en-keyword=Transcriptome
kn-keyword=Transcriptome
END

start-ver=1.4
cd-journal=joma
no-vol=6
cd-vols=
no-issue=5
article-no=
start-page=e70094
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202510
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Seaweed Extracts Improve Salinity Tolerance in Cereal Crops—A Meta‐Analysis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Seaweeds are considered an essential component of the blue economy. Because seaweed extracts are rich in bioactive compounds that enhance plant stress resilience, exploiting this resource could offer a sustainable solution for crop production. Salinity is a major abiotic challenge that significantly impacts crop yield and food security. Through meta-analysis, we explored whether the exogenous application of seaweed extracts improves the salt tolerance of cereal crops. All the studies chosen for this study utilized aqueous seaweed extracts as foliar sprays. A multi-level meta-analysis with a mixed effects model was performed to determine the effect size. This meta-analysis demonstrated that applying aqueous seaweed extracts enhanced the shoot and root biomass under normal and salinity stress conditions, suggesting that seaweed extract can help improve crop stress tolerance. The seaweeds studied belonged to three classes: Phaeophyceae, Rhodophyta, and Chlorophyta, with extracts from Chlorophyta and Phaeophyceae significantly enhancing biomass production under salinity conditions. Applying aqueous seaweed extracts effectively improved salinity tolerance at both 34.2–100 mM and 101–400 mM NaCl equivalent salinity stress. Moreover, exogenous foliar application of ≤ 25% aqueous seaweed extracts was most effective for improving salinity tolerance in cereals. The impact of seaweed extracts on cereal crop yields has not been extensively reported; therefore, further studies should focus on this aspect.
en-copyright=
kn-copyright=

en-aut-name=NuruzzamanMd.
en-aut-sei=Nuruzzaman
en-aut-mei=Md.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=Tahjib‐Ul‐ArifMd.
en-aut-sei=Tahjib‐Ul‐Arif
en-aut-mei=Md.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HannanMd. Abdul
en-aut-sei=Hannan
en-aut-mei=Md. Abdul
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MurataYoshiyuki
en-aut-sei=Murata
en-aut-mei=Yoshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HossainM. Afzal
en-aut-sei=Hossain
en-aut-mei=M. Afzal
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Department of Plant Resources, College of Industrial Sciences, Kongju National University
kn-affil=

affil-num=2
en-affil=Department of Biochemistry and Molecular Biology, Bangladesh Agricultural University
kn-affil=

affil-num=3
en-affil=Department of Biochemistry and Molecular Biology, Bangladesh Agricultural University
kn-affil=

affil-num=4
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Biochemistry and Molecular Biology, Bangladesh Agricultural University
kn-affil=
en-keyword=abiotic stress
kn-keyword=abiotic stress
en-keyword=crop tolerance
kn-keyword=crop tolerance
en-keyword=marine algae
kn-keyword=marine algae
en-keyword=plant growth
kn-keyword=plant growth
en-keyword=salt stress
kn-keyword=salt stress
en-keyword=sustainable agriculture
kn-keyword=sustainable agriculture
END

start-ver=1.4
cd-journal=joma
no-vol=64
cd-vols=
no-issue=20
article-no=
start-page=4309
end-page=4317
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20251009
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Characterization of Autonomous and Ca2+/Calmodulin-Dependent Activities of CaMKK Isoforms In Vitro and in Mouse Tissues
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Ca2+/CaM-dependent protein kinase kinase (CaMKK) phosphorylates and activates downstream kinases, including CaMKI, CaMKIV, PKB, and AMPK, regulating various cellular functions such as neuronal morphogenesis, metabolic control, and pathophysiological pathways, such as cancer progression. CaMKKα/1 is tightly regulated by an autoinhibitory mechanism. CaMKKβ/2 activity is highly Ca2+/CaM-independent (autonomous activity) in vitro and Ca2+/CaM-dependent in cultured cells. Whether these two activity states of CaMKKβ/2 exist in vivo and the detailed regulatory mechanisms for the transition of both activity states remain unclear due to the difficulty in distinguishing the two activity states. In this study, we detected Ca2+-dependent and autonomous CaMKK activity in HeLa cells and successfully separated both activity states of CaMKKβ/2 in mouse brain and testis extracts using a recently developed CaMKK inhibitor (TIM-063)-coupled sepharose, which binds to the catalytic domain in the active state but not in the autoinhibited state. Furthermore, lambda protein phosphatase treatment converted the Ca2+/CaM-dependent form to the autonomous form of CaMKKβ/2, which was not affected by Ala mutation of Ser128, Ser132, and Ser136. The two activity forms of CaMKKβ/2 had equivalent Ca2+/CaM-binding ability. The findings demonstrate the presence of autonomous and Ca2+/CaM-dependent forms of CaMKKβ/2 independently in mouse tissues and cultured cells. The transition of these states of CaMKKβ/2 may be dynamically regulated by the phosphorylation/dephosphorylation of serine residues in the N-terminal regulatory domain.
en-copyright=
kn-copyright=

en-aut-name=OhtsukaSatomi
en-aut-sei=Ohtsuka
en-aut-mei=Satomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ChenYerun
en-aut-sei=Chen
en-aut-mei=Yerun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MagariMasaki
en-aut-sei=Magari
en-aut-mei=Masaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=IshikawaTeruhiko
en-aut-sei=Ishikawa
en-aut-mei=Teruhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SakagamiHiroyuki
en-aut-sei=Sakagami
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SuizuFutoshi
en-aut-sei=Suizu
en-aut-mei=Futoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TokumitsuHiroshi
en-aut-sei=Tokumitsu
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Applied Cell Biology, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=2
en-affil=Applied Cell Biology, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=3
en-affil=Applied Cell Biology, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Science Education, Graduate School of Education, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Anatomy, Kitasato University School of Medicine
kn-affil=

affil-num=6
en-affil=Clinical Examination Department, Kagawa Prefectural University of Health Sciences
kn-affil=

affil-num=7
en-affil=Applied Cell Biology, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=10
cd-vols=
no-issue=11
article-no=
start-page=105889
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202511
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Association between adjuvant chemotherapy and outcomes in resected locoregional recurrence of hormone receptor-positive HER2-negative breast cancer: a multi-institutional retrospective study
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: To evaluate the association of adjuvant chemotherapy and prognosis for locoregional recurrence (LRR) in hormone receptor (HR)-positive human epidermal growth factor receptor 2 (HER2)-negative subtype breast cancer.<br>
Patients and methods: We carried out a multi-institutional retrospective cohort study in patients with breast cancer who developed HR-positive HER2-negative LRR. Patients who underwent curative surgery for LRR between 2014 and 2018 were categorized based on whether they received adjuvant chemotherapy for LRR (CTx versus no-CTx). Invasive disease-free survival (iDFS) was evaluated between the groups by Cox proportional hazards analysis. The primary analysis used a double-robust Cox model incorporating inverse probability of treatment weighting, and a sensitivity analysis using propensity score matching was also carried out.<br>
Results: A total of 958 patients were included. The median time from the primary surgery to LRR diagnosis was 9.5 years (interquartile range 3.1-10.1 years). There were 235 patients (25%) in the CTx group and 722 (75%) in the no-CTx group. Among all patients, the 5-year iDFS rate was 75.4% [95% confidence interval (CI) 72.4% to 78.2%]. Multivariate analysis showed better iDFS in the CTx group (hazard ratio 0.70, 95% CI 0.49-0.99, P = 0.045). Sensitivity analysis supported these findings. Subgroup analyses showed that the CTx group had better iDFS in cases with non-ipsilateral breast tumor recurrence (IBTR), recurrences during adjuvant endocrine therapy for primary breast cancer, and without perioperative chemotherapy for primary breast cancer. Secondary analysis showed no significant difference with a worse trend toward overall survival in the CTx group with multivariate Cox proportional hazards analysis.<br>
Conclusion: Adjuvant chemotherapy for HR-positive HER2-negative LRR was associated with better iDFS, particularly in cases of non-IBTR, recurrences during adjuvant endocrine therapy, and no prior perioperative chemotherapy for their primary tumor. However, the retrospective design and inability to distinguish true recurrences from new primary tumors in IBTR warrant cautious interpretation.
en-copyright=
kn-copyright=

en-aut-name=OzakiY.
en-aut-sei=Ozaki
en-aut-mei=Y.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TokudaE.
en-aut-sei=Tokuda
en-aut-mei=E.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SagaraY.
en-aut-sei=Sagara
en-aut-mei=Y.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HaraF.
en-aut-sei=Hara
en-aut-mei=F.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SasadaS.
en-aut-sei=Sasada
en-aut-mei=S.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SawakiM.
en-aut-sei=Sawaki
en-aut-mei=M.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KanbayashiC.
en-aut-sei=Kanbayashi
en-aut-mei=C.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YamanakaT.
en-aut-sei=Yamanaka
en-aut-mei=T.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=OnishiT.
en-aut-sei=Onishi
en-aut-mei=T.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=FujikiY.
en-aut-sei=Fujiki
en-aut-mei=Y.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=SutoA.
en-aut-sei=Suto
en-aut-mei=A.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=TakahashiY.
en-aut-sei=Takahashi
en-aut-mei=Y.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=TokunagaE.
en-aut-sei=Tokunaga
en-aut-mei=E.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=ArugaT.
en-aut-sei=Aruga
en-aut-mei=T.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=NakamuraR.
en-aut-sei=Nakamura
en-aut-mei=R.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=FujisawaT.
en-aut-sei=Fujisawa
en-aut-mei=T.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=SajiS.
en-aut-sei=Saji
en-aut-mei=S.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=IwataH.
en-aut-sei=Iwata
en-aut-mei=H.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=ShienT.
en-aut-sei=Shien
en-aut-mei=T.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

affil-num=1
en-affil=Department of Breast Medical Oncology, Cancer Institute Hospital of Japanese Foundation for Cancer Research
kn-affil=

affil-num=2
en-affil=Department of Medical Oncology, Fukushima Medical University
kn-affil=

affil-num=3
en-affil=Department of Breast Surgery, Social Medical Corporation Hakuaikai Sagara Hospital
kn-affil=

affil-num=4
en-affil=Department of Breast Oncology, Aichi Cancer Center Hospital
kn-affil=

affil-num=5
en-affil=Department of Surgical Oncology, Research Institute for Radiation Biology and Medicine, Hiroshima University
kn-affil=

affil-num=6
en-affil=Department of Breast Oncology, Aichi Cancer Center Hospital
kn-affil=

affil-num=7
en-affil=Department of Breast Oncology, Niigata Cancer Center Hospital
kn-affil=

affil-num=8
en-affil=Department of Breast Surgery and Oncology, Kanagawa Cancer Center
kn-affil=

affil-num=9
en-affil=Department of Breast Oncology, National Cancer Center Hospital East
kn-affil=

affil-num=10
en-affil=Department of Breast Surgery, Social Medical Corporation Hakuaikai Sagara Hospital
kn-affil=

affil-num=11
en-affil=Department of Breast Oncology, National Cancer Center Hospital
kn-affil=

affil-num=12
en-affil=Department of Breast and Endocrine Surgery, Okayama University Hospital
kn-affil=

affil-num=13
en-affil=Department of Breast Oncology, National Hospital Organization Kyushu Cancer Center
kn-affil=

affil-num=14
en-affil=Tokyo Metropolitan Cancer and Infectious Diseases Center, Komagome Hospital
kn-affil=

affil-num=15
en-affil=Division of Breast Surgery, Chiba Cancer Center
kn-affil=

affil-num=16
en-affil=Department of Breast Oncology, Gunma Prefectural Cancer Center
kn-affil=

affil-num=17
en-affil=Department of Medical Oncology, Fukushima Medical University
kn-affil=

affil-num=18
en-affil=Department of Advanced Clinical Research and Development, Nagoya City University
kn-affil=

affil-num=19
en-affil=Department of Breast and Endocrine Surgery, Okayama University Hospital
kn-affil=
en-keyword=breast cancer
kn-keyword=breast cancer
en-keyword=locoregional recurrence
kn-keyword=locoregional recurrence
en-keyword=adjuvant chemotherapy
kn-keyword=adjuvant chemotherapy
en-keyword=inverse probability of treatment weighting
kn-keyword=inverse probability of treatment weighting
END

start-ver=1.4
cd-journal=joma
no-vol=13
cd-vols=
no-issue=
article-no=
start-page=RP99936
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250811
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Redistribution of fragmented mitochondria ensures symmetric organelle partitioning and faithful chromosome segregation in mitotic mouse zygotes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=In cleavage-stage embryos, preexisting organelles partition evenly into daughter blastomeres without significant cell growth after symmetric cell division. The presence of mitochondrial DNA within mitochondria and its restricted replication during preimplantation development makes their inheritance particularly important. While chromosomes are precisely segregated by the mitotic spindle, the mechanisms controlling mitochondrial partitioning remain poorly understood. In this study, we investigate the mechanism by which Dynamin-related protein 1 (Drp1) controls the mitochondrial redistribution and partitioning during embryonic cleavage. Depletion of Drp1 in mouse zygotes causes marked mitochondrial aggregation, and the majority of embryos arrest at the 2 cell stage. Clumped mitochondria are located in the center of mitotic Drp1-depleted zygotes with less uniform distribution, thereby preventing their symmetric partitioning. Asymmetric mitochondrial inheritance is accompanied by functionally inequivalent blastomeres with biased ATP and endoplasmic reticulum Ca2+ levels. We also find that marked mitochondrial centration in Drp1-depleted zygotes prevents the assembly of parental chromosomes, resulting in chromosome segregation defects and binucleation. Thus, mitochondrial fragmentation mediated by Drp1 ensures proper organelle positioning and partitioning into functional daughters during the first embryonic cleavage.
en-copyright=
kn-copyright=

en-aut-name=GekkoHaruna
en-aut-sei=Gekko
en-aut-mei=Haruna
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NomuraRuri
en-aut-sei=Nomura
en-aut-mei=Ruri
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KuzuharaDaiki
en-aut-sei=Kuzuhara
en-aut-mei=Daiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KaneyasuMasato
en-aut-sei=Kaneyasu
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KosekiGenpei
en-aut-sei=Koseki
en-aut-mei=Genpei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=AdhikariDeepak
en-aut-sei=Adhikari
en-aut-mei=Deepak
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MioYasuyuki
en-aut-sei=Mio
en-aut-mei=Yasuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=CarrollJohn
en-aut-sei=Carroll
en-aut-mei=John
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KonoTomohiro
en-aut-sei=Kono
en-aut-mei=Tomohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=FunahashiHiroaki
en-aut-sei=Funahashi
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=WakaiTakuya
en-aut-sei=Wakai
en-aut-mei=Takuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

affil-num=1
en-affil=Department of Animal Science, Graduate School of Environment and Life Science, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Animal Science, Graduate School of Environment and Life Science, Okayama University
kn-affil=

affil-num=3
en-affil=Reproductive Centre, Mio Fertility Clinic
kn-affil=

affil-num=4
en-affil=Department of Animal Science, Graduate School of Environment and Life Science, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Animal Science, Graduate School of Environment and Life Science, Okayama University
kn-affil=

affil-num=6
en-affil=Development and Stem Cell Program and Department of Anatomy and Developmental Biology, Monash Biomedicine Discovery Institute, Monash University
kn-affil=

affil-num=7
en-affil=Reproductive Centre, Mio Fertility Clinic
kn-affil=

affil-num=8
en-affil=Development and Stem Cell Program and Department of Anatomy and Developmental Biology, Monash Biomedicine Discovery Institute, Monash University
kn-affil=

affil-num=9
en-affil=Department of Bioscience, Tokyo University of Agriculture
kn-affil=

affil-num=10
en-affil=Department of Animal Science, Graduate School of Environment and Life Science, Okayama University
kn-affil=

affil-num=11
en-affil=Department of Animal Science, Graduate School of Environment and Life Science, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=53
cd-vols=
no-issue=22
article-no=
start-page=gkaf1322
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20251126
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=eIF2D promotes 40S ribosomal subunit recycling during intrinsic ribosome destabilization
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Although eukaryotic initiation factor 2D (eIF2D) is implicated in translation initiation, reinitiation, and ribosome recycling, its precise role remains unclear. Here, we show that eIF2D promotes 40S ribosome recycling during intrinsic ribosome destabilization (IRD), a process in which ribosomes stochastically destabilize while translating proteins with consecutive acidic amino acids at their NH2-terminus. Unrecycled 40S ribosomes accumulate in eIF2D-deficient cells, leading to 80S ribosome stalling. Selective translation complex profiling (TCP-seq) reveals that eIF2D preferentially associates with IRD-prone regions. The winged helix domain, unique to eIF2D but absent in MCTS1–DENR, enhances its binding to 40S subunits, but likely clashes with ABCE1 during stop-codon-associated recycling. Loss of eIF2D reduces the expression of IRD-inducing proteins, including splicing factors. Together, these findings define a previously unappreciated role for eIF2D in 40S recycling and clarify its mechanistic divergence from the MCTS1–DENR complex.
en-copyright=
kn-copyright=

en-aut-name=IchiharaKazuya
en-aut-sei=Ichihara
en-aut-mei=Kazuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ShiraishiTaichi
en-aut-sei=Shiraishi
en-aut-mei=Taichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ChadaniYuhei
en-aut-sei=Chadani
en-aut-mei=Yuhei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KitoYuki
en-aut-sei=Kito
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ShiraishiChisa
en-aut-sei=Shiraishi
en-aut-mei=Chisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=HirataMina
en-aut-sei=Hirata
en-aut-mei=Mina
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TakahashiYuta
en-aut-sei=Takahashi
en-aut-mei=Yuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KoboAkinao
en-aut-sei=Kobo
en-aut-mei=Akinao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=HatanoAtsushi
en-aut-sei=Hatano
en-aut-mei=Atsushi
kn-aut-name=
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en-aut-name=MatsumotoMasaki
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en-aut-name=MachidaKodai
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ORCID=

en-aut-name=ImatakaHiroaki
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ORCID=

en-aut-name=ToyodaAtsushi
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ORCID=

en-aut-name=Mishiro-SatoEmi
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aut-affil-num=14
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en-aut-name=NojimaTakayuki
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en-aut-name=ItoTakuhiro
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en-aut-name=TaguchiHideki
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aut-affil-num=17
ORCID=

en-aut-name=NakayamaKeiichi I
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aut-affil-num=18
ORCID=

en-aut-name=MatsumotoAkinobu
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affil-num=1
en-affil=Division of Biological Science, Graduate School of Science, Nagoya University
kn-affil=

affil-num=2
en-affil=Division of Biological Science, Graduate School of Science, Nagoya University
kn-affil=

affil-num=3
en-affil=Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=4
en-affil=Division of Cell Biology, Medical Institute of Bioregulation, Kyushu University
kn-affil=

affil-num=5
en-affil=Division of Biological Science, Graduate School of Science, Nagoya University
kn-affil=

affil-num=6
en-affil=Division of Biological Science, Graduate School of Science, Nagoya University
kn-affil=

affil-num=7
en-affil=Division of Biological Science, Graduate School of Science, Nagoya University
kn-affil=

affil-num=8
en-affil=School of Life Science and Technology, Institute of Science Tokyo
kn-affil=

affil-num=9
en-affil=Department of Omics and Systems Biology, Graduate School of Medical and Dental Sciences, Niigata University
kn-affil=

affil-num=10
en-affil=Department of Omics and Systems Biology, Graduate School of Medical and Dental Sciences, Niigata University
kn-affil=

affil-num=11
en-affil=Graduate School of Engineering, University of Hyogo
kn-affil=

affil-num=12
en-affil=Graduate School of Engineering, University of Hyogo
kn-affil=

affil-num=13
en-affil=Advanced Genomics Center, National Institute of Genetics
kn-affil=

affil-num=14
en-affil=Institute of Transformative Bio-Molecules (WPI-ITbM), Nagoya University
kn-affil=

affil-num=15
en-affil=Medical Institute of Bioregulation, Kyushu University
kn-affil=

affil-num=16
en-affil=Laboratory for Translation Structural Biology, RIKEN Center for Integrative Medical Sciences
kn-affil=

affil-num=17
en-affil=School of Life Science and Technology, Institute of Science Tokyo 
kn-affil=

affil-num=18
en-affil=Division of Cell Biology, Medical Institute of Bioregulation, Kyushu University
kn-affil=

affil-num=19
en-affil=Division of Biological Science, Graduate School of Science, Nagoya University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=38
cd-vols=
no-issue=2
article-no=
start-page=222
end-page=225
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250104
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Ethical Use of Cadaveric Images in Anatomical Textbooks, Atlases, and Journals: A Consensus Response From Authors and Editors
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Nowadays, consent to use donor bodies for medical education and research is obtained from the body donors and their families before the donation. Recently, the International Federation of Associations of Anatomists (IFAA) published guidelines that could restrict the appearance of cadaveric images in commercial anatomical resources such as textbooks and other educational products. These guidelines state that the donor must expressly consent to using such images for this purpose. Cadaveric photos and drawings made from dissections of cadavers have been used in anatomy textbooks and atlases for hundreds of years. They are invaluable for anatomy students and clinical/surgical practitioners. The IFAA guidelines should not restrict the use of those older books; to do so would infringe the rights of those seeking knowledge from these resources. As the images in such textbooks and atlases are anonymized and are used for teaching and research, and the donors and their families are informed about this before the donation, we believe no additional consent is needed. It is impossible to separate educational from “commercial” usage entirely in any situation, e.g., publications from publishers and the use of cadavers in medical schools. Therefore, our best efforts to avoid unethical use of cadaveric images by following traditional consent processes are still needed so that more people will reap the benefits from them. As senior textbook/atlas authors/editors from over 10 countries, we believe that using cadaveric images in anatomy textbooks is appropriate, and no additional consent should be necessary. Such usage falls within the good faith of professionals using these invaluable gifts.
en-copyright=
kn-copyright=

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en-aut-name=ReinaMiguel Angel
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en-aut-name=AbrahamsPeter H.
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en-aut-name=AndersonRobert H.
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ORCID=

en-aut-name=IbaragiSoichiro
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aut-affil-num=33
ORCID=

en-aut-name=LoukasMarios
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ORCID=

en-aut-name=TubbsR. Shane
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kn-aut-mei=
aut-affil-num=35
ORCID=

affil-num=1
en-affil=Department of Neurosurgery, Tulane University School of Medicine
kn-affil=

affil-num=2
en-affil=Division in Anatomy & Development Biology, Department of Oral Biology, Yonsei University College of Dentistry
kn-affil=

affil-num=3
en-affil=Department of Clinical Anatomy, Tokyo Medical and Dental University (TMDU)
kn-affil=

affil-num=4
en-affil=UK
kn-affil=

affil-num=5
en-affil=UK
kn-affil=

affil-num=6
en-affil=Department of Integral Adult Dentistry, Center for Research in Dental Sciences (CICO), Dental School, Universidad de La Frontera
kn-affil=

affil-num=7
en-affil=Department of Neurosurgery, Tokai University School of Medicine
kn-affil=

affil-num=8
en-affil=Department of Anatomy, Rama Medical College & Research Centre
kn-affil=

affil-num=9
en-affil=Department of Anatomical Sciences, School of Medicine, St. George's University
kn-affil=

affil-num=10
en-affil=Department of Anatomy, Kasturba Medical College Mangalore, Manipal Academy of Higher Education
kn-affil=

affil-num=11
en-affil=Department of Neurologic Surgery, Mayo Clinic
kn-affil=

affil-num=12
en-affil=Department of Anatomy, University of Valencia
kn-affil=

affil-num=13
en-affil=Department of Anatomy, Faculty of Medicine, Ankara University
kn-affil=

affil-num=14
en-affil=Department of Neurological Surgery, University of Wisconsin
kn-affil=

affil-num=15
en-affil=Department of Neuroplastic and Reconstructive Surgery Social Medical Corporation Kotobukikai Tominaga Hospital
kn-affil=

affil-num=16
en-affil=Department of Neurosurgery, Stanford University School of Medicine
kn-affil=

affil-num=17
en-affil=Department of Anatomy, Daegu Catholic University School of Medicine
kn-affil=

affil-num=18
en-affil=Department of Medical Education, Dr. Kiran C. Patel College of Allopathic Medicine, Nova Southeastern University (NSU) 
kn-affil=

affil-num=19
en-affil=Department of Radiological Sciences, David Geffen School of Medicine at UCLA, Ronald Reagan UCLA Medical Center 
kn-affil=

affil-num=20
en-affil=Medical Sciences Department, Faculty of Medicine, Clinical Anatomy, Embryology and Neuroscience Research Group, University of Girona
kn-affil=

affil-num=21
en-affil=Division of Gross and Clinical Anatomy, Department of Anatomy, Kurume University School of Medicine
kn-affil=

affil-num=22
en-affil=Medical Sciences Department, Faculty of Medicine, Clinical Anatomy, Embryology and Neuroscience Research Group, University of Girona
kn-affil=

affil-num=23
en-affil=University Hospital of North Durham
kn-affil=

affil-num=24
en-affil=Cardiac Morphology, Royal Brompton & Harefield Hospitals
kn-affil=

affil-num=25
en-affil=University of California Los Angeles (UCLA) Cardiac Arrhythmia Center, Cardiovascular and Interventional Programs, UCLA Health System, David Geffen School of Medicine at UCLA 
kn-affil=

affil-num=26
en-affil=Department of Otorhinolaryngology, Graduate School of Medical Sciences, Kyushu University
kn-affil=

affil-num=27
en-affil=Division of Gross and Clinical Anatomy, Department of Anatomy, Kurume University School of Medicine
kn-affil=

affil-num=28
en-affil=Laboratory of Surgical NeuroAnatomy (LSNA), director of the Body Donation and Dissection Rooms Service, Faculty of Medicine and Health of Science, University of Barcelona
kn-affil=

affil-num=29
en-affil=Surgery Specialties Department, University of Valencia
kn-affil=

affil-num=30
en-affil=CEU‐San‐Pablo University School of Medicine
kn-affil=

affil-num=31
en-affil=Warwick Medical School
kn-affil=

affil-num=32
en-affil=Biosciences Institute, Newcastle University
kn-affil=

affil-num=33
en-affil=Department of Oral and Maxillofacial Surgery, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=34
en-affil=Department of Anatomical Sciences, School of Medicine, St. George's University
kn-affil=

affil-num=35
en-affil=Department of Neurosurgery, Tulane University School of Medicine
kn-affil=
en-keyword=anatomy
kn-keyword=anatomy
en-keyword=cadaver
kn-keyword=cadaver
en-keyword=commercial
kn-keyword=commercial
en-keyword=consent
kn-keyword=consent
en-keyword=dissection
kn-keyword=dissection
en-keyword=donors
kn-keyword=donors
en-keyword=medical education
kn-keyword=medical education
en-keyword=medical ethics
kn-keyword=medical ethics
en-keyword=publishing
kn-keyword=publishing
END

start-ver=1.4
cd-journal=joma
no-vol=8
cd-vols=
no-issue=1
article-no=
start-page=1720
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20251205
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A genome-wide association study identifies the GPM6A locus associated with age at onset in ALS
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Amyotrophic lateral sclerosis (ALS) exhibits considerable clinical variability, such as differences in age at onset (AAO). Multiple factors, including genetic factors, may underlie this variability; however, the specific determinants remain unclear. To identify genes affecting AAO, we have conducted a genome-wide association study in Japanese patients with ALS (discovery cohort: n = 1808; replication cohort: n = 207). Here, we show that the minor A allele of rs113161727 at the ADAM29-GPM6A locus is associated with a younger AAO in the discovery cohort (effect, -4.27 years; p = 4.60 × 10-8); this finding has been confirmed in the replication cohort (p = 0.0068) and meta-analysis (p = 1.08 × 10−9). Among 65 ALS patients with a SOD1 mutation, the AAO has been found to be 10.2 years younger in those with the A allele than in those without it (p = 0.002). This variant correlates with GPM6A upregulation in iPSC-derived motor neurons, suggesting GPM6A as a candidate AAO modifier. Overall, our study highlights the impact of genetic modifiers on ALS heterogeneity and provides a potential target for delaying disease onset.
en-copyright=
kn-copyright=

en-aut-name=NakamuraRyoichi
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ORCID=

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ORCID=

en-aut-name=AtsutaNaoki
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aut-affil-num=3
ORCID=

en-aut-name=MatsudaYumi
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aut-affil-num=4
ORCID=

en-aut-name=MorimotoSatoru
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aut-affil-num=5
ORCID=

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ORCID=

en-aut-name=KatsunoMasahisa
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aut-affil-num=7
ORCID=

en-aut-name=IzumiYuishin
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aut-affil-num=8
ORCID=

en-aut-name=MoritaMitsuya
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aut-affil-num=9
ORCID=

en-aut-name=IwataIkuko
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kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=YabeIchiro
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en-aut-mei=Ichiro
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kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=NakazatoTomoko
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en-aut-mei=Tomoko
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kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=HattoriNobutaka
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kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=HirayamaTakehisa
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kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=KanoOsamu
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aut-affil-num=15
ORCID=

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aut-affil-num=16
ORCID=

en-aut-name=SuzukiNaoki
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kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=AokiMasashi
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affil-num=1
en-affil=Department of Neurology, Aichi Medical University School of Medicine
kn-affil=

affil-num=2
en-affil=Division of ALS Research, Aichi Medical University School of Medicine
kn-affil=

affil-num=3
en-affil=Department of Neurology, Aichi Medical University School of Medicine
kn-affil=

affil-num=4
en-affil=Public Health Informatics Unit, Department of Integrated Health Sciences, Nagoya University Graduate School of Medicine
kn-affil=

affil-num=5
en-affil=Keio University Regenerative Medicine Research Center, Kawasaki
kn-affil=

affil-num=6
en-affil=Department of Neurology, Nagoya University Graduate School of Medicine
kn-affil=

affil-num=7
en-affil=Department of Neurology, Nagoya University Graduate School of Medicine
kn-affil=

affil-num=8
en-affil=Department of Neurology, Tokushima University Graduate School of Biomedical Sciences
kn-affil=

affil-num=9
en-affil=Division of Neurology, Department of Internal Medicine, Jichi Medical University
kn-affil=

affil-num=10
en-affil=Department of Neurology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University
kn-affil=

affil-num=11
en-affil=Department of Neurology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University
kn-affil=

affil-num=12
en-affil=Department of Neurology, Juntendo University School of Medicine
kn-affil=

affil-num=13
en-affil=Department of Neurology, Juntendo University School of Medicine
kn-affil=

affil-num=14
en-affil=Department of Neurology, Toho University Faculty of Medicine
kn-affil=

affil-num=15
en-affil=Department of Neurology, Toho University Faculty of Medicine
kn-affil=

affil-num=16
en-affil=Department of Neurology, Mie University Graduate School of Medicine
kn-affil=

affil-num=17
en-affil=Department of Neurology, Tohoku University Graduate School of Medicine
kn-affil=

affil-num=18
en-affil=Department of Neurology, Tohoku University Graduate School of Medicine
kn-affil=

affil-num=19
en-affil=Department of Neurology, Graduate School of Medicine, Chiba University
kn-affil=

affil-num=20
en-affil=Department of Neurology, Graduate School of Medicine, Chiba University
kn-affil=

affil-num=21
en-affil=Department of Neurology, Vihara Hananosato Hospital
kn-affil=

affil-num=22
en-affil=Department of Neurology, NHO Higashinagoya National Hospital
kn-affil=

affil-num=23
en-affil=Department of Neurology, NHO Higashinagoya National Hospital
kn-affil=

affil-num=24
en-affil=Department of Neurology, Brain Research Institute, Niigata University
kn-affil=

affil-num=25
en-affil=Department of Neurology, Brain Research Institute, Niigata University
kn-affil=

affil-num=26
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=27
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=28
en-affil=Department of Neurology, Tokyo Metropolitan Neurological Hospital
kn-affil=

affil-num=29
en-affil=Department of Neurology, Tokyo Metropolitan Neurological Hospital
kn-affil=

affil-num=30
en-affil=Department of Neurology, Gunma University Graduate School of Medicine
kn-affil=

affil-num=31
en-affil=Division of Neurology, NHO Sagamihara National Hospital
kn-affil=

affil-num=32
en-affil=Department of Neurology and Stroke Medicine, Yokohama City University Graduate School of Medicine
kn-affil=

affil-num=33
en-affil=Department of Neurology and Neurological Science, NucleoTIDE and PepTIDE Drug Discovery Center (TIDE), Institute of Science Tokyo
kn-affil=

affil-num=34
en-affil=Department of Neurology, Fukushima Medical University School of Medicine
kn-affil=

affil-num=35
en-affil=Department of Neurology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine
kn-affil=

affil-num=36
en-affil=Department of Neurology, Tokushima University Graduate School of Biomedical Sciences
kn-affil=

affil-num=37
en-affil=Department of Neurology, Fujita Health University
kn-affil=

affil-num=38
en-affil=Division of ALS Research, Aichi Medical University School of Medicine
kn-affil=

affil-num=39
en-affil=Division of ALS Research, Aichi Medical University School of Medicine
kn-affil=

affil-num=40
en-affil=Division of ALS Research, Aichi Medical University School of Medicine
kn-affil=

affil-num=41
en-affil=Department of Neurology, Aichi Medical University School of Medicine
kn-affil=

affil-num=42
en-affil=Department of Neurology, Aichi Medical University School of Medicine
kn-affil=

affil-num=43
en-affil=Department of Neurology, Aichi Medical University School of Medicine
kn-affil=

affil-num=44
en-affil=Keio University Regenerative Medicine Research Center, Kawasaki
kn-affil=

affil-num=45
en-affil=Keio University Regenerative Medicine Research Center, Kawasaki
kn-affil=

affil-num=46
en-affil=Keio University Regenerative Medicine Research Center, Kawasaki
kn-affil=

affil-num=47
en-affil=Public Health Informatics Unit, Department of Integrated Health Sciences, Nagoya University Graduate School of Medicine
kn-affil=

affil-num=48
en-affil=Division of ALS Research, Aichi Medical University School of Medicine
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=445
cd-vols=
no-issue=
article-no=
start-page=134071
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=20260215
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Cardiac characteristics of Fabry disease from baseline enrolment data in a nationwide prospective Japanese registry
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Fabry disease (FD) is an important disease in the cardiovascular field because a significant proportion of patients with FD die from cardiac lesions.<br>
Methods: A multicenter prospective registration study of patients with FD throughout Japan was designed. The baseline clinical characteristics of 175 patients are presented here.<br>
Results: The mean ages at enrolment and at diagnosis were 52 ± 16 and 43 ± 18 years, respectively, with men accounting for 38 % of the patients. In the cohort, 24 % of the patients had the classical hemizygote male type, whereas 14 % had the late-onset male type, and 62 % had the heterozygote female type. On electrocardiography data at enrolment in 92 patients with left ventricular hypertrophy (LVH) (maximum LV wall thickness > 12 mm), 12 % showed a short PQ interval (< 120 msec), and 33 % had a short PendQ interval (≤ 40 msec). The Sokolow-Lyon voltage was high (6.1 ± 13.1 mv). Regarding the distribution of LVH patterns, 77 % of the patients showed concentric diffuse LVH, 16 % of the patients had asymmetric septal hypertrophy, and 1 % of the patients had hypertrophy confined to the LV apex. With regard to implantation of cardiac devices, permanent pacemakers had been implanted in 5 % of the patients and defibrillators had been implanted in 12 patients (7 %), for primary prevention in nine patients and for secondary prevention in three patients.<br>
Conclusion: As the first large-scale prospective registry of FD patients in Japan, this study has provided valuable baseline data for the cardiac features and management of FD.
en-copyright=
kn-copyright=

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en-aut-name=NakamuraKazuto
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en-aut-name=NakamuraKazufumi
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en-aut-name=IkenagaHiroki
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aut-affil-num=24
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en-aut-name=KandaTakahiro
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aut-affil-num=25
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en-aut-name=KinugasaYoshiharu
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en-aut-name=ItoHiromasa
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aut-affil-num=27
ORCID=

en-aut-name=OnoueKenji
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kn-aut-mei=
aut-affil-num=28
ORCID=

en-aut-name=KanamoriHiromitsu
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aut-affil-num=29
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en-aut-name=KitaokaHiroaki
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kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=30
ORCID=

affil-num=1
en-affil=Department of Cardiology and Geriatrics, Kochi Medical School, Kochi University
kn-affil=

affil-num=2
en-affil=Division of Cardiology, Internal Medicine III, Hamamatsu University School of Medicine
kn-affil=

affil-num=3
en-affil=Division of Cardiology, Department of Internal Medicine, The Jikei University School of Medicine
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Tohoku University Graduate School of Medicine
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, Osaka Metropolitan University, Graduate School of Medicine
kn-affil=

affil-num=6
en-affil=Department of Cardiology, Keio University School of Medicine
kn-affil=

affil-num=7
en-affil=Department of Cardiovascular, Renal and Metabolic Medicine, Sapporo Medical University School of Medicine
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Medicine and Hypertension, Graduate School of Medical and Dental Sciences, Kagoshima University
kn-affil=

affil-num=9
en-affil=Department of Cardiovascular Medicine, The University of Osaka Graduate School of Medicine
kn-affil=

affil-num=10
en-affil=Division of Cardiology and Nephrology, Department of Internal Medicine, Asahikawa Medical University
kn-affil=

affil-num=11
en-affil=Department of Heart Failure and Transplantation, National Cerebral and Cardiovascular Center
kn-affil=

affil-num=12
en-affil=Department of Cardiology, Institute of Medicine, University of Tsukuba
kn-affil=

affil-num=13
en-affil=Department of Cardiovascular Medicine, Fukushima Medical University
kn-affil=

affil-num=14
en-affil=Department of Cardiovascular Medicine, Kitasato University School of Medicine
kn-affil=

affil-num=15
en-affil=Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University
kn-affil=

affil-num=16
en-affil=Department of Cardiovascular Biology and Medicine, Juntendo University Graduate School of Medicine
kn-affil=

affil-num=17
en-affil=Department of Cardiology, Fujita Health University
kn-affil=

affil-num=18
en-affil=Department of Cardiology, Tokyo Women's Medical University
kn-affil=

affil-num=19
en-affil=Department of Cardiology, National Defense Medical College
kn-affil=

affil-num=20
en-affil=Department of Cardiovascular Medicine, Faculty of Medicine and Graduate School of Medicine, Hokkaido University
kn-affil=

affil-num=21
en-affil=Department of Pharmacology, St. Marianna University School of Medicine
kn-affil=

affil-num=22
en-affil=Department of Cardiovascular Medicine, University of Yamanashi, Faculty of Medicine
kn-affil=

affil-num=23
en-affil=Center for Advanced Heart Failure, Okayama University Hospital
kn-affil=

affil-num=24
en-affil=Department of Cardiovascular Medicine, Hiroshima University Graduate School of Biomedical and Health Sciences
kn-affil=

affil-num=25
en-affil=Department of Internal Medicine, Division of Cardiology, Hamamatsu Red Cross Hospital
kn-affil=

affil-num=26
en-affil=Department of Cardiovascular Medicine and Endocrinology and Metabolism, Faculty of Medicine, Tottori University
kn-affil=

affil-num=27
en-affil=Department of Cardiology, Mie University Hospital
kn-affil=

affil-num=28
en-affil=Department of Cardiovascular Medicine, Nara Medical University
kn-affil=

affil-num=29
en-affil=Department of Cardiology, Gifu University Graduate School of Medicine
kn-affil=

affil-num=30
en-affil=Department of Cardiology and Geriatrics, Kochi Medical School, Kochi University
kn-affil=
en-keyword=Fabry disease
kn-keyword=Fabry disease
en-keyword=Prospective study
kn-keyword=Prospective study
en-keyword=Left ventricular hypertrophy
kn-keyword=Left ventricular hypertrophy
en-keyword=Treatment
kn-keyword=Treatment
END

start-ver=1.4
cd-journal=joma
no-vol=8
cd-vols=
no-issue=1
article-no=
start-page=1773
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20251216
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Single-cell and spatial transcriptomic characterization of pulmonary pleomorphic carcinoma
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Pulmonary pleomorphic carcinoma (PPC) is a rare subtype of lung cancer that comprises both epithelial and sarcomatoid components. The molecular basis of PPC, including the cellular dynamics of its components, remains largely unknown. To elucidate potential therapeutic targets for PPC, we perform a multi-omics analysis incorporating digital spatial profiling and single-cell RNA sequencing (scRNA-seq). PPC exhibits diverse driver gene alterations, including MET exon 14 skipping mutation (METex14) and ALK fusion. In spatial transcriptomics, MET gene and protein are overexpressed exclusively within the epithelial component and not in the sarcomatoid component, even in patients harboring METex14. Epithelial-mesenchymal transition (EMT)-related transcriptional changes, along with extracellular matrix (ECM) remodeling between the epithelial and sarcomatoid components, are observed. scRNA-seq identifies cell populations within the epithelial component that contribute to the malignant transformation and differentiation of the sarcomatoid component. They are characterized by an intermediate EMT state with ECM remodeling signature, suggesting their potential as novel therapeutic targets for PPC.
en-copyright=
kn-copyright=

en-aut-name=MatsuokaAtsushi
en-aut-sei=Matsuoka
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ShienKazuhiko
en-aut-sei=Shien
en-aut-mei=Kazuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TomidaShuta
en-aut-sei=Tomida
en-aut-mei=Shuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OhkiMasayoshi
en-aut-sei=Ohki
en-aut-mei=Masayoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HisamatsuKazuya
en-aut-sei=Hisamatsu
en-aut-mei=Kazuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=FujiwaraRyota
en-aut-sei=Fujiwara
en-aut-mei=Ryota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=IshimuraKosei
en-aut-sei=Ishimura
en-aut-mei=Kosei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=FujiiRyunosuke
en-aut-sei=Fujii
en-aut-mei=Ryunosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=HigashiharaTomoaki
en-aut-sei=Higashihara
en-aut-mei=Tomoaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=HayashiNaohiro
en-aut-sei=Hayashi
en-aut-mei=Naohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=OkadaKazuhiro
en-aut-sei=Okada
en-aut-mei=Kazuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=YoshichikaRyo
en-aut-sei=Yoshichika
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=MukoharaFumiaki
en-aut-sei=Mukohara
en-aut-mei=Fumiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=YoshikawaMao
en-aut-sei=Yoshikawa
en-aut-mei=Mao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=FukumotoYuma
en-aut-sei=Fukumoto
en-aut-mei=Yuma
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=SuzawaKen
en-aut-sei=Suzawa
en-aut-mei=Ken
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=TomiokaYasuaki
en-aut-sei=Tomioka
en-aut-mei=Yasuaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=TanakaShin
en-aut-sei=Tanaka
en-aut-mei=Shin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=MiyoshiKentaroh
en-aut-sei=Miyoshi
en-aut-mei=Kentaroh
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=OkazakiMikio
en-aut-sei=Okazaki
en-aut-mei=Mikio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

en-aut-name=SugimotoSeiichiro
en-aut-sei=Sugimoto
en-aut-mei=Seiichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=21
ORCID=

en-aut-name=OtaniYusuke
en-aut-sei=Otani
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=22
ORCID=

en-aut-name=TanakaAtsushi
en-aut-sei=Tanaka
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=23
ORCID=

en-aut-name=InoueHirofumi
en-aut-sei=Inoue
en-aut-mei=Hirofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=24
ORCID=

en-aut-name=TogashiYosuke
en-aut-sei=Togashi
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=25
ORCID=

en-aut-name=YamamotoHidetaka
en-aut-sei=Yamamoto
en-aut-mei=Hidetaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=26
ORCID=

en-aut-name=EnnishiDaisuke
en-aut-sei=Ennishi
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=27
ORCID=

en-aut-name=ToyookaShinichi
en-aut-sei=Toyooka
en-aut-mei=Shinichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=28
ORCID=

affil-num=1
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=
kn-affil=

affil-num=4
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=12
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=13
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=14
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=15
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=16
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=17
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=18
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=19
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=20
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=21
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=22
en-affil=Department of Pathology, Beth Israel Deaconess Medical Center
kn-affil=

affil-num=23
en-affil=Department of Pathology, Beth Israel Deaconess Medical Center
kn-affil=

affil-num=24
en-affil=Center for Comprehensive Genomic Medicine, Okayama University Hospital
kn-affil=

affil-num=25
en-affil=Department of Tumor Microenvironment, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=26
en-affil=Department of Pathology and Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=27
en-affil=Center for Comprehensive Genomic Medicine, Okayama University Hospital
kn-affil=

affil-num=28
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=32
cd-vols=
no-issue=6
article-no=
start-page=dsaf030
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20251022
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=MedakaBase as a unified genomic resource platform for medaka fish biology
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Medaka, a group of small, mostly freshwater fishes in the teleost order Beloniformes, includes the rice fish Oryzias latipes, a useful model organism studied in diverse biological fields. Chromosome-scale genome sequences of the Hd-rR strain of this species were obtained in 2007, and its improved version has facilitated various genome-wide studies. However, despite its widespread utility, omics data for O. latipes are dispersed across various public databases and lack a unified platform. To address this, the medaka section of the National Bioresource Project (NBRP) of Japan established a genome informatics team in 2022 tasked with providing various in silico solutions for bench biologists. This initiative led to the launch of MedakaBase (https://medakabase.nbrp.jp), a web server that enables gene-oriented analysis including exhaustive sequence similarity searches. MedakaBase also provides on-demand browsing of diverse genome-wide datasets, including tissue-specific transcriptomes and intraspecific genomic variations, integrated with gene models from different sources. Additionally, the platform offers gene models optimized for single-cell transcriptome analysis, which often requires coverage of the 3′ untranslated region (UTR) of transcripts. Currently, MedakaBase provides genome-wide data for seven Oryzias species, including original data for O. mekongensis and O. luzonensis produced by the NBRP team. This article outlines technical details behind the data provided by MedakaBase.
en-copyright=
kn-copyright=

en-aut-name=MorikamiKenji
en-aut-sei=Morikami
en-aut-mei=Kenji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TanizawaYasuhiro
en-aut-sei=Tanizawa
en-aut-mei=Yasuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YaguraMasaru
en-aut-sei=Yagura
en-aut-mei=Masaru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SakamotoMika
en-aut-sei=Sakamoto
en-aut-mei=Mika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KawamotoShoko
en-aut-sei=Kawamoto
en-aut-mei=Shoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NakamuraYasukazu
en-aut-sei=Nakamura
en-aut-mei=Yasukazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YamaguchiKatsushi
en-aut-sei=Yamaguchi
en-aut-mei=Katsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=ShigenobuShuji
en-aut-sei=Shigenobu
en-aut-mei=Shuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=NaruseKiyoshi
en-aut-sei=Naruse
en-aut-mei=Kiyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=AnsaiSatoshi
en-aut-sei=Ansai
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=KurakuShigehiro
en-aut-sei=Kuraku
en-aut-mei=Shigehiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

affil-num=1
en-affil=Molecular Life History Laboratory, Department of Genomics and Evolutionary Biology, National Institute of Genetics, Research Organization of Information and Systems
kn-affil=

affil-num=2
en-affil=Genome Informatics Laboratory, National Institute of Genetics, Research Organization of Information and Systems
kn-affil=

affil-num=3
en-affil=Molecular Life History Laboratory, Department of Genomics and Evolutionary Biology, National Institute of Genetics, Research Organization of Information and Systems
kn-affil=

affil-num=4
en-affil=Genome Informatics Laboratory, National Institute of Genetics, Research Organization of Information and Systems
kn-affil=

affil-num=5
en-affil=Department of Genetics, Sokendai (Graduate University for Advanced Studies)
kn-affil=

affil-num=6
en-affil=Genome Informatics Laboratory, National Institute of Genetics, Research Organization of Information and Systems
kn-affil=

affil-num=7
en-affil=Trans-Omics Facility, National Institute for Basic Biology
kn-affil=

affil-num=8
en-affil=Trans-Omics Facility, National Institute for Basic Biology
kn-affil=

affil-num=9
en-affil=Laboratory of Bioresources, National Institute for Basic Biology, National Institutes of Natural Sciences
kn-affil=

affil-num=10
en-affil=Ushimado Marine Institute, Okayama University
kn-affil=

affil-num=11
en-affil=Molecular Life History Laboratory, Department of Genomics and Evolutionary Biology, National Institute of Genetics, Research Organization of Information and Systems
kn-affil=
en-keyword=medaka
kn-keyword=medaka
en-keyword=comparative genomics
kn-keyword=comparative genomics
en-keyword=genome browser
kn-keyword=genome browser
en-keyword=MedakaBase
kn-keyword=MedakaBase
en-keyword=Beloniformes
kn-keyword=Beloniformes
END

start-ver=1.4
cd-journal=joma
no-vol=23
cd-vols=
no-issue=1
article-no=
start-page=1387
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20251208
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Tumor marker–guided precision BNCT for CA19-9–positive cancers: a new paradigm in molecularly targeted chemoradiation therapy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Boron neutron capture therapy (BNCT) is a molecularly targeted chemoradiation modality that relies on boron delivery agents such as p-borophenylalanine (BPA), which require LAT1 (L-type amino acid transporter 1) for tumor uptake. However, the limited efficacy of BPA in LAT1-low tumors restricts its therapeutic scope. To address this limitation, we developed a tumor marker–guided BNCT strategy targeting cancers overexpressing the clinically validated glycan biomarker CA19-9.<br>
Methods: We conducted transcriptomic analyses using The Cancer Genome Atlas (TCGA) datasets to identify LAT1-low cancers with high CA19-9 expression. These analyses revealed elevated expression of fucosyltransferase 3 (FUT3), which underlies CA19-9 biosynthesis, in pancreatic, biliary, and ovarian malignancies. Based on this, we synthesized a novel boron compound, fucose-BSH, designed to selectively accumulate in CA19-9–positive tumors. We evaluated its physicochemical properties, pharmacokinetics, biodistribution, and antitumor efficacy in cell lines and xenograft models, comparing its performance to that of BPA.<br>
Results: Fucose-BSH demonstrated significantly greater boron uptake in CA19-9–positive cell lines (AsPC-1, Panc 04.03, HuCCT-1, HSKTC, OVISE) compared to CA19-9–negative PANC-1. In HuCCT-1 xenografts, boron accumulation reached 36.2 ppm with a tumor/normal tissue ratio of 2.1, outperforming BPA. Upon neutron irradiation, fucose-BSH–mediated BNCT achieved > 80% tumor growth inhibition. Notably, fucose-BSH retained therapeutic efficacy in LAT1-deficient models where BPA was ineffective, confirming LAT1-independent targeting.<br>
Conclusions: This study establishes a novel precision BNCT approach by leveraging CA19-9 as a tumor-selective glycan marker for boron delivery. Fucose-BSH offers a promising platform for expanding BNCT to previously inaccessible LAT1-low malignancies, including pancreatic, biliary, and ovarian cancers. These findings provide a clinically actionable strategy for tumor marker–driven chemoradiation and lay the foundation for translational application in BNCT. This strategy has the potential to support companion diagnostic development and precision stratification in ongoing and future BNCT clinical trials.<br>
Translational Relevance: Malignancies with elevated CA19-9 expression, such as pancreatic, biliary, and ovarian cancers, are associated with poor prognosis and limited response to current therapies. This study presents a tumor marker–guided strategy for boron neutron capture therapy (BNCT) by leveraging CA19-9 glycan biology to enable selective tumor targeting via fucose-BSH, a novel boron compound. Through transcriptomic data mining and preclinical validation, fucose-BSH demonstrated LAT1-independent boron delivery, potent BNCT-mediated cytotoxicity, and tumor-specific accumulation in CA19-9–positive models. These findings support a precision chemoradiation approach that addresses a critical gap in BNCT applicability, offering a clinically actionable pathway for patient stratification and therapeutic development in CA19-9–expressing cancers.
en-copyright=
kn-copyright=

en-aut-name=KanehiraNoriyuki
en-aut-sei=Kanehira
en-aut-mei=Noriyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TeraishiFuminori
en-aut-sei=Teraishi
en-aut-mei=Fuminori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TajimaTomoyuki
en-aut-sei=Tajima
en-aut-mei=Tomoyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OsoneTatsunori
en-aut-sei=Osone
en-aut-mei=Tatsunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=GotohKazuyoshi
en-aut-sei=Gotoh
en-aut-mei=Kazuyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=FujimotoTakuya
en-aut-sei=Fujimoto
en-aut-mei=Takuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SakuraiYoshinori
en-aut-sei=Sakurai
en-aut-mei=Yoshinori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KondoNatsuko
en-aut-sei=Kondo
en-aut-mei=Natsuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=NagahisaNarikazu
en-aut-sei=Nagahisa
en-aut-mei=Narikazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=KameiKaoru
en-aut-sei=Kamei
en-aut-mei=Kaoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=FujitaTaiga
en-aut-sei=Fujita
en-aut-mei=Taiga
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=MoriharaAkira
en-aut-sei=Morihara
en-aut-mei=Akira
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=TakaguchiYutaka
en-aut-sei=Takaguchi
en-aut-mei=Yutaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=KitamatsuMizuki
en-aut-sei=Kitamatsu
en-aut-mei=Mizuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=TakaradaTakeshi
en-aut-sei=Takarada
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=ShigeyasuKunitoshi
en-aut-sei=Shigeyasu
en-aut-mei=Kunitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=SuzukiMinoru
en-aut-sei=Suzuki
en-aut-mei=Minoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=FujiwaraToshiyoshi
en-aut-sei=Fujiwara
en-aut-mei=Toshiyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=MichiueHiroyuki
en-aut-sei=Michiue
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

affil-num=1
en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Regenerative Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Medical Laboratory Science, Okayama University Graduate School of Health Sciences
kn-affil=

affil-num=6
en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Institute for Integrated Radiation and Nuclear Science, Kyoto University
kn-affil=

affil-num=8
en-affil=Institute for Integrated Radiation and Nuclear Science, Kyoto University
kn-affil=

affil-num=9
en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=11
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=12
en-affil=Graduate School of Environmental, Life Science, Okayama University
kn-affil=

affil-num=13
en-affil=Faculty of Sustainable Design, Department of Material Design and Engineering, University of Toyama
kn-affil=

affil-num=14
en-affil=Department of Applied Chemistry, Kindai University
kn-affil=

affil-num=15
en-affil=Department of Regenerative Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=16
en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=17
en-affil=Institute for Integrated Radiation and Nuclear Science, Kyoto University
kn-affil=

affil-num=18
en-affil=Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=19
en-affil=Neutron Therapy Research Center, Okayama University
kn-affil=
en-keyword=Boron neutron capture therapy (BNCT)
kn-keyword=Boron neutron capture therapy (BNCT)
en-keyword=Precision BNCT
kn-keyword=Precision BNCT
en-keyword=Fucose-conjugated medicine
kn-keyword=Fucose-conjugated medicine
en-keyword=CA19-9
kn-keyword=CA19-9
en-keyword=Drug discovery
kn-keyword=Drug discovery
END

start-ver=1.4
cd-journal=joma
no-vol=68
cd-vols=
no-issue=1
article-no=
start-page=100720
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=202602
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Dynamin 2 is involved in osteoblast migration by regulating the organization of F-actin
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Objectives: Dynamin, a GTPase that regulates membrane dynamics, has recently been implicated in actin cytoskeletal remodeling. This study aimed to elucidate the role of dynamin in osteoblast migration by examining the effects of dynamin inhibition on the localization and organization of F-actin and dynamin 2 in MC3T3-E1 cells.<br>
Methods: MC3T3-E1 cells were treated with dynamin inhibitors (Dyngo 4a and Dynole 34-2), and cell migration was assessed using a wound-healing assay. Fluorescent staining was performed to analyze the intracellular localization of F-actin and dynamin 2.<br>
Results: Dynamin inhibition significantly reduced the migration of MC3T3-E1 cells. Fluorescence analysis revealed a marked decrease in the accumulation and colocalization of F-actin and dynamin 2 at the protrusion edge. Additionally, dynamin inhibition suppressed the formation of lamellipodia and stress fibers while promoting the appearance of abnormal F-actin clusters in the cytoplasm.<br>
Conclusions: These findings suggest that dynamin plays an essential role in osteoblast migration by regulating actin cytoskeletal remodeling, particularly through the formation of lamellipodia and stress fibers.
en-copyright=
kn-copyright=

en-aut-name=MoriyaTakumi
en-aut-sei=Moriya
en-aut-mei=Takumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SurongA.
en-aut-sei=Surong
en-aut-mei=A.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TatsumiNanami
en-aut-sei=Tatsumi
en-aut-mei=Nanami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YamadaHiroshi
en-aut-sei=Yamada
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TakemotoFumiko
en-aut-sei=Takemoto
en-aut-mei=Fumiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KamiokaHiroshi
en-aut-sei=Kamioka
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=OkamuraHirohiko
en-aut-sei=Okamura
en-aut-mei=Hirohiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=IkegameMika
en-aut-sei=Ikegame
en-aut-mei=Mika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Oral Morphology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Neuroscience, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Neuroscience, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Neuroscience, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Orthodontics, Okayama University Hospital
kn-affil=

affil-num=6
en-affil=Department of Orthodontics, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Oral Morphology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Oral Morphology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Dynamin
kn-keyword=Dynamin
en-keyword=Cell migration
kn-keyword=Cell migration
en-keyword=Osteoblasts
kn-keyword=Osteoblasts
en-keyword=F-actin
kn-keyword=F-actin
END

start-ver=1.4
cd-journal=joma
no-vol=26
cd-vols=
no-issue=19
article-no=
start-page=9630
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20251002
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Critical Requirement of Senescence-Associated CCN3 Expression in CD44-Positive Stem Cells for Osteoarthritis Progression
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Osteoarthritis (OA) is a degenerative joint disease characterized by progressive cartilage breakdown, synovial inflammation, and subchondral bone remodeling. Previous studies have shown that cellular communication network factor 3 (CCN3) expression increases with age in cartilage, and its overexpression promotes OA-like changes by inducing senescence-associated secretory phenotypes. This study aimed to investigate the effect of Ccn3 knockout (KO) on OA development using a murine OA model. Destabilization of the medial meniscus (DMM) surgery was performed in wild-type (WT) and Ccn3-KO mice. Histological scoring and staining were used to assess cartilage degeneration and proteoglycan loss. Gene and protein expressions of catabolic enzyme (Mmp9), hypertrophic chondrocyte marker (Col10a1), senescence marker, and cyclin-dependent kinase inhibitor 1A (Cdkn1a) were evaluated. Single-cell RNA sequencing (scRNA-seq) data from WT and Sox9-deficient cartilage were reanalyzed to identify Ccn3+ progenitor populations. Immunofluorescence staining assessed CD44 and Ki67 expression in articular cartilage. The effects of Ccn3 knockdown on IL-1β-induced Mmp13 and Adamts5 expression in chondrocytes were examined in vitro. Ccn3 KO mice exhibited reduced cartilage degradation and catabolic gene expression compared with WT mice post-DMM. scRNA-seq revealed enriched Ccn3-Cd44 double-positive cells in osteoblast progenitor, synovial mesenchymal stem cell, and mesenchymal stem cell clusters. Immunofluorescence showed increased CCN3+/CD44+ cells in femoral and tibial cartilage and meniscus. Ki67+ cells were significantly increased in DMM-treated Ccn3 KO cartilage, mostly CD44+. In vitro Ccn3 knockdown attenuated IL-1β-induced Mmp13 and Adamts5 expressions in chondrocytes. Ccn3 contributes to OA pathogenesis by promoting matrix degradation, inducing hypertrophic changes, and restricting progenitor cell proliferation, highlighting Ccn3 as a potential therapeutic target for OA.
en-copyright=
kn-copyright=

en-aut-name=HabumugishaJanvier
en-aut-sei=Habumugisha
en-aut-mei=Janvier
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OkudaRyuichiro
en-aut-sei=Okuda
en-aut-mei=Ryuichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HiroseKazuki
en-aut-sei=Hirose
en-aut-mei=Kazuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KuwaharaMiho
en-aut-sei=Kuwahara
en-aut-mei=Miho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=WangZiyi
en-aut-sei=Wang
en-aut-mei=Ziyi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OnoMitsuaki
en-aut-sei=Ono
en-aut-mei=Mitsuaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KamiokaHiroshi
en-aut-sei=Kamioka
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KubotaSatoshi
en-aut-sei=Kubota
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=HattoriTakako
en-aut-sei=Hattori
en-aut-mei=Takako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Biochemistry and Molecular Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Biochemistry and Molecular Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Biochemistry and Molecular Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Biochemistry and Molecular Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Oral Rehabilitation and Regenerative Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Orthodontics, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Biochemistry and Molecular Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Biochemistry and Molecular Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=articular
kn-keyword=articular
en-keyword=cartilage
kn-keyword=cartilage
en-keyword=mesenchymal stem cells
kn-keyword=mesenchymal stem cells
en-keyword=nephroblastoma overexpressed protein
kn-keyword=nephroblastoma overexpressed protein
en-keyword=osteoarthritis
kn-keyword=osteoarthritis
END

start-ver=1.4
cd-journal=joma
no-vol=68
cd-vols=
no-issue=1
article-no=
start-page=100718
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=202602
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Evaluation of Mycobacterium-derived plasmids for application in oral Actinomyces species
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Objectives: Genetic manipulation tools are essential for elucidating the pathogenic mechanisms of microorganisms. Several species of Actinomyces, including A. israelii, are present in the oral cavity and they are the causative agents of actinomycosis. However, efficient gene-editing tools for these species have not yet been developed. In this study, the aim was to evaluate the introduction of foreign genes into Actinomyces using plasmids derived from Mycobacterium, which belong to the same class as Actinomycetes.<br>
Methods: A truncated derivative of pYT923, pYT923S, which contains the replication origin of the M. scrofulaceum plasmid pMSC262 was constructed and introduced into A. israelii by electrotransformation.<br>
Results: pYT923S was successfully introduced into A. israelii. The transformation efficiency of A. israelii was approximately 7–66 CFU/μg of DNA, and all transformed colonies harbored pYT923S. The plasmid recovered from A. israelii replicated in Escherichia coli.<br>
Conclusions: pYT923S was introduced into and maintained within A. israelii. Therefore, the pYT923S vector represents a useful genetic tool for Actinomyces and it is expected to facilitate future studies on the biology and pathogenicity of Actinomyces.
en-copyright=
kn-copyright=

en-aut-name=OharaSakiko
en-aut-sei=Ohara
en-aut-mei=Sakiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ShengYijuan
en-aut-sei=Sheng
en-aut-mei=Yijuan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NishiyaYuki
en-aut-sei=Nishiya
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TosaIkue
en-aut-sei=Tosa
en-aut-mei=Ikue
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TakebeKatsuki
en-aut-sei=Takebe
en-aut-mei=Katsuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ArimuraYuki
en-aut-sei=Arimura
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MeseHiroshi
en-aut-sei=Mese
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=OharaNaoko
en-aut-sei=Ohara
en-aut-mei=Naoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=OharaNaoya
en-aut-sei=Ohara
en-aut-mei=Naoya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Oral Microbiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Oral Microbiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Oral Microbiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Oral Microbiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Dental Pharmacology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Oral and Maxillofacial Reconstructive Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Dentistry and Oral Surgery, Fukuyama City Hospital
kn-affil=

affil-num=8
en-affil=Department of Operative Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Oral Microbiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Actinomyces
kn-keyword=Actinomyces
en-keyword=Plasmid
kn-keyword=Plasmid
en-keyword=Shuttle vector
kn-keyword=Shuttle vector
en-keyword=Transformation
kn-keyword=Transformation
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=1
article-no=
start-page=5762
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250217
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Hypoglycemia and hyperinsulinemia induced by phenolic uremic toxins in CKD and DKD patients
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Patients with end-stage renal disease have lower fasting plasma glucose and HbA1c levels, with significantly higher insulin levels. For a long time, it has been believed that this higher insulin level in renal failure is due to decreased insulin clearance caused by reduced renal function. However, here we reported that accumulation of the gut microbiota-derived uremic toxin, phenyl sulfate (PS) in the renal failure, increased insulin secretion from the pancreas by enhanced glucose-stimulated insulin secretion. Other endogenous sulfides compounds which accumulated as in the renal failure also increased glucose-stimulated insulin secretion from β-cell. With RNA-seq analyses and gene knock down, we demonstrated that insulin secretion evoked by PS was mediated by Ddah2. In addition, we also found that PS increased insulin resistance through lncRNA expression and Erk phosphorylation in the adipocytes. To confirm the relationship between PS and glucose metabolism in human, we recruited 2 clinical cohort studies (DKD and CKD) including 462 patients, and found that there was a weak negative correlation between PS and HbA1c. Because these trials did not measure fasting insulin level, we alternatively used the urinary C-peptide/creatinine ratio (UCPCR) as an indicator of insulin resistance. We found that PS may induce insulin resistance in patients with eGFR < 60 mL/min/1.73 m2. These data suggest that the accumulation of uremic toxins modulates glucose metabolism and induced insulin resistance in CKD and DKD patients. Considering HbA1c as a reflection of chronic hyperglycemia and UCPCR as a reflection of chronic hyperinsulinemia, our findings indicate that PS is negatively associated with hyperglycemia independent of CKD, and positively associated with hyperinsulinemia in DKD patients.
en-copyright=
kn-copyright=

en-aut-name=TonguYoshiyasu
en-aut-sei=Tongu
en-aut-mei=Yoshiyasu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KasaharaTomoko
en-aut-sei=Kasahara
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=AkiyamaYasutoshi
en-aut-sei=Akiyama
en-aut-mei=Yasutoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SuzukiTakehiro
en-aut-sei=Suzuki
en-aut-mei=Takehiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HoHsin-Jung
en-aut-sei=Ho
en-aut-mei=Hsin-Jung
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MatsumotoYotaro
en-aut-sei=Matsumoto
en-aut-mei=Yotaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KujiraiRyota
en-aut-sei=Kujirai
en-aut-mei=Ryota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KikuchiKoichi
en-aut-sei=Kikuchi
en-aut-mei=Koichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=NataKoji
en-aut-sei=Nata
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=KanzakiMakoto
en-aut-sei=Kanzaki
en-aut-mei=Makoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=SuzukiKenshin
en-aut-sei=Suzuki
en-aut-mei=Kenshin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=WatanabeShun
en-aut-sei=Watanabe
en-aut-mei=Shun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=KawabeChiharu
en-aut-sei=Kawabe
en-aut-mei=Chiharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=MiyataYui
en-aut-sei=Miyata
en-aut-mei=Yui
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=ItaiShun
en-aut-sei=Itai
en-aut-mei=Shun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=ToyoharaTakafumi
en-aut-sei=Toyohara
en-aut-mei=Takafumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=SuzukiChitose
en-aut-sei=Suzuki
en-aut-mei=Chitose
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=TanakaTetsuhiro
en-aut-sei=Tanaka
en-aut-mei=Tetsuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=WadaJun
en-aut-sei=Wada
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=TomiokaYoshihisa
en-aut-sei=Tomioka
en-aut-mei=Yoshihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

en-aut-name=AbeTakaaki
en-aut-sei=Abe
en-aut-mei=Takaaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=21
ORCID=

affil-num=1
en-affil=Tohoku University School of Medicine
kn-affil=

affil-num=2
en-affil=Department of Clinical Biology and Hormonal Regulation, Tohoku University Graduate School of Medicine
kn-affil=

affil-num=3
en-affil=Laboratory of Oncology, Pharmacy Practice and Sciences, Tohoku University Graduate School of Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Clinical Biology and Hormonal Regulation, Tohoku University Graduate School of Medicine
kn-affil=

affil-num=5
en-affil=Department of Clinical Biology and Hormonal Regulation, Tohoku University Graduate School of Medicine
kn-affil=

affil-num=6
en-affil=Laboratory of Oncology, Pharmacy Practice and Sciences, Tohoku University Graduate School of Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Laboratory of Oncology, Pharmacy Practice and Sciences, Tohoku University Graduate School of Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Clinical Biology and Hormonal Regulation, Tohoku University Graduate School of Medicine
kn-affil=

affil-num=9
en-affil=Department of Medical Biochemistry, School of Pharmacy, Iwate Medical University
kn-affil=

affil-num=10
en-affil=Department of Biomedical Engineering, Tohoku University
kn-affil=

affil-num=11
en-affil=Tohoku University School of Medicine
kn-affil=

affil-num=12
en-affil=Department of Clinical Biology and Hormonal Regulation, Tohoku University Graduate School of Medicine
kn-affil=

affil-num=13
en-affil=Department of Clinical Biology and Hormonal Regulation, Tohoku University Graduate School of Medicine
kn-affil=

affil-num=14
en-affil=Department of Clinical Biology and Hormonal Regulation, Tohoku University Graduate School of Medicine
kn-affil=

affil-num=15
en-affil=Department of Clinical Biology and Hormonal Regulation, Tohoku University Graduate School of Medicine
kn-affil=

affil-num=16
en-affil=Department of Clinical Biology and Hormonal Regulation, Tohoku University Graduate School of Medicine
kn-affil=

affil-num=17
en-affil=Department of Clinical Biology and Hormonal Regulation, Tohoku University Graduate School of Medicine
kn-affil=

affil-num=18
en-affil=Division of Nephrology, Endocrinology, and Vascular Medicine, Tohoku University Graduate School of Medicine
kn-affil=

affil-num=19
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=20
en-affil=Laboratory of Oncology, Pharmacy Practice and Sciences, Tohoku University Graduate School of Pharmaceutical Sciences
kn-affil=

affil-num=21
en-affil=Department of Clinical Biology and Hormonal Regulation, Tohoku University Graduate School of Medicine
kn-affil=
en-keyword=CKD, DKD, Phenyl sulfate, Uremic toxin, Insulin secretion, Insulin resistance, Gut microbiota
kn-keyword=CKD, DKD, Phenyl sulfate, Uremic toxin, Insulin secretion, Insulin resistance, Gut microbiota
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250908
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Efficacy of ciclosporin monotherapy in non-severe aplastic anaemia not requiring transfusions: Results from a multicentre phase II study
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The efficacy of ciclosporin (CsA) to treat transfusion-independent non-severe aplastic anaemia (TI-NSAA) has not yet been systematically evaluated. We conducted a prospective trial in patients with TI-NSAA treated with CsA monotherapy. CsA (3.5 mg/kg/day) was administered to patients with TI-NSAA aged ≥16. The CsA dose was adjusted to maintain a blood CsA level of ≥600 ng/mL at 2 h post-administration. Blood cell counts were assessed after 8, 16 and 52 weeks of therapy. Thirty-two evaluable patients from 21 institutions were enrolled. The median age was 63.5 (range: 16–83) years. At 8 weeks, haematological improvement, with increases in haemoglobin (Hb) ≥1.5 g/dL (haematological improvement in erythrocytes [HI-E]) and platelet count ≥30 × 109/L (haematological improvement in platelets [HI-P]), was observed in 0/25 (0%) and 6/32 (19%) evaluable cases respectively. HI-E and HI-P occurred in 1/25 (4%) and 10/32 (31%) patients at 16 weeks, respectively, and at 52 weeks in 5/25 (20%) and 16/32 (50%) patients respectively. Nine grade 3 adverse events (AEs) occurred in six patients, but there were no grade ≥4 AEs. Ten of the 32 patients experienced grade 2 renal toxicity. Low-dose CsA is effective in TI-NSAA patients and demonstrates minimal renal toxicity. However, at least 16 weeks are necessary to adequately evaluate its efficacy.
en-copyright=
kn-copyright=

en-aut-name=IshiyamaKen
en-aut-sei=Ishiyama
en-aut-mei=Ken
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YamazakiMasahide
en-aut-sei=Yamazaki
en-aut-mei=Masahide
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MaruyamaHiroyuki
en-aut-sei=Maruyama
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HosonoNaoko
en-aut-sei=Hosono
en-aut-mei=Naoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YamaguchiHiroki
en-aut-sei=Yamaguchi
en-aut-mei=Hiroki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=AsadaNoboru
en-aut-sei=Asada
en-aut-mei=Noboru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TanimotoKazuki
en-aut-sei=Tanimoto
en-aut-mei=Kazuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=SugiuraHiroyuki
en-aut-sei=Sugiura
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=UsukiKensuke
en-aut-sei=Usuki
en-aut-mei=Kensuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=YoshimuraKenichi
en-aut-sei=Yoshimura
en-aut-mei=Kenichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=OgawaSeishi
en-aut-sei=Ogawa
en-aut-mei=Seishi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=KanakuraYuzuru
en-aut-sei=Kanakura
en-aut-mei=Yuzuru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=MatsumuraItaru
en-aut-sei=Matsumura
en-aut-mei=Itaru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=AkashiKoichi
en-aut-sei=Akashi
en-aut-mei=Koichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=NakaoShinji
en-aut-sei=Nakao
en-aut-mei=Shinji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

affil-num=1
en-affil=Department of Hematology, Kanazawa University Hospital
kn-affil=

affil-num=2
en-affil=Department of Internal Medicine, Keiju Medical Center
kn-affil=

affil-num=3
en-affil=Department of Hematology, Kanazawa University Hospital
kn-affil=

affil-num=4
en-affil=Department of Hematology and Oncology, University of Fukui Hospital
kn-affil=

affil-num=5
en-affil=Department of Hematology, Nippon Medical School
kn-affil=

affil-num=6
en-affil=Department of Hematology and Oncology, Okayama University Hospital
kn-affil=

affil-num=7
en-affil=Department of Hematology and Oncology, Japanese Red Cross Fukuoka Hospital
kn-affil=

affil-num=8
en-affil=Department of Hematology, Chugoku Central Hospital of Japan Mutual Aid Association of Public School Teachers
kn-affil=

affil-num=9
en-affil=Department of Hematology, NTT Medical Center Tokyo
kn-affil=

affil-num=10
en-affil=Department of Biostatistics and Health Data Science, Graduate School of Medical Science, Nagoya City University
kn-affil=

affil-num=11
en-affil=Department of Pathology and Tumor Biology, Institute for the Advanced Study of Human Biology (WPI-ASHBi), Kyoto University
kn-affil=

affil-num=12
en-affil=Sumitomo Hospital
kn-affil=

affil-num=13
en-affil=Department of Hematology and Rheumatology, Kindai University Faculty of Medicine
kn-affil=

affil-num=14
en-affil=Department of Medicine and Biosystemic Science, Kyushu University Graduate School of Medical Sciences
kn-affil=

affil-num=15
en-affil=Department of Hematology, Kanazawa University Hospital
kn-affil=
en-keyword=ciclosporin
kn-keyword=ciclosporin
en-keyword=prospective study
kn-keyword=prospective study
en-keyword=renal toxicity
kn-keyword=renal toxicity
en-keyword=transfusion-independent non-severe aplastic anaemia
kn-keyword=transfusion-independent non-severe aplastic anaemia
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250807
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Performance Assessment of ChatGPT for the Board Qualification Examination of the Japanese Society for Oral and Maxillofacial Radiology
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The aim of this study is to assess the performance and utility of ChatGPT for the board qualification examination of the Japanese Society for Oral and Maxillofacial Radiology (JSOMR). We assessed ChatGPT responses to 149 multiple-choice questions written in Japanese for the board qualification examination of the JSOMR for the 3 years from 2020 to 2022. The questions were directly entered into ChatGPT-3.5 and ChatGPT-4 models manually one by one as a prompt. The accuracy rate was calculated and classified by year, type of multiple-choice question, and level of intellectual ability, and significant differences were noted. The accuracy rate of GPT-3.5 for the 3 years was 45.0% (51.0% for 2020, 34.0% for 2021, and 50.0% for 2022), while the accuracy rate of GPT-4 was 68.5% (73.5% for 2020, 62.0% for 2021, and 70.0% for 2022) for the board qualification examination of the JSOMR. GPT-4 had a significantly higher accuracy rate than GPT-3.5 in each year. On performance classified by the type of multiple-choice questions, GPT-4 performed significantly better than GPT-3.5. However, neither model performed well with questions that required interpretation or knowledge of Japanese law. The performance of GPT-4 was significantly superior to GPT-3.5 in the board qualification examination of the JSOMR, suggesting that the use of Chat GPT, especially ChatGPT-4, would be effective as a tool for learning and preparing for the examination.
en-copyright=
kn-copyright=

en-aut-name=TakeshitaYohei
en-aut-sei=Takeshita
en-aut-mei=Yohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KawazuToshiyuki
en-aut-sei=Kawazu
en-aut-mei=Toshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HisatomiMiki
en-aut-sei=Hisatomi
en-aut-mei=Miki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OkadaShunsuke
en-aut-sei=Okada
en-aut-mei=Shunsuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=FujikuraMamiko
en-aut-sei=Fujikura
en-aut-mei=Mamiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NambaYuri
en-aut-sei=Namba
en-aut-mei=Yuri
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YoshidaSuzuka
en-aut-sei=Yoshida
en-aut-mei=Suzuka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YoshidaSaori
en-aut-sei=Yoshida
en-aut-mei=Saori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=YanagiYoshinobu
en-aut-sei=Yanagi
en-aut-mei=Yoshinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=AsaumiJunichi
en-aut-sei=Asaumi
en-aut-mei=Junichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of Oral and Maxillofacial Radiology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Oral and Maxillofacial Radiology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Oral and Maxillofacial Radiology, Okayama University Hospital
kn-affil=

affil-num=4
en-affil=Department of Oral and Maxillofacial Radiology, Okayama University Hospital
kn-affil=

affil-num=5
en-affil=Department of Oral and Maxillofacial Radiology, Okayama University Hospital
kn-affil=

affil-num=6
en-affil=Department of Oral and Maxillofacial Radiology, Okayama University Hospital
kn-affil=

affil-num=7
en-affil=Department of Oral and Maxillofacial Radiology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=8
en-affil=Preliminary Examination Room, Okayama University Hospital
kn-affil=

affil-num=9
en-affil=Preliminary Examination Room, Okayama University Hospital
kn-affil=

affil-num=10
en-affil=Department of Oral and Maxillofacial Radiology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=ChatGPT
kn-keyword=ChatGPT
en-keyword=GPT-3.5
kn-keyword=GPT-3.5
en-keyword=GPT-4
kn-keyword=GPT-4
en-keyword=Generative AI
kn-keyword=Generative AI
en-keyword=Large language model
kn-keyword=Large language model
en-keyword=Japanese Society for Oral and Maxillofacial Radiology
kn-keyword=Japanese Society for Oral and Maxillofacial Radiology
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250924
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=DSOK-0011 Potentially Regulates Circadian Misalignment and Affects Gut Microbiota Composition in Activity-Based Anorexia Model
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Objective: Anorexia nervosa (AN) is a metabolic-psychiatric disorder characterized by severe weight loss, hypercortisolemia, and hypothalamic–pituitary–adrenal (HPA) axis activation. In this study, we investigated the effect of inhibiting cortisol regeneration via the enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) on the pathophysiology of AN.<br>
Method: Female C57BL/6J mice underwent a 7-day activity-based anorexia (ABA) paradigm, involving 3 h daily feeding and free access to wheels, until 25% body weight loss or experiment completion. Mice were orally treated once daily with a potent 11β-HSD1 inhibitor, DSOK-0011, or vehicle. Body weight, food intake, and activity transitions were recorded; plasma corticosterone and cholesterol levels were measured using a fluorometric assay; gut microbiota were analyzed using 16S rRNA sequencing; and hippocampal glial cells were analyzed using immunohistochemistry.<br>
Results: DSOK-0011-treated mice exhibited a modest but significant increase in postprandial wheel-running activity compared to baseline (4–5 p.m., p = 0.018; 5–6 p.m., p = 0.043), whereas vehicle-treated mice showed higher preprandial activity (9–10 a.m., p = 0.0229). Gut microbiota analysis revealed increased alpha diversity in ABA mice, with a specific enrichment of the Lachnospiraceae family in the DSOK-0011 group. However, DSOK-0011 did not significantly affect body weight, food intake, corticosterone, and lipid levels, or hippocampal glial cell populations.<br>
Conclusion: Inhibition of 11β-HSD1 by DSOK-0011 was associated with microbiota alterations and subtle shifts in activity timing under energy-deficient conditions. These findings suggest that peripheral glucocorticoid metabolism may influence microbial and behavioral responses in the ABA model, although its metabolic impact appears limited in the acute phase.
en-copyright=
kn-copyright=

en-aut-name=KawaiHiroki
en-aut-sei=Kawai
en-aut-mei=Hiroki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=WadaNanami
en-aut-sei=Wada
en-aut-mei=Nanami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SakamotoShinji
en-aut-sei=Sakamoto
en-aut-mei=Shinji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MiyazakiKenji
en-aut-sei=Miyazaki
en-aut-mei=Kenji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KatoTaro
en-aut-sei=Kato
en-aut-mei=Taro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=HoriuchiYoshihiro
en-aut-sei=Horiuchi
en-aut-mei=Yoshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KiriiHiroshi
en-aut-sei=Kirii
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NguyenHoang Duy
en-aut-sei=Nguyen
en-aut-mei=Hoang Duy
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=HinotsuKenji
en-aut-sei=Hinotsu
en-aut-mei=Kenji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=OhyaYoshio
en-aut-sei=Ohya
en-aut-mei=Yoshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=AsadaTakahiro
en-aut-sei=Asada
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=YokodeAkiyoshi
en-aut-sei=Yokode
en-aut-mei=Akiyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=OkahisaYuko
en-aut-sei=Okahisa
en-aut-mei=Yuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=MiyazakiHaruko
en-aut-sei=Miyazaki
en-aut-mei=Haruko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=OohashiToshitaka
en-aut-sei=Oohashi
en-aut-mei=Toshitaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=TakakiManabu
en-aut-sei=Takaki
en-aut-mei=Manabu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

affil-num=1
en-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Sumitomo Pharma Co. Ltd
kn-affil=

affil-num=5
en-affil=Sumitomo Pharma Co. Ltd
kn-affil=

affil-num=6
en-affil=Sumitomo Pharma Co. Ltd
kn-affil=

affil-num=7
en-affil=Department of Animal Applied Microbiology, Okayama University Graduate School of Environmental, Life, Natural Science and Technology
kn-affil=

affil-num=8
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Neuropsychiatry, Okayama University Hospital
kn-affil=

affil-num=10
en-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=12
en-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=13
en-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=14
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=15
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=16
en-affil=Department of Neuropsychiatry, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=11β-HSD1
kn-keyword=11β-HSD1
en-keyword=activity-based anorexia
kn-keyword=activity-based anorexia
en-keyword=anorexia nervosa
kn-keyword=anorexia nervosa
en-keyword=corticosterone
kn-keyword=corticosterone
en-keyword=eating disorders
kn-keyword=eating disorders
en-keyword=microbiota
kn-keyword=microbiota
END

start-ver=1.4
cd-journal=joma
no-vol=106
cd-vols=
no-issue=7
article-no=
start-page=002115
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250725
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Summary of taxonomy changes ratified by the International Committee on Taxonomy of Viruses (ICTV) from the Fungal and Protist Viruses Subcommittee, 2025
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The Fungal and Protist Viruses Subcommittee (SC) of the International Committee on Taxonomy of Viruses (ICTV) has received a total of eight taxonomic proposals for the 2024 annual cycle. The extent of proposed changes varied, including nomenclatural updates, creation of new taxa and reorganization of established taxa. Following the ICTV procedures, all proposals were reviewed and voted upon by the members of the Executive Committee with ratification in March 2025. As a result, a total of 52 species in the families Botourmiaviridae and Marnaviridae were renamed to comply with the mandated binomial format. A new genus has been added to the dsRNA virus family Amalgaviridae, while two new families, Splipalmiviridae (Wolframvirales) and Mycoalphaviridae (Hepelivirales), were created to classify new groups of positive-sense (+) RNA mycoviruses. The class Arfiviricetes (Cressdnaviricota) was expanded by a new order Lineavirales and a new family Oomyviridae of ssDNA viruses. Additionally, a new class Orpoviricetes was created in the kingdom Orthornavirae to classify a group of bisegmented (+)RNA viruses reported from fungi and oomycetes. Finally, the order Pimascovirales was reorganized to better depict evolutionary relationships of pithoviruses and related viruses with large dsDNA genomes. The summary of updates in the taxonomy of fungal and protist viruses presented here is limited to taxa within the remit of this Subcommittee. For information on taxonomy changes on other fungal viruses closely related to animal and/or plant viruses, please see reports from sister ICTV Subcommittees (i.e. Plant Virus SC and Animal dsRNA and ssRNA(−) Viruses SC).
en-copyright=
kn-copyright=

en-aut-name=SabanadzovicSead
en-aut-sei=Sabanadzovic
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en-aut-name=AbergelChantal
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ORCID=

en-aut-name=AyllónMarı́a A.
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en-aut-mei=Marı́a A.
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en-aut-name=BotellaLeticia
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en-aut-name=CanutiMarta
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en-aut-name=ChibaYuto
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en-aut-name=ClaverieJean-Michel
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en-aut-mei=Jean-Michel
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aut-affil-num=7
ORCID=

en-aut-name=CouttsRobert H.A.
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en-aut-mei=Robert H.A.
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en-aut-name=DaghinoStefania
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ORCID=

en-aut-name=ForgiaMarco
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ORCID=

en-aut-name=HejnaOndřej
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ORCID=

en-aut-name=JiaJichun
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ORCID=

en-aut-name=JiangDaohong
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aut-affil-num=14
ORCID=

en-aut-name=Kotta-LoizouIoly
en-aut-sei=Kotta-Loizou
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aut-affil-num=15
ORCID=

en-aut-name=KrupovicMart
en-aut-sei=Krupovic
en-aut-mei=Mart
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=LangAndrew S.
en-aut-sei=Lang
en-aut-mei=Andrew S.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=LegendreMatthieu
en-aut-sei=Legendre
en-aut-mei=Matthieu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=Lee MarzanoShin-Yi
en-aut-sei=Lee Marzano
en-aut-mei=Shin-Yi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=NervaLuca
en-aut-sei=Nerva
en-aut-mei=Luca
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kn-aut-sei=
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aut-affil-num=20
ORCID=

en-aut-name=PénzesJudit
en-aut-sei=Pénzes
en-aut-mei=Judit
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aut-affil-num=21
ORCID=

en-aut-name=PoimalaAnna
en-aut-sei=Poimala
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ORCID=

en-aut-name=RigouSofia
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kn-aut-sei=
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aut-affil-num=23
ORCID=

en-aut-name=SatoYukiyo
en-aut-sei=Sato
en-aut-mei=Yukiyo
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kn-aut-sei=
kn-aut-mei=
aut-affil-num=24
ORCID=

en-aut-name=ShamsiWajeeha
en-aut-sei=Shamsi
en-aut-mei=Wajeeha
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=25
ORCID=

en-aut-name=SuzukiNobuhiro
en-aut-sei=Suzuki
en-aut-mei=Nobuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=26
ORCID=

en-aut-name=TurinaMassimo
en-aut-sei=Turina
en-aut-mei=Massimo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=27
ORCID=

en-aut-name=UrayamaSyun-ichi
en-aut-sei=Urayama
en-aut-mei=Syun-ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=28
ORCID=

en-aut-name=VainioEeva J.
en-aut-sei=Vainio
en-aut-mei=Eeva J.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=29
ORCID=

en-aut-name=XieJiatao
en-aut-sei=Xie
en-aut-mei=Jiatao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=30
ORCID=

affil-num=1
en-affil=Institute for Genomics, Biocomputing and Biotechnology, Mississippi State University
kn-affil=

affil-num=2
en-affil=Information Génomique & Structurale, UMR7256, CNRS & Aix-Marseille Université, Marseille, IMM, IM2B, IOM
kn-affil=

affil-num=3
en-affil=Departamento de Biotecnología-Biología Vegetal, Escuela Técnica Superior de Ingeniería Agronómica, Alimentaria y de Biosistemas, Universidad Politécnica de Madrid (UPM)
kn-affil=

affil-num=4
en-affil=Forest Protection and Wildlife Management Mendel University in Brno
kn-affil=

affil-num=5
en-affil=Department of Veterinary and Animal Sciences, University of Copenhagen
kn-affil=

affil-num=6
en-affil=School of Agriculture, Meiji University
kn-affil=

affil-num=7
en-affil=Information Génomique & Structurale, UMR7256, CNRS & Aix-Marseille Université, Marseille, IMM, IM2B, IOM
kn-affil=

affil-num=8
en-affil=School of Health, Medicine and Life Sciences, University of Hertfordshire
kn-affil=

affil-num=9
en-affil=Institute for Sustainable Plant Protection, National Research Council of Italy
kn-affil=

affil-num=10
en-affil=Centro de Edafología y Biología Aplicada del Segura-CSIC
kn-affil=

affil-num=11
en-affil=Institute for Sustainable Plant Protection, CNR
kn-affil=

affil-num=12
en-affil=Department of Genetics and Biotechnologies, University of South Bohemia
kn-affil=

affil-num=13
en-affil=College of Plant Protection, Shanxi Agricultural University
kn-affil=

affil-num=14
en-affil=College of Plant Science and Technology, Huazhong Agricultural University
kn-affil=

affil-num=15
en-affil=School of Health, Medicine and Life Sciences, University of Hertfordshire
kn-affil=

affil-num=16
en-affil=Institut Pasteur, Université Paris Cité, CNRS UMR6047, Archaeal Virology Unit
kn-affil=

affil-num=17
en-affil=Department of Biology, Memorial University of Newfoundland
kn-affil=

affil-num=18
en-affil=Information Génomique & Structurale, UMR7256, CNRS & Aix-Marseille Université, Marseille, IMM, IM2B, IOM
kn-affil=

affil-num=19
en-affil=United States Department of Agriculture, Agricultural Research Service, Application Technology Research Unit
kn-affil=

affil-num=20
en-affil=Council for Agricultural Research and Economics - Research Centre for Viticulture and Enology
kn-affil=

affil-num=21
en-affil=Department of Entomology, Texas A&M University
kn-affil=

affil-num=22
en-affil=Natural Resources Institute Finland (Luke)
kn-affil=

affil-num=23
en-affil=Information Génomique & Structurale, UMR7256, CNRS & Aix-Marseille Université, Marseille, IMM, IM2B, IOM
kn-affil=

affil-num=24
en-affil=Department of Biology, Institute for Plant Sciences, University of Cologne
kn-affil=

affil-num=25
en-affil=Department of Molecular Biology and Genetics, Aarhus University
kn-affil=

affil-num=26
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=27
en-affil=Department of Plant Protection, School of Agriculture, The University of Jordan
kn-affil=

affil-num=28
en-affil=Department of Life and Environmental Sciences, University of Tsukuba
kn-affil=

affil-num=29
en-affil=Natural Resources Institute Finland (Luke)
kn-affil=

affil-num=30
en-affil=College of Plant Science and Technology, Huazhong Agricultural University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=106
cd-vols=
no-issue=7
article-no=
start-page=002079
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250725
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Virus taxonomy proposal summaries: a searchable and citable resource to disseminate virus taxonomy advances
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Taxonomic classification of cellular organisms requires the publication of descriptions and proposed names of species and the deposition of specimens. Virus taxonomy is developed through a different system of annual submission of formal taxonomy proposals (TPs) that can be submitted by anyone but are typically prepared by a study group appointed by the International Committee on Taxonomy of Viruses (ICTV) and consisting of experts on a particular group of viruses. These are initially evaluated by an expert subcommittee and by the executive committee (EC) of the ICTV. EC-approved TPs are then submitted for evaluation and a ratification vote by the wider ICTV membership. Following ratification, the new taxonomy is annually updated in the Master Species List, associated databases and bioinformatic resources. The process is consistent, creates traceability in assignments and supports a fully evaluated, hierarchical classification and nomenclature of all taxonomic ranks from species to realms. The structure also facilitates large-scale and coordinated changes to virus taxonomy, such as the recent introduction of a binomial species nomenclature.<br>
TPs are available on the ICTV website after ratification, but they are not indexed in bibliographic databases and are not easily cited. Authors of TPs do not receive citation credit for adopted proposals, and their voluntary contributions are largely invisible in the published literature. For greater visibility of TPs and their authors, the ICTV will commence the annual publication of summaries of all TPs from each ICTV subcommittee. These summaries will provide a searchable compendium of all annual taxonomy changes and additions as well as direct links to the Master Species List and other ICTV bioinformatic resources. Their publication will provide due credit and citations for their authors, form the basis for disseminating taxonomy decisions and promote greater visibility and accessibility to taxonomy changes for the virology community.
en-copyright=
kn-copyright=

en-aut-name=MayneRichard
en-aut-sei=Mayne
en-aut-mei=Richard
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SimmondsPeter
en-aut-sei=Simmonds
en-aut-mei=Peter
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SmithDonald B.
en-aut-sei=Smith
en-aut-mei=Donald B.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=AdriaenssensEvelien M.
en-aut-sei=Adriaenssens
en-aut-mei=Evelien M.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=LefkowitzElliot J.
en-aut-sei=Lefkowitz
en-aut-mei=Elliot J.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OksanenHanna M.
en-aut-sei=Oksanen
en-aut-mei=Hanna M.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=ZerbiniFrancisco Murilo
en-aut-sei=Zerbini
en-aut-mei=Francisco Murilo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=Alfenas-ZerbiniPoliane
en-aut-sei=Alfenas-Zerbini
en-aut-mei=Poliane
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=AylwardFrank O
en-aut-sei=Aylward
en-aut-mei=Frank O
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=Freitas-AstúaJuliana
en-aut-sei=Freitas-Astúa
en-aut-mei=Juliana
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=HendricksonR. Curtis
en-aut-sei=Hendrickson
en-aut-mei=R. Curtis
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=HughesHolly R.
en-aut-sei=Hughes
en-aut-mei=Holly R.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=KrupovicMart
en-aut-sei=Krupovic
en-aut-mei=Mart
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=KuhnJens H.
en-aut-sei=Kuhn
en-aut-mei=Jens H.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=ŁobockaMałgorzata
en-aut-sei=Łobocka
en-aut-mei=Małgorzata
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=MushegianArcady R.
en-aut-sei=Mushegian
en-aut-mei=Arcady R.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=PenzesJudit
en-aut-sei=Penzes
en-aut-mei=Judit
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=MuñozAlejandro Reyes
en-aut-sei=Muñoz
en-aut-mei=Alejandro Reyes
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=RobertsonDavid L.
en-aut-sei=Robertson
en-aut-mei=David L.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=RouxSimon
en-aut-sei=Roux
en-aut-mei=Simon
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

en-aut-name=RubinoLuisa
en-aut-sei=Rubino
en-aut-mei=Luisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=21
ORCID=

en-aut-name=SabanadzovicSead
en-aut-sei=Sabanadzovic
en-aut-mei=Sead
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=22
ORCID=

en-aut-name=SuzukiNobuhiro
en-aut-sei=Suzuki
en-aut-mei=Nobuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=23
ORCID=

en-aut-name=TurnerDann
en-aut-sei=Turner
en-aut-mei=Dann
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=24
ORCID=

en-aut-name=Van DoorslaerKoenraad
en-aut-sei=Van Doorslaer
en-aut-mei=Koenraad
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=25
ORCID=

en-aut-name=VarsaniArvind
en-aut-sei=Varsani
en-aut-mei=Arvind
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=26
ORCID=

affil-num=1
en-affil=Nuffield Department of Medicine, University of Oxford
kn-affil=

affil-num=2
en-affil=Nuffield Department of Medicine, University of Oxford
kn-affil=

affil-num=3
en-affil=Nuffield Department of Medicine, University of Oxford
kn-affil=

affil-num=4
en-affil=Quadram Institute Bioscience
kn-affil=

affil-num=5
en-affil=Department of Microbiology, University of Alabama at Birmingham
kn-affil=

affil-num=6
en-affil=Molecular and Integrative Biosciences Research Programme, Faculty of Biological and Environmental Sciences, University of Helsinki
kn-affil=

affil-num=7
en-affil=Departamento de Fitopatologia/BIOAGRO, Universidade Federal de Viçosa
kn-affil=

affil-num=8
en-affil=Departamento de Microbiologia, Universidade Federal de Viçosa
kn-affil=

affil-num=9
en-affil=Department of Biological Sciences, Virginia Tech
kn-affil=

affil-num=10
en-affil=Embrapa Cassava and Fruits, Cruz das Almas
kn-affil=

affil-num=11
en-affil=Department of Microbiology, University of Alabama at Birmingham
kn-affil=

affil-num=12
en-affil=Centers for Disease Control and Prevention
kn-affil=

affil-num=13
en-affil=Institut Pasteur, Université Paris Cité, CNRS UMR6047, Archaeal Virology Unit
kn-affil=

affil-num=14
en-affil=Integrated Research Facility at Fort Detrick, National Institute of Allergy and Infectious Diseases, National Institutes of Health
kn-affil=

affil-num=15
en-affil=Institute of Biochemistry and Biophysics of the Polish Academy of Sciences
kn-affil=

affil-num=16
en-affil=Division of Molecular and Cellular Biosciences, National Science Foundation
kn-affil=

affil-num=17
en-affil=Institute for Quantitative Biomedicine, Rutgers University
kn-affil=

affil-num=18
en-affil=Departamento de Ciencias Biológicas, Universidad de los Andes
kn-affil=

affil-num=19
en-affil=MRC-University of Glasgow Centre for Virus Research
kn-affil=

affil-num=20
en-affil=Department of Energy, Joint Genome Institute, Lawrence Berkeley National Laboratory
kn-affil=

affil-num=21
en-affil=Consiglio Nazionale delle Ricerche, Istituto per la Protezione Sostenibile delle Piante, Sede Secondaria di Bari
kn-affil=

affil-num=22
en-affil=Department of Agricultural Science and Plant Protection, Mississippi State University
kn-affil=

affil-num=23
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=24
en-affil=Molecular Biology, University of the West of England
kn-affil=

affil-num=25
en-affil=Department of Immunobiology, School of Animal and Comparative Biomedical Sciences, BIO5 Institute, University of Arizona Cancer Center
kn-affil=

affil-num=26
en-affil=The Biodesign Center for Fundamental and Applied Microbiomics, School of Life Sciences, Center for Evolution and Medicine, Arizona State University
kn-affil=
en-keyword=ICTV
kn-keyword=ICTV
en-keyword=master species list
kn-keyword=master species list
en-keyword=taxonomy proposal
kn-keyword=taxonomy proposal
en-keyword=virus taxonomy
kn-keyword=virus taxonomy
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=e06572
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250908
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A Viral RNA Silencing Suppressor Modulates Reactive Oxygen Species Levels to Induce the Autophagic Degradation of Dicer‐Like and Argonaute‐Like Proteins
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Mounting evidence indicates that viruses exploit elevated reactive oxygen species (ROS) levels to promote replication and pathogenesis, yet the mechanistic underpinnings of this viral strategy remain elusive for many viral systems. This study uncovers a sophisticated viral counter-defense mechanism in the Cryphonectria hypovirus 1 (CHV1)-Fusarium graminearum system, where the viral p29 protein subverts host redox homeostasis to overcome antiviral responses. That p29 directly interacts with and inhibits the enzymatic activity of fungal NAD(P)H-dependent FMN reductase 1 (FMR1), leading to increased ROS accumulation and subsequent autophagy activation is demonstrated. Strikingly, this ROS-induced autophagy selectively targets for degradation two core antiviral RNA silencing components against CHV1 in F. graminearum, Dicer-like 2 (DCL2) and Argonaute-like 1 (AGL1), thereby compromising the host's primary antiviral defense system. Genetic analysis confirms this coordinated hijacking of host machineries, as CHV1 shows enhanced accumulation in the FMR1 knockout and reduced accumulation in autophagy-deficient fungal strains. This work reveals a tripartite interplay among oxidative stress, autophagy, and RNA silencing that CHV1 manipulates through p29 multifunctional activity. These findings provide a model for how viruses coordinately regulate distinct host defense systems to optimize infection.
en-copyright=
kn-copyright=

en-aut-name=ZhaiShiyu
en-aut-sei=Zhai
en-aut-mei=Shiyu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=PangTianxing
en-aut-sei=Pang
en-aut-mei=Tianxing
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=PengShiyu
en-aut-sei=Peng
en-aut-mei=Shiyu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ZouShenshen
en-aut-sei=Zou
en-aut-mei=Shenshen
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=DengZhiping
en-aut-sei=Deng
en-aut-mei=Zhiping
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SuzukiNobuhiro
en-aut-sei=Suzuki
en-aut-mei=Nobuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KangZhensheng
en-aut-sei=Kang
en-aut-mei=Zhensheng
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=AndikaIda Bagus
en-aut-sei=Andika
en-aut-mei=Ida Bagus
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=SunLiying
en-aut-sei=Sun
en-aut-mei=Liying
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=State Key Laboratory of Crop Stress Biology for Arid Areas and College of Plant Protection, Northwest A&F University
kn-affil=

affil-num=2
en-affil=State Key Laboratory of Crop Stress Biology for Arid Areas and College of Plant Protection, Northwest A&F University
kn-affil=

affil-num=3
en-affil=State Key Laboratory of Crop Stress Biology for Arid Areas and College of Plant Protection, Northwest A&F University
kn-affil=

affil-num=4
en-affil=Department of Plant Pathology, College of Plant Protection, Shandong Agricultural University
kn-affil=

affil-num=5
en-affil=Institute of Virology and Biotechnology, Zhejiang Academy of Agricultural Sciences
kn-affil=

affil-num=6
en-affil=Institute of Plant Science and Resources (IPSR), Okayama University
kn-affil=

affil-num=7
en-affil=State Key Laboratory of Crop Stress Biology for Arid Areas and College of Plant Protection, Northwest A&F University
kn-affil=

affil-num=8
en-affil=State Key Laboratory of Crop Stress Biology for Arid Areas and College of Plant Protection, Northwest A&F University
kn-affil=

affil-num=9
en-affil=State Key Laboratory of Crop Stress Biology for Arid Areas and College of Plant Protection, Northwest A&F University
kn-affil=
en-keyword=argonaute
kn-keyword=argonaute
en-keyword=autophagic degradation
kn-keyword=autophagic degradation
en-keyword=cryphonectria hypovirus 1
kn-keyword=cryphonectria hypovirus 1
en-keyword=dicer
kn-keyword=dicer
en-keyword=reactive oxygen species
kn-keyword=reactive oxygen species
en-keyword=RNA silencing suppressor
kn-keyword=RNA silencing suppressor
END

start-ver=1.4
cd-journal=joma
no-vol=13
cd-vols=
no-issue=1
article-no=
start-page=234
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20251114
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Rotenone targets midbrain astrocytes to produce glial dysfunction-mediated dopaminergic neurodegeneration
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Exposure to pesticides, such as rotenone or paraquat, is an environmental factor that plays an important role in the pathogenesis of Parkinson's disease (PD). Rotenone induces PD-like pathology and is therefore used to develop parkinsonian animal models. Dopaminergic neurotoxicity caused by rotenone has been attributed to the inhibition of mitochondrial complex I, oxidative stress and neuroinflammation; however, the mechanisms underlying selective dopaminergic neurodegeneration by rotenone remain unclear. To resolve this, we focused on glial diversity and examined whether the brain region-specific glial response to rotenone could determine the vulnerability of dopaminergic neurons using primary cultured neurons, astrocytes and microglia from the midbrain and striatum of rat embryos and rotenone-injected PD model mice. Direct neuronal treatment with low-dose rotenone failed to damage dopaminergic neurons. Conversely, rotenone exposure in the presence of midbrain astrocyte and microglia or conditioned media from rotenone-treated midbrain glial cultures containing astrocytes and microglia produced dopaminergic neurotoxicity, but striatal glia did not. Surprisingly, conditioned media from rotenone-treated midbrain astrocytes or microglia monocultures did not affect neuronal survival. We also demonstrated that rotenone targeted midbrain astrocytes prior to microglia to induce dopaminergic neurotoxicity. Rotenone-treated astrocytes produced secreted protein acidic and rich in cysteine (SPARC) extracellularly, which induced microglial proliferation, increase in IL-1β and TNF-α, and NF-κB (p65) nuclear translocation in microglia, resulting in dopaminergic neurodegeneration. In addition, rotenone exposure caused the secretion of NFAT-related inflammatory cytokines and a reduction in the level of an antioxidant metallothionein (MT)-1 from midbrain glia. Furthermore, we observed microglial proliferation and a decrease in the number of MT-positive astrocytes in the substantia nigra, but not the striatum, of low-dose rotenone-injected PD model mice. Our data highlight that rotenone targets midbrain astrocytes, leading to SPARC secretion, which promotes the neurotoxic conversion of microglia and leads to glial dysfunction-mediated dopaminergic neurodegeneration.
en-copyright=
kn-copyright=

en-aut-name=MiyazakiIkuko
en-aut-sei=Miyazaki
en-aut-mei=Ikuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=IsookaNami
en-aut-sei=Isooka
en-aut-mei=Nami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KikuokaRyo
en-aut-sei=Kikuoka
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ImafukuFuminori
en-aut-sei=Imafuku
en-aut-mei=Fuminori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MasaiKaori
en-aut-sei=Masai
en-aut-mei=Kaori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TomimotoKana
en-aut-sei=Tomimoto
en-aut-mei=Kana
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SakaguchiMasakiyo
en-aut-sei=Sakaguchi
en-aut-mei=Masakiyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=SogawaChiharu
en-aut-sei=Sogawa
en-aut-mei=Chiharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=SogawaNorio
en-aut-sei=Sogawa
en-aut-mei=Norio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=KitamuraYoshihisa
en-aut-sei=Kitamura
en-aut-mei=Yoshihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=AsanumaMasato
en-aut-sei=Asanuma
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

affil-num=1
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Food and Health Sciences, Faculty of Environmental Studies, Hiroshima Institute of Technology
kn-affil=

affil-num=9
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Pharmacotherapy, School of Pharmacy, Shujitsu University
kn-affil=

affil-num=11
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Rotenone
kn-keyword=Rotenone
en-keyword=Astrocyte
kn-keyword=Astrocyte
en-keyword=Microglia
kn-keyword=Microglia
en-keyword=SPARC
kn-keyword=SPARC
en-keyword=Parkinson's disease
kn-keyword=Parkinson's disease
END

start-ver=1.4
cd-journal=joma
no-vol=281
cd-vols=
no-issue=
article-no=
start-page=111174
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2026
dt-pub=202601
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=N-terminal domains and site-specific glycosylation regulate the secretion of avian melanocortin inverse agonists, agouti signaling protein (ASIP) and agouti-related protein (AGRP)
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Agouti signaling protein (ASIP) and agouti-related protein (AGRP) are paralogous inverse agonists of melanocortin receptors with distinct physiological roles, but their structural and biochemical properties in birds remain poorly understood. Here, we characterized chicken ASIP and AGRP proteins. Analysis of available sequences revealed that a motif resembling the mammalian proprotein convertase 1/3 (PC1/3, also known as PCSK1) cleavage site is conserved across a broad range of avian orders, but Western blot analysis of transfected Chinese hamster ovary (CHO-K1) cells and chicken hypothalamus detected no cleavage, suggesting that avian AGRP may not be post-translationally processed at this site. Chicken ASIP mRNA contains an in-frame upstream ATG (uATG) and a putative N-linked glycosylation site at Asn-42, both conserved across multiple avian orders. Overexpression in CHO-K1 cells showed that ASIP translated from either ATG produces a mature protein of the same size that is N-glycosylated at Asn-42 and exhibits markedly lower secretion efficiency than AGRP. Domain-swapping experiments revealed that the N-terminal domain reduces secretion, whereas a naturally occurring ASIP-b variant with an additional N-glycan at Asn-47 shows enhanced secretion. Proteasome inhibition increased intracellular ASIP, and endoglycosidase H (Endo H) sensitivity indicated endoplasmic reticulum (ER) retention, suggesting that the N-terminal domain limits secretion via ER-associated proteasomal degradation. These findings reveal species-specific post-translational regulation of avian melanocortin inverse agonists, in which N-terminal features and site-specific N-glycosylation determine secretion efficiency, likely contributing to their distinct roles in pigmentation and hypothalamic energy balance.
en-copyright=
kn-copyright=

en-aut-name=FukuchiHibiki
en-aut-sei=Fukuchi
en-aut-mei=Hibiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=WatanabeRyoya
en-aut-sei=Watanabe
en-aut-mei=Ryoya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=IidaYuna
en-aut-sei=Iida
en-aut-mei=Yuna
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NakanoSaya
en-aut-sei=Nakano
en-aut-mei=Saya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MizutaniAya
en-aut-sei=Mizutani
en-aut-mei=Aya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=AboTatsuhiko
en-aut-sei=Abo
en-aut-mei=Tatsuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=AizawaSayaka
en-aut-sei=Aizawa
en-aut-mei=Sayaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TakeuchiSakae
en-aut-sei=Takeuchi
en-aut-mei=Sakae
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=4
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=5
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=6
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=7
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=8
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=
en-keyword=Agouti signaling protein
kn-keyword=Agouti signaling protein
en-keyword=Agouti-related protein
kn-keyword=Agouti-related protein
en-keyword=Avian melanocortin inverse agonists
kn-keyword=Avian melanocortin inverse agonists
en-keyword=Post-translational modification
kn-keyword=Post-translational modification
en-keyword=N-linked glycosylation
kn-keyword=N-linked glycosylation
en-keyword=Protein secretion
kn-keyword=Protein secretion
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250912
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Radiological assessment of dissected cervical lymph nodes in level III affected by the area of supraomohyoid neck dissection
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Objectives: To compare the number of dissected cervical lymph nodes in the anatomical level III with that in supraomohyoid neck dissection (SOHND) level III affected by the anatomical relationship between the omohyoid muscle and cricoid cartilage using contrast-enhanced CT (CE-CT) images to assess the validity of the current SOHND.<br>
Methods: CE-CT images of the patients who suffered from malignant tumours in the oral and maxillofacial regions were reviewed. The number of cervical lymph nodes both in the anatomical level III (area between the centre of the inferior border of the hyoid bone [HB] and the inferior border of the cricoid cartilage [CC]) and SOHND level III (area between HB and the intersection of the omohyoid muscle and internal jugular vein [OM-IJ]) were recorded, respectively.<br>
Results: The rate of patients whose number of lymph nodes in level III was affected by the positional relationship between the OM-IJ and CC was almost equal in males and females. As for the patients with OM-IJ below the CC, the number of lymph nodes in SOHND level III increased from that of anatomical level III. Females showed significantly higher values than males (P < .05). Meanwhile, for patients with OM-IJ at or above the CC, the number of lymph nodes in SOHND level III decreased from that of anatomical level III.<br>
Conclusions: The number of dissected cervical lymph nodes differed between the SOHND dissection area and levels I, II, and III. In most cases, SOHND dissects more cervical lymph nodes, especially in female patients.
en-copyright=
kn-copyright=

en-aut-name=TakeshitaYohei
en-aut-sei=Takeshita
en-aut-mei=Yohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OhyamaYoshio
en-aut-sei=Ohyama
en-aut-mei=Yoshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=IbaragiSoichiro
en-aut-sei=Ibaragi
en-aut-mei=Soichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MatsushitaYuki
en-aut-sei=Matsushita
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TubbsR Shane
en-aut-sei=Tubbs
en-aut-mei=R Shane
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KitagawaNorio
en-aut-sei=Kitagawa
en-aut-mei=Norio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KawazuToshiyuki
en-aut-sei=Kawazu
en-aut-mei=Toshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=HisatomiMiki
en-aut-sei=Hisatomi
en-aut-mei=Miki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=OkadaShunsuke
en-aut-sei=Okada
en-aut-mei=Shunsuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=FujikuraMamiko
en-aut-sei=Fujikura
en-aut-mei=Mamiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=YanagiYoshinobu
en-aut-sei=Yanagi
en-aut-mei=Yoshinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=IwanagaJoe
en-aut-sei=Iwanaga
en-aut-mei=Joe
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

affil-num=1
en-affil=Department of Oral and Maxillofacial Radiology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Clinical Anatomy Research Association in Oral and Maxillofacial Surgery
kn-affil=

affil-num=3
en-affil=Department of Oral and Maxillofacial Surgery, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Clinical Anatomy Research Association in Oral and Maxillofacial Surgery
kn-affil=

affil-num=5
en-affil=Clinical Anatomy Research Association in Oral and Maxillofacial Surgery
kn-affil=

affil-num=6
en-affil=Clinical Anatomy Research Association in Oral and Maxillofacial Surgery
kn-affil=

affil-num=7
en-affil=Department of Oral and Maxillofacial Radiology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Oral and Maxillofacial Radiology, Okayama University Hospital
kn-affil=

affil-num=9
en-affil=Department of Oral and Maxillofacial Radiology, Okayama University Hospital
kn-affil=

affil-num=10
en-affil=Department of Oral and Maxillofacial Radiology, Okayama University Hospital
kn-affil=

affil-num=11
en-affil=Department of Oral and Maxillofacial Radiology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=12
en-affil=Clinical Anatomy Research Association in Oral and Maxillofacial Surgery
kn-affil=
en-keyword=omohyoid muscle
kn-keyword=omohyoid muscle
en-keyword=CT
kn-keyword=CT
en-keyword=neck dissection
kn-keyword=neck dissection
en-keyword=cervical lymph nodes
kn-keyword=cervical lymph nodes
en-keyword=cancer
kn-keyword=cancer
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20251005
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Artificial Selections for Life-History Traits Affect Effective Cumulative Temperature and Developmental Zero Point in Zeugoducus cucurbitae
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Effective cumulative temperature and developmental zero point are important indicators for estimating the timing of organism development and the area of distribution. These indicators are generally considered to have unique values for different species of organisms and are also important for predicting the distribution range of animals and plants, especially insect pests. These values generally are species-specific, but there is variation within populations in traits having a genetic component. However, there are no studies on what kind of selection pressure affects these indicator values. To address this issue, it would be worthwhile to compare these values using individuals of strains that have been artificially selected for life-history traits by rearing them at various temperatures and calculating these indicators from developmental days and temperatures. In the present study, eggs were taken from adults of strains with many generations of artificial selection on two life-history traits (age at reproduction and developmental period) of the melon fly, Zeugodacus cucurbitae, under constant temperature conditions. Eggs were reared at five different temperatures, and the effective cumulative temperatures and developmental zero points of the larval and developmental periods were compared. The results demonstrate that artificial selection on life-history traits in Z. cucurbitae induces evolutionary changes in both the effective cumulative temperature and the developmental zero point across successive generations.
en-copyright=
kn-copyright=

en-aut-name=MiyatakeTakahisa
en-aut-sei=Miyatake
en-aut-mei=Takahisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MatsumuraKentarou
en-aut-sei=Matsumura
en-aut-mei=Kentarou
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

affil-num=1
en-affil=Graduate School of Environment, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Department of General Systems Studies, Graduate School of Arts and Sciences, the University of Tokyo
kn-affil=
en-keyword=age at reproduction
kn-keyword=age at reproduction
en-keyword=development time
kn-keyword=development time
en-keyword=developmental period
kn-keyword=developmental period
en-keyword=larval period
kn-keyword=larval period
en-keyword=melon fly
kn-keyword=melon fly
en-keyword=Tephritidae
kn-keyword=Tephritidae
en-keyword=thermal biology
kn-keyword=thermal biology
en-keyword=trade-offs
kn-keyword=trade-offs
END

start-ver=1.4
cd-journal=joma
no-vol=26
cd-vols=
no-issue=20
article-no=
start-page=10072
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20251016
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Neurofibromin Encoded by the Neurofibromatosis Type 1 (NF1) Gene Promotes the Membrane Translocation of SPRED2, Thereby Inhibiting the ERK Pathway in Breast Cancer Cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Neurofibromin (NF) inhibits the RAS/RAF/ERK pathway through its interaction with SPRED1 (Sprouty-related EVH1 domain-containing protein 1). Here, we investigated the functional relationship between NF and SPRED2 in breast cancer (BC). Human BC cell lines were transfected to downregulate or overexpress NF and SPRED2 and subsequently subjected to functional assays. Protein and mRNA levels were analyzed by Western blotting and RT-qPCR, respectively. Protein–protein interactions were examined by immunoprecipitation. Database analyses and immunohistochemistry (IHC) of BC tissues were performed to validate the in vitro findings. Downregulating NF or SPRED2 expression in BC cells enhanced cell proliferation, migration and invasion accompanied by RAF/ERK activation, whereas overexpression produced opposite effects. NF formed a protein complex with SPRED2 and facilitated its translocation to the plasma membrane. By IHC, SPRED2 membrane localization was absent in NF-negative luminal A and triple-negative BC (TNBC) but present in a subset of luminal A BC. By database analyses, both NF1 and SPRED2 mRNA levels were reduced in BC tissues, and luminal A BC patients with high expression of both NF1 and SPRED2 mRNA exhibited improved relapse-free survival. These results suggest a critical role for the NF–SPRED2 axis in BC progression and highlight it as a potential therapeutic target.
en-copyright=
kn-copyright=

en-aut-name=Su PwintNang Thee
en-aut-sei=Su Pwint
en-aut-mei=Nang Thee
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=LiChunning
en-aut-sei=Li
en-aut-mei=Chunning
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=GaoTong
en-aut-sei=Gao
en-aut-mei=Tong
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=WangYuze
en-aut-sei=Wang
en-aut-mei=Yuze
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=FujisawaMasayoshi
en-aut-sei=Fujisawa
en-aut-mei=Masayoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OharaToshiaki
en-aut-sei=Ohara
en-aut-mei=Toshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SakaguchiMasakiyo
en-aut-sei=Sakaguchi
en-aut-mei=Masakiyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YoshimuraTeizo
en-aut-sei=Yoshimura
en-aut-mei=Teizo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MatsukawaAkihiro
en-aut-sei=Matsukawa
en-aut-mei=Akihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Pathology and Experimental Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Pathology and Experimental Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Pathology and Experimental Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Pathology and Experimental Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Pathology and Experimental Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Pathology and Experimental Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Cell Biology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Pathology and Experimental Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Pathology and Experimental Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=breast cancer
kn-keyword=breast cancer
en-keyword=SPRED2
kn-keyword=SPRED2
en-keyword=neurofibromatosis type 1
kn-keyword=neurofibromatosis type 1
en-keyword=neurofibromin
kn-keyword=neurofibromin
en-keyword=RAS/RAF/ERK
kn-keyword=RAS/RAF/ERK
END

start-ver=1.4
cd-journal=joma
no-vol=42
cd-vols=
no-issue=3
article-no=
start-page=215
end-page=227
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Root-exuded sugars as drivers of rhizosphere microbiome assembly
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Sugars in root exudates play a pivotal role in shaping plant-microbe interactions in the rhizosphere, serving as carbon sources and signaling molecules that orchestrate microbial behavior, community structure, and plant resilience. Recent research has shed light on the dynamics of sugar levels in root exudates, the factors that influence their secretion, and the mechanisms by which these sugars drive microbial colonization and community assembly in the rhizosphere. Microbial communities, in turn, contribute to plant physiological changes that enhance growth and stress tolerance. While well-studied sugars such as glucose, sucrose, and fructose are known to promote chemotaxis, motility, and biofilm formation, emerging evidence suggests that less-studied sugars like arabinose and trehalose may also play significant roles in microbial interactions and stress resilience. Key challenges remain, including the accurate measurement of labile sugars that are rapidly metabolized by microbes, and the elucidation of genetic mechanisms underlying rhizosphere metabolic interactions in both host plants and microbes. Addressing these challenges will advance our understanding of sugar-mediated interactions and inform the development of sustainable agricultural innovations.
en-copyright=
kn-copyright=

en-aut-name=HemeldaNiarsi Merry
en-aut-sei=Hemelda
en-aut-mei=Niarsi Merry
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NoutoshiYoshiteru
en-aut-sei=Noutoshi
en-aut-mei=Yoshiteru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

affil-num=1
en-affil=Department of Biology, Faculty of Mathematics and Natural Sciences, University of Indonesia
kn-affil=

affil-num=2
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=
en-keyword=carbon sources
kn-keyword=carbon sources
en-keyword=plant-derived sugars
kn-keyword=plant-derived sugars
en-keyword=plant-microbe interactions
kn-keyword=plant-microbe interactions
en-keyword=rhizosphere
kn-keyword=rhizosphere
en-keyword=root exudate
kn-keyword=root exudate
END

start-ver=1.4
cd-journal=joma
no-vol=34
cd-vols=
no-issue=1
article-no=
start-page=46
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20251009
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Highly efficient transgenesis mediated by Tip100 transposon system in medaka
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Transgenesis mediated by transposon is an effective approach for introducing exogenous DNA into the nuclear genome and establishing stable transgenic strains that efficiently express genetic tools. Although the DNA transposon Tol2 is widely used for transgenesis in zebrafish, its endogenous transpositional activity can lead to unintended transgene mobilization, making it unsuitable for transgenesis in medaka (Oryzias latipes). Here, we demonstrated that the DNA transposon Tip100, originally identified in the common morning glory (Ipomoea purpurea), an ornamental plant, can serve as a useful tool for transgenesis in Japanese medaka. The GFP transgene cassette, when co-injected with Tip100 transposase mRNA, was expressed in significantly higher number of somatic cells in the injected fish. Furthermore, a transgene flanked by truncated recognition sequences (100 bp each) exhibited expression levels comparable to those of the original vector containing the full 2.2 kb recognition sequence. Injection of a transgene driven by a germline-specific promoter revealed that fish injected with Tip100 mRNA exhibited a significantly higher germline transmission rate (42/68; 62.7%) compared to those injected without the mRNA (13/62; 21.0%). We successfully established transgenic strains by outcrossing injected founders with GFP-positive germ cells (7/7; 100%) and demonstrated that the transgenes were randomly integrated into the medaka genome, generating 8-bp duplications at the insertional sites–an insertional signature of the hAT superfamily of transposons. Our findings indicate that the Tip100 system is a promising tool for generating stable transgenic strains that express various genetic tools in medaka and potentially other fish species.
en-copyright=
kn-copyright=

en-aut-name=TanakaYoshitaka
en-aut-sei=Tanaka
en-aut-mei=Yoshitaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SekiTakahide
en-aut-sei=Seki
en-aut-mei=Takahide
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HoshinoAtsushi
en-aut-sei=Hoshino
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=AnsaiSatoshi
en-aut-sei=Ansai
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=Ushimado Marine Institute (UMI), Okayama University
kn-affil=

affil-num=2
en-affil=Department of Integrative Life Sciences, Graduate School of Life Sciences, Tohoku University
kn-affil=

affil-num=3
en-affil=National Institute for Basic Biology
kn-affil=

affil-num=4
en-affil=Ushimado Marine Institute (UMI), Okayama University
kn-affil=
en-keyword=Fish
kn-keyword=Fish
en-keyword=Medaka
kn-keyword=Medaka
en-keyword=Morning glory
kn-keyword=Morning glory
en-keyword=Transgenic
kn-keyword=Transgenic
en-keyword=Transposon
kn-keyword=Transposon
END

start-ver=1.4
cd-journal=joma
no-vol=18
cd-vols=
no-issue=10
article-no=
start-page=1623
end-page=1625
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20251006
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The OsATG8–OsATG1–SPIN6 module: Linking nutrient sensing to OsRac1-mediated rice immunity via autophagy-independent mechanisms
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=KouYanjun
en-aut-sei=Kou
en-aut-mei=Yanjun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KawanoYoji
en-aut-sei=Kawano
en-aut-mei=Yoji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

affil-num=1
en-affil=State Key Laboratory of Rice Biology and Breeding, China National Rice Research Institute
kn-affil=

affil-num=2
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=16
cd-vols=
no-issue=1
article-no=
start-page=519
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250926
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Specific induction of right ventricular-like cardiomyocytes from human pluripotent stem cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background Applications employing human pluripotent stem cell-derived cardiomyocytes (hPSC-CMs) require well-characterized, chamber-specific hPSC-CMs. Distinct first heart field (FHF) and second heart field (SHF) cardiac progenitor populations give rise to the left ventricular (LV) and right ventricular (RV) cardiomyocytes, respectively. This developmental difference in cardiomyocyte origin suggests that chamber-specific cardiomyocytes have unique characteristics. Therefore, efficient strategies to differentiate human pluripotent stem cells (hPSCs) specifically to LV-like or RV-like cardiomyocytes are needed and it is still unknown whether there is a phenotypic difference between LV-like cardiomyocytes and RV-like cardiomyocytes derived from hPSCs.<br>
Methods An established hPSC cardiac differentiation protocol employing sequential GSK3β inhibition followed by Wnt inhibition (GiWi) was modified by addition of insulin or BMP antagonists during mesoderm formation. Cardiac progenitor populations were evaluated for FHF and SHF markers, and differentiated hPSC-CMs were characterized for chamber-specific markers.<br>
Results The GiWi protocol produced mainly FHF-like progenitor cells that gave rise to LV-like cardiomyocytes. Inhibition of endogenous BMP signaling during mesoderm induction using insulin or BMP antagonists reduced expression of FHF markers and increased expression of SHF markers in cardiac progenitor cells. hPSC-CMs arising from the SHF-like progenitor cells showed an RV-like gene expression pattern and exhibited phenotypic differences in spontaneous contraction rate, Ca2+ transients, and cell size compared to control LV-like cardiomyocytes.<br>
Conclusion This study establishes methodology to generate RV-like hPSC-CMs to support the development of disease modeling research using chamber-specific hPSC-CMs.
en-copyright=
kn-copyright=

en-aut-name=SaitoYukihiro
en-aut-sei=Saito
en-aut-mei=Yukihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KatanosakaYuki
en-aut-sei=Katanosaka
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=IidaToshihiro
en-aut-sei=Iida
en-aut-mei=Toshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KusumotoDai
en-aut-sei=Kusumoto
en-aut-mei=Dai
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SatoRyushi
en-aut-sei=Sato
en-aut-mei=Ryushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=AdachiRiki
en-aut-sei=Adachi
en-aut-mei=Riki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=ShimizuSatoshi
en-aut-sei=Shimizu
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KurokawaJunko
en-aut-sei=Kurokawa
en-aut-mei=Junko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=AkagiSatoshi
en-aut-sei=Akagi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=YoshidaMasashi
en-aut-sei=Yoshida
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=MiyoshiToru
en-aut-sei=Miyoshi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=MoritaHiroshi
en-aut-sei=Morita
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=NaruseKeiji
en-aut-sei=Naruse
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=NishidaMikako
en-aut-sei=Nishida
en-aut-mei=Mikako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=UdonoHeiichiro
en-aut-sei=Udono
en-aut-mei=Heiichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=ZhangJianhua
en-aut-sei=Zhang
en-aut-mei=Jianhua
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=YuasaShinsuke
en-aut-sei=Yuasa
en-aut-mei=Shinsuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=KampTimothy J.
en-aut-sei=Kamp
en-aut-mei=Timothy J.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=ItoHiroshi
en-aut-sei=Ito
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Hospital
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Okayama University Hospital
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Physiology, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Biomedical Informatics and Molecular Biology, The Sakaguchi Laboratory, Keio University School of Medicine
kn-affil=

affil-num=6
en-affil=Department of Bio-Informational Pharmacology, School of Pharmaceutical Sciences, University of Shizuoka
kn-affil=

affil-num=7
en-affil=Department of Bio-Informational Pharmacology, School of Pharmaceutical Sciences, University of Shizuoka
kn-affil=

affil-num=8
en-affil=Department of Bio-Informational Pharmacology, School of Pharmaceutical Sciences, University of Shizuoka
kn-affil=

affil-num=9
en-affil=Department of Bio-Informational Pharmacology, School of Pharmaceutical Sciences, University of Shizuoka
kn-affil=

affil-num=10
en-affil=Department of Cardiovascular Medicine, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Department of Chronic Kidney Disease and Cardiovascular Disease, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=12
en-affil=Department of Cardiovascular Medicine, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=13
en-affil=Department of Cardiovascular Therapeutics, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=14
en-affil=Department of Cardiovascular Physiology, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=15
en-affil=Department of Metabolic Immune Regulation, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=16
en-affil=Department of Metabolic Immune Regulation, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=17
en-affil=Department of Medicine, University of Wisconsin School of Medicine and Public Health
kn-affil=

affil-num=18
en-affil=Department of Cardiovascular Medicine, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=19
en-affil=Department of Medicine, University of Wisconsin School of Medicine and Public Health
kn-affil=

affil-num=20
en-affil=Department of Cardiovascular Medicine, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Human pluripotent stem cell-derived cardiomyocytes
kn-keyword=Human pluripotent stem cell-derived cardiomyocytes
en-keyword=Anterior second heart field
kn-keyword=Anterior second heart field
en-keyword=Right ventricle
kn-keyword=Right ventricle
en-keyword=Bone morphogenetic protein
kn-keyword=Bone morphogenetic protein
END

start-ver=1.4
cd-journal=joma
no-vol=18
cd-vols=
no-issue=2
article-no=
start-page=22
end-page=32
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250805
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Data inventory, processing, and reporting on plant blindness among high school students in three schools in West Java
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Plant blindness is a problem related to a person's inability to realize, recognize, and know the benefits and roles of plants. After some research, there was a shift in the term, from Plant Blindness to Plant Awareness Disparity. This study aims to find out the prevalence of Plant Blindness in three high schools in West Java. The method used in this study is descriptive Cross sectional. The results of this study revealed that there were differences in the level of plant awareness in the three schools studied. One of the schools in the city of Bandung showed the highest plant awareness rate. In addition, it was also found that students who had a high level of plant awareness had a high perception of plant awareness. As a follow-up, further research can be carried out to collect more data so that it becomes a whole population. In addition, researchers can then use additional instruments so that more things can be revealed about plant blindness.
en-copyright=
kn-copyright=

en-aut-name=SorayaPuan Helwa Rezha
en-aut-sei=Soraya
en-aut-mei=Puan Helwa Rezha
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SolihatRini
en-aut-sei=Solihat
en-aut-mei=Rini
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SanjayaYayan
en-aut-sei=Sanjaya
en-aut-mei=Yayan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HaradaTaro
en-aut-sei=Harada
en-aut-mei=Taro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=Biology Education, Faculty of Mathematics and Science Education, Universitas Pendidikan Indonesia
kn-affil=

affil-num=2
en-affil=Biology Education, Faculty of Mathematics and Science Education, Universitas Pendidikan Indonesia
kn-affil=

affil-num=3
en-affil=Biology Education, Faculty of Mathematics and Science Education, Universitas Pendidikan Indonesia
kn-affil=

affil-num=4
en-affil=Graduate School of Education, Okayama University
kn-affil=
en-keyword=Descriptive statistics
kn-keyword=Descriptive statistics
en-keyword=Inferential statistics
kn-keyword=Inferential statistics
en-keyword=Plant Blindness
kn-keyword=Plant Blindness
END

start-ver=1.4
cd-journal=joma
no-vol=40
cd-vols=
no-issue=4
article-no=
start-page=463
end-page=474
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241225
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Nationwide diversity of symbolic “city flowers” in Japan is increasing
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Recognizing and maintaining locally rooted human–nature interactions is essential for utilizing ecosystem services. Although the general public's awareness of biodiversity and ecosystem services has been examined using various proxies, it remains unclear how local governments—key sectors in creating conservation policies—appreciate them within a solid local context. Here, we focused on the “city flower,” an official symbolic species of Japanese cities, as a new proxy for measuring governmental attitudes toward biota and its services. We aimed to capture temporal changes in the awareness of species with locally relevant value at the city government level by examining the changes in city flowers over more than half a century. Data from the official websites of municipalities, including the names, the adoption years, and the reasons for adoption, revealed two major periods of adoption, with a notable increase in species diversity in and after 1993. This increase could be attributed to a recent reduction in bias toward popular flowers and growing interest in alternative, less popular flowers. Analysis of the reasons for adoption suggested that the temporal change in adopted flower species was related to the increasing emphasis on species with an explicit local context, especially those with instrumental value to the city. Our findings indicate the tendency for local governments to increasingly recognize their biocultural backgrounds and the ecosystem services of plants within their regions. The growing awareness of the local governments regarding their biocultural background is a positive sign for the conservation of biodiversity and ecosystem services.
en-copyright=
kn-copyright=

en-aut-name=TsuzukiYoichi
en-aut-sei=Tsuzuki
en-aut-mei=Yoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OhsakiHaruna
en-aut-sei=Ohsaki
en-aut-mei=Haruna
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KawaguchiYawako W.
en-aut-sei=Kawaguchi
en-aut-mei=Yawako W.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SuzukiSayaka
en-aut-sei=Suzuki
en-aut-mei=Sayaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HaradaShogo
en-aut-sei=Harada
en-aut-mei=Shogo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OtakeYurie
en-aut-sei=Otake
en-aut-mei=Yurie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=ShinoharaNaoto
en-aut-sei=Shinohara
en-aut-mei=Naoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KatsuharaKoki R.
en-aut-sei=Katsuhara
en-aut-mei=Koki R.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Health and Environmental Risk Division, National Institute for Environmental Studies
kn-affil=

affil-num=2
en-affil=Department of Biological Sciences, Tokyo Metropolitan University
kn-affil=

affil-num=3
en-affil=Department of Biological Sciences, Graduate School of Science, The University of Tokyo
kn-affil=

affil-num=4
en-affil=Center for Ecological Research, Kyoto University
kn-affil=

affil-num=5
en-affil=Department of Biology, Graduate School of Science, Osaka City University
kn-affil=

affil-num=6
en-affil=Center for Ecological Research, Kyoto University
kn-affil=

affil-num=7
en-affil=Center for Ecological Research, Kyoto University
kn-affil=

affil-num=8
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=
en-keyword=awareness of local governments
kn-keyword=awareness of local governments
en-keyword=biocultural diversity
kn-keyword=biocultural diversity
en-keyword=ecosystem services
kn-keyword=ecosystem services
en-keyword=manual web scraping
kn-keyword=manual web scraping
en-keyword=temporal trend
kn-keyword=temporal trend
END

start-ver=1.4
cd-journal=joma
no-vol=19
cd-vols=
no-issue=3
article-no=
start-page=e70004
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202509
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Oregon Wolfe barley genetic stocks – Research and teaching tools for next generation scientists
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The Oregon Wolfe Barley (OWB) mapping population (Reg. no. MP-4, NSL 554937 MAP) is a resource for genetics research and instruction. The OWBs are a set of doubled haploid barley (Hordeum vulgare L.) lines developed at Oregon State University from the F1 of a cross between Dr. Robert Wolfe's dominant and recessive marker stocks. Exhibiting a high level of genetic and phenotypic diversity, the OWBs are used throughout the world as a research tool for barley genetics. To date, these endeavors have led to 56 peer-reviewed publications, as well as three reports in the Barley Genetics Newsletter. At the same time, the OWBs are widely used as an instructor resource at the K–12, undergraduate, graduate, and professional levels. They are currently used at universities and/or institutes in German, Italy, Norway, Spain, and the United States and are currently being developed further for educational use in other countries. Genotype and phenotype data, lesson plans, and seed availability information are available herein and online.
en-copyright=
kn-copyright=

en-aut-name=KrauseMargaret R.
en-aut-sei=Krause
en-aut-mei=Margaret R.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ArbelaezJuan David
en-aut-sei=Arbelaez
en-aut-mei=Juan David
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=AsdalÅsmund
en-aut-sei=Asdal
en-aut-mei=Åsmund
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=BelkodjaRamzi
en-aut-sei=Belkodja
en-aut-mei=Ramzi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=BouryNancy
en-aut-sei=Boury
en-aut-mei=Nancy
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=BlakeVictoria C.
en-aut-sei=Blake
en-aut-mei=Victoria C.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=BrownPatrick J.
en-aut-sei=Brown
en-aut-mei=Patrick J.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=CasasAna
en-aut-sei=Casas
en-aut-mei=Ana
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=CistuéLuis
en-aut-sei=Cistué
en-aut-mei=Luis
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=Farré‐MartínezAlba
en-aut-sei=Farré‐Martínez
en-aut-mei=Alba
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=FiskScott
en-aut-sei=Fisk
en-aut-mei=Scott
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=FuerstGregory S.
en-aut-sei=Fuerst
en-aut-mei=Gregory S.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=GiménezEstela
en-aut-sei=Giménez
en-aut-mei=Estela
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=Guijarro‐RealCarla
en-aut-sei=Guijarro‐Real
en-aut-mei=Carla
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=GuthrieKaty
en-aut-sei=Guthrie
en-aut-mei=Katy
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=HalsteadMargaret
en-aut-sei=Halstead
en-aut-mei=Margaret
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=HelgersonLaura
en-aut-sei=Helgerson
en-aut-mei=Laura
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=HisanoHiroshi
en-aut-sei=Hisano
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=IgartuaErnesto
en-aut-sei=Igartua
en-aut-mei=Ernesto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=LillemoMorten
en-aut-sei=Lillemo
en-aut-mei=Morten
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

en-aut-name=Martínez‐GarcíaMarina
en-aut-sei=Martínez‐García
en-aut-mei=Marina
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=21
ORCID=

en-aut-name=Martínez‐SubiràMariona
en-aut-sei=Martínez‐Subirà
en-aut-mei=Mariona
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=22
ORCID=

en-aut-name=McCouchSusan
en-aut-sei=McCouch
en-aut-mei=Susan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=23
ORCID=

en-aut-name=McGheeLaurie
en-aut-sei=McGhee
en-aut-mei=Laurie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=24
ORCID=

en-aut-name=NickolsTravis
en-aut-sei=Nickols
en-aut-mei=Travis
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=25
ORCID=

en-aut-name=PetersNick
en-aut-sei=Peters
en-aut-mei=Nick
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=26
ORCID=

en-aut-name=PorterRaymond
en-aut-sei=Porter
en-aut-mei=Raymond
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=27
ORCID=

en-aut-name=RomagosaIgnacio
en-aut-sei=Romagosa
en-aut-mei=Ignacio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=28
ORCID=

en-aut-name=RuudAnja Karine
en-aut-sei=Ruud
en-aut-mei=Anja Karine
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=29
ORCID=

en-aut-name=SatoKazuhiro
en-aut-sei=Sato
en-aut-mei=Kazuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=30
ORCID=

en-aut-name=SalviSilvio
en-aut-sei=Salvi
en-aut-mei=Silvio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=31
ORCID=

en-aut-name=SangiorgiGiuseppe
en-aut-sei=Sangiorgi
en-aut-mei=Giuseppe
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=32
ORCID=

en-aut-name=SchüllerRebekka
en-aut-sei=Schüller
en-aut-mei=Rebekka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=33
ORCID=

en-aut-name=SenTaner Z.
en-aut-sei=Sen
en-aut-mei=Taner Z.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=34
ORCID=

en-aut-name=SorianoJosé Miguel
en-aut-sei=Soriano
en-aut-mei=José Miguel
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=35
ORCID=

en-aut-name=StuparRobert M.
en-aut-sei=Stupar
en-aut-mei=Robert M.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=36
ORCID=

en-aut-name=TingTo‐Chia
en-aut-sei=Ting
en-aut-mei=To‐Chia
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=37
ORCID=

en-aut-name=ViningKelly
en-aut-sei=Vining
en-aut-mei=Kelly
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=38
ORCID=

en-aut-name=von KorffMaria
en-aut-sei=von Korff
en-aut-mei=Maria
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=39
ORCID=

en-aut-name=WallaAgatha
en-aut-sei=Walla
en-aut-mei=Agatha
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=40
ORCID=

en-aut-name=WangDiane R.
en-aut-sei=Wang
en-aut-mei=Diane R.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=41
ORCID=

en-aut-name=WaughRobbie
en-aut-sei=Waugh
en-aut-mei=Robbie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=42
ORCID=

en-aut-name=WiseRoger P.
en-aut-sei=Wise
en-aut-mei=Roger P.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=43
ORCID=

en-aut-name=WolfeRobert
en-aut-sei=Wolfe
en-aut-mei=Robert
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=44
ORCID=

en-aut-name=YaoEric
en-aut-sei=Yao
en-aut-mei=Eric
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=45
ORCID=

en-aut-name=HayesPatrick M.
en-aut-sei=Hayes
en-aut-mei=Patrick M.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=46
ORCID=

affil-num=1
en-affil=Department of Crop and Soil Science, Oregon State University
kn-affil=

affil-num=2
en-affil=Department of Crop Sciences, University of Illinois at Urbana-Champaign
kn-affil=

affil-num=3
en-affil=Nordic Genetic Resource Centre
kn-affil=

affil-num=4
en-affil=CIHEAM-Zaragoza
kn-affil=

affil-num=5
en-affil=Department of Plant Pathology, Entomology, and Microbiology, Iowa State University
kn-affil=

affil-num=6
en-affil=Department of Plant Sciences and Plant Pathology, Montana State University
kn-affil=

affil-num=7
en-affil=Department of Plant Sciences, University of California-Davis
kn-affil=

affil-num=8
en-affil=Departamento de Genética y Producción Vegetal, Estación Experimental Aula Dei–CSIC
kn-affil=

affil-num=9
en-affil=Departamento de Genética y Producción Vegetal, Estación Experimental Aula Dei–CSIC
kn-affil=

affil-num=10
en-affil=AGROTECNIO-CERCA Center, Universidad de Lleida
kn-affil=

affil-num=11
en-affil=Department of Crop and Soil Science, Oregon State University
kn-affil=

affil-num=12
en-affil=U.S. Department of Agriculture-Agricultural Research Service, Corn Insects and Crop Genetics Research Unit, Iowa State University
kn-affil=

affil-num=13
en-affil=Department of Biotechnology-Plant Biology, School of Agricultural, Food and Biosystems Engineering, Universidad Politécnica de Madrid
kn-affil=

affil-num=14
en-affil=Department of Biotechnology-Plant Biology, School of Agricultural, Food and Biosystems Engineering, Universidad Politécnica de Madrid
kn-affil=

affil-num=15
en-affil=Department of Agronomy and Plant Genetics, University of Minnesota
kn-affil=

affil-num=16
en-affil=Aardevo North America
kn-affil=

affil-num=17
en-affil=Department of Crop and Soil Science, Oregon State University
kn-affil=

affil-num=18
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=19
en-affil=Departamento de Genética y Producción Vegetal, Estación Experimental Aula Dei–CSIC
kn-affil=

affil-num=20
en-affil=Department of Plant Sciences, Norwegian University of Life Sciences
kn-affil=

affil-num=21
en-affil=Department of Biotechnology-Plant Biology, School of Agricultural, Food and Biosystems Engineering, Universidad Politécnica de Madrid
kn-affil=

affil-num=22
en-affil=AGROTECNIO-CERCA Center, Universidad de Lleida
kn-affil=

affil-num=23
en-affil=Plant Breeding and Genetics Section, School of Integrative Plant Science, Cornell University
kn-affil=

affil-num=24
en-affil=Colfax-Mingo Community High School
kn-affil=

affil-num=25
en-affil=Department of Crop and Soil Science, Oregon State University
kn-affil=

affil-num=26
en-affil=Department of Plant Pathology, Entomology, and Microbiology, Iowa State University
kn-affil=

affil-num=27
en-affil=Haupert Institute for Agricultural Studies, Huntington University
kn-affil=

affil-num=28
en-affil=AGROTECNIO-CERCA Center, Universidad de Lleida
kn-affil=

affil-num=29
en-affil=Department of Plant Sciences, Norwegian University of Life Sciences
kn-affil=

affil-num=30
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=31
en-affil=Department of Agricultural and Food Sciences, University of Bologna
kn-affil=

affil-num=32
en-affil=Department of Agricultural and Food Sciences, University of Bologna
kn-affil=

affil-num=33
en-affil=Department of Crop Sciences, University of Illinois at Urbana-Champaign
kn-affil=

affil-num=34
en-affil=Crop Improvement and Genetics Research Unit, U.S. Department of Agriculture-Agricultural Research Service
kn-affil=

affil-num=35
en-affil=AGROTECNIO-CERCA Center, Universidad de Lleida
kn-affil=

affil-num=36
en-affil=Department of Agronomy and Plant Genetics, University of Minnesota
kn-affil=

affil-num=37
en-affil=Agronomy Department, Purdue University
kn-affil=

affil-num=38
en-affil=Department of Crop and Soil Science, Oregon State University
kn-affil=

affil-num=39
en-affil=Institute of Plant Genetics, Heinrich-Heine-Universität Düsseldorf
kn-affil=

affil-num=40
en-affil=Institute of Plant Genetics, Heinrich-Heine-Universität Düsseldorf
kn-affil=

affil-num=41
en-affil=Agronomy Department, Purdue University
kn-affil=

affil-num=42
en-affil=Division of Plant Sciences, School of Life Sciences, University of Dundee
kn-affil=

affil-num=43
en-affil=Department of Plant Pathology, Entomology, and Microbiology, Iowa State University
kn-affil=

affil-num=44
en-affil=Agriculture and Agri-Food Canada
kn-affil=

affil-num=45
en-affil=Crop Improvement and Genetics Research Unit, U.S. Department of Agriculture-Agricultural Research Service
kn-affil=

affil-num=46
en-affil=Department of Crop and Soil Science, Oregon State University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=1869
cd-vols=
no-issue=12
article-no=
start-page=130860
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250913
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The F54L mutation of Thioredoxin shows protein instability and increased fluctuations of the catalytic center
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Thioredoxin is a ubiquitous redox protein that acts as an electron donor via its conserved dithiol motif (C32GPC35), catalyzing dithiol–disulfide exchange to regulate the redox state of target proteins. It supports antioxidant defense via peroxiredoxins, facilitates DNA synthesis by donating electrons to ribonucleotide reductase, and regulates redox-sensitive signaling pathways, including those controlling transcription and apoptosis. Neuronal degeneration and chronic kidney disease have been observed in Txn-F54L mutant rats; however, the details of why the Txn mutation causes these phenomena remain unknown. The present study aimed to elucidate the functional and structural changes caused by the F54L mutation. The Thioredoxin-F54L showed less insulin-reducing activity and more thermosensitivity to denaturation in the body temperature range compared to the wild type. The crystal structure revealed that F54 forms hydrophobic interactions with the surrounding hydrophobic amino acids. In addition, molecular dynamics simulation predicts increased fluctuations around the F54L mutation and a tendency for the distance between residues C32 and C35 at the catalytic center to be widened. The increased distance between residues C32 and C35 of the catalytic center may affect the reducing activity of the enzyme on the substrate. The finding that Thioredoxin-F54L is prone to denaturation at normal body temperature may reduce the normally functioning Thioredoxin. These molecular characteristics of Thioredoxin-F54L may be related to brain and kidney disease development in the Txn-F54L rats.
en-copyright=
kn-copyright=

en-aut-name=BabaTakumi
en-aut-sei=Baba
en-aut-mei=Takumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=UenoGo
en-aut-sei=Ueno
en-aut-mei=Go
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OheChika
en-aut-sei=Ohe
en-aut-mei=Chika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SajiShuku
en-aut-sei=Saji
en-aut-mei=Shuku
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YamamotoSachiko
en-aut-sei=Yamamoto
en-aut-mei=Sachiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YamamotoMasaki
en-aut-sei=Yamamoto
en-aut-mei=Masaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NakagawaHiroshi
en-aut-sei=Nakagawa
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=OkazakiNobuo
en-aut-sei=Okazaki
en-aut-mei=Nobuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=OuchidaMamoru
en-aut-sei=Ouchida
en-aut-mei=Mamoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=Kawasaki-OhmoriIori
en-aut-sei=Kawasaki-Ohmori
en-aut-mei=Iori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=TakeshitaKohei
en-aut-sei=Takeshita
en-aut-mei=Kohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

affil-num=1
en-affil=Life Science Research Infrastructure Group, Advanced Photon Technology Division, RIKEN SPring-8 Center
kn-affil=

affil-num=2
en-affil=Life Science Research Infrastructure Group, Advanced Photon Technology Division, RIKEN SPring-8 Center
kn-affil=

affil-num=3
en-affil=Life Science Research Infrastructure Group, Advanced Photon Technology Division, RIKEN SPring-8 Center
kn-affil=

affil-num=4
en-affil=Structural Biology Division, Japan Synchrotron Radiation Research Institute
kn-affil=

affil-num=5
en-affil=Structural Biology Division, Japan Synchrotron Radiation Research Institute
kn-affil=

affil-num=6
en-affil=Life Science Research Infrastructure Group, Advanced Photon Technology Division, RIKEN SPring-8 Center
kn-affil=

affil-num=7
en-affil=Materials Sciences Research Center, Japan Atomic Energy Agency
kn-affil=

affil-num=8
en-affil=Neutron Science and Technology Center, Comprehensive Research Organization for Science and Society (CROSS)
kn-affil=

affil-num=9
en-affil=Department of Molecular Oncology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=10
en-affil=Section of Developmental Physiology and Pathology, Faculty of Education, Okayama University
kn-affil=

affil-num=11
en-affil=Life Science Research Infrastructure Group, Advanced Photon Technology Division, RIKEN SPring-8 Center
kn-affil=
en-keyword=Txn
kn-keyword=Txn
en-keyword=Thioredoxin
kn-keyword=Thioredoxin
en-keyword=Protein instability
kn-keyword=Protein instability
en-keyword=Thermosensitivity
kn-keyword=Thermosensitivity
en-keyword=Crystal structure
kn-keyword=Crystal structure
en-keyword=Molecular dynamics simulation
kn-keyword=Molecular dynamics simulation
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=1
end-page=3
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250919
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Dual-action intranasal oxytocin enhances both male sexual performance and fertility in rats
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=EnomotoChica
en-aut-sei=Enomoto
en-aut-mei=Chica
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OtiTakumi
en-aut-sei=Oti
en-aut-mei=Takumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YamanakaTakahiro
en-aut-sei=Yamanaka
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ShimadaMasayuki
en-aut-sei=Shimada
en-aut-mei=Masayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SakamotoHirotaka
en-aut-sei=Sakamoto
en-aut-mei=Hirotaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Department of Biology, Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Biology, Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=3
en-affil=Laboratory of Reproductive Endocrinology, Graduate School of Integrated Sciences for Life, Hiroshima University
kn-affil=

affil-num=4
en-affil=Laboratory of Reproductive Endocrinology, Graduate School of Integrated Sciences for Life, Hiroshima University
kn-affil=

affil-num=5
en-affil=Department of Biology, Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=
en-keyword=oxytocin
kn-keyword=oxytocin
en-keyword=intranasal administration
kn-keyword=intranasal administration
en-keyword=sexual behavior
kn-keyword=sexual behavior
en-keyword=sperm motility
kn-keyword=sperm motility
en-keyword=paraventricular nucleus
kn-keyword=paraventricular nucleus
en-keyword=male sexual function
kn-keyword=male sexual function
en-keyword=androgen signaling
kn-keyword=androgen signaling
END

start-ver=1.4
cd-journal=joma
no-vol=18
cd-vols=
no-issue=1
article-no=
start-page=wrae175
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202401
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Cyanorhodopsin-II represents a yellow-absorbing proton-pumping rhodopsin clade within cyanobacteria
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Microbial rhodopsins are prevalent in many cyanobacterial groups as a light-energy-harvesting system in addition to the photosynthetic system. It has been suggested that this dual system allows efficient capture of sunlight energy using complementary ranges of absorption wavelengths. However, the diversity of cyanobacterial rhodopsins, particularly in accumulated metagenomic data, remains underexplored. Here, we used a metagenomic mining approach, which led to the identification of a novel rhodopsin clade unique to cyanobacteria, cyanorhodopsin-II (CyR-II). CyR-IIs function as light-driven outward H+ pumps. CyR-IIs, together with previously identified cyanorhodopsins (CyRs) and cyanobacterial halorhodopsins (CyHRs), constitute cyanobacterial ion-pumping rhodopsins (CyipRs), a phylogenetically distinct family of rhodopsins. The CyR-II clade is further divided into two subclades, YCyR-II and GCyR-II, based on their specific absorption wavelength. YCyR-II absorbed yellow light (λmax = 570 nm), whereas GCyR-II absorbed green light (λmax = 550 nm). X-ray crystallography and mutational analysis revealed that the difference in absorption wavelengths is attributable to slight changes in the side chain structure near the retinal chromophore. The evolutionary trajectory of cyanobacterial rhodopsins suggests that the function and light-absorbing range of these rhodopsins have been adapted to a wide range of habitats with variable light and environmental conditions. Collectively, these findings shed light on the importance of rhodopsins in the evolution and environmental adaptation of cyanobacteria.
en-copyright=
kn-copyright=

en-aut-name=Hasegawa-TakanoMasumi
en-aut-sei=Hasegawa-Takano
en-aut-mei=Masumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HosakaToshiaki
en-aut-sei=Hosaka
en-aut-mei=Toshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KojimaKeiichi
en-aut-sei=Kojima
en-aut-mei=Keiichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NishimuraYosuke
en-aut-sei=Nishimura
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KuriharaMarie
en-aut-sei=Kurihara
en-aut-mei=Marie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NakajimaYu
en-aut-sei=Nakajima
en-aut-mei=Yu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=Ishizuka-KatsuraYoshiko
en-aut-sei=Ishizuka-Katsura
en-aut-mei=Yoshiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=Kimura-SomeyaTomomi
en-aut-sei=Kimura-Someya
en-aut-mei=Tomomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=ShirouzuMikako
en-aut-sei=Shirouzu
en-aut-mei=Mikako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=SudoYuki
en-aut-sei=Sudo
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=YoshizawaSusumu
en-aut-sei=Yoshizawa
en-aut-mei=Susumu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

affil-num=1
en-affil=Atmosphere and Ocean Research Institute, The University of Tokyo
kn-affil=

affil-num=2
en-affil=Laboratory for Protein Functional and Structural Biology, RIKEN Center for Biosystems Dynamics Research
kn-affil=

affil-num=3
en-affil=Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Atmosphere and Ocean Research Institute, The University of Tokyo
kn-affil=

affil-num=5
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Atmosphere and Ocean Research Institute, The University of Tokyo
kn-affil=

affil-num=7
en-affil=Laboratory for Protein Functional and Structural Biology, RIKEN Center for Biosystems Dynamics Research
kn-affil=

affil-num=8
en-affil=Laboratory for Protein Functional and Structural Biology, RIKEN Center for Biosystems Dynamics Research
kn-affil=

affil-num=9
en-affil=Laboratory for Protein Functional and Structural Biology, RIKEN Center for Biosystems Dynamics Research
kn-affil=

affil-num=10
en-affil=Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=11
en-affil=Atmosphere and Ocean Research Institute, The University of Tokyo
kn-affil=
en-keyword=cyanobacteria
kn-keyword=cyanobacteria
en-keyword=microbial rhodopsin
kn-keyword=microbial rhodopsin
en-keyword=ecology
kn-keyword=ecology
en-keyword=evolution
kn-keyword=evolution
END

start-ver=1.4
cd-journal=joma
no-vol=26
cd-vols=
no-issue=10
article-no=
start-page=4724
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250515
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Stem Cell Factors BAM1 and WOX1 Suppressing Longitudinal Cell Division of Margin Cells Evoked by Low-Concentration Auxin in Young Cotyledon of Arabidopsis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Highly differentiated tissues and organs play essential biological functions in multicellular organisms. Coordination of organ developmental process with tissue differentiation is necessary to achieve proper development of mature organs, but mechanisms for such coordination are not well understood. We used cotyledon margin cells from Arabidopsis plant as a new model system to investigate cell elongation and cell division during organ growth and found that margin cells endured a developmental phase transition from the “elongation” phase to the “elongation and division” phase at the early stage in germinating seedlings. We also discovered that the stem cell factors BARELY ANY MERISTEM 1 (BAM1) and WUSCHEL-related homeobox1 (WOX1) are involved in the regulation of margin cell developmental phase transition. Furthermore, exogenous auxin treatment (1 nanomolar,nM) promotes cell division, especially longitudinal cell division. This promotion of cell division did not occur in bam1 and wox1 mutants. Based on these findings, we hypothesized a new “moderate auxin concentration” model which emphasizes that a moderate auxin concentration is the key to triggering the developmental transition of meristematic cells.
en-copyright=
kn-copyright=

en-aut-name=JiangYuli
en-aut-sei=Jiang
en-aut-mei=Yuli
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=LiangJian
en-aut-sei=Liang
en-aut-mei=Jian
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=WangChunyan
en-aut-sei=Wang
en-aut-mei=Chunyan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TanLi
en-aut-sei=Tan
en-aut-mei=Li
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KawanoYoji
en-aut-sei=Kawano
en-aut-mei=Yoji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NagawaShingo
en-aut-sei=Nagawa
en-aut-mei=Shingo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Institute for Translational Brain Reaearch, Fudan University
kn-affil=

affil-num=2
en-affil=Center for Excellence in Molecular Plant Science, Chinese Academy of Sciences
kn-affil=

affil-num=3
en-affil=Center for Excellence in Molecular Plant Science, Chinese Academy of Sciences
kn-affil=

affil-num=4
en-affil=Center for Excellence in Molecular Plant Science, Chinese Academy of Sciences
kn-affil=

affil-num=5
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=6
en-affil=Center for Excellence in Molecular Plant Science, Chinese Academy of Sciences
kn-affil=
en-keyword=BAM1
kn-keyword=BAM1
en-keyword=WOX1
kn-keyword=WOX1
en-keyword=margin cells
kn-keyword=margin cells
en-keyword=auxin
kn-keyword=auxin
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250909
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=S100A8/A9-MCAM signaling promotes gastric cancer cell progression via ERK-c-Jun activation
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=S100 protein family members S100A8 and S100A9 function primarily as a heterodimer complex (S100A8/A9) in vivo. This complex has been implicated in various cancers, including gastric cancer (GC). Recent studies suggest that these proteins play significant roles in tumor progression, inflammation, and metastasis. However, the exact mechanisms by which S100A8/A9 contributes to GC pathogenesis remain unclear. This study investigates the role of S100A8/A9 and its receptor in GC. Immunohistochemical analysis was performed on GC tissue samples to assess the expression of the S100A8/A9 receptor melanoma cell adhesion molecule (MCAM). In vitro transwell migration and invasion assays were used to evaluate the motility and invasiveness of GC cells. Cell proliferation was assessed using a growth assay, and Western blotting (WB) was employed to examine downstream signaling pathways, including ERK and the transcription factor c-Jun, in response to S100A8/A9–MCAM interaction. S100A8/A9 stimulation enhanced both proliferation and migration through MCAM binding in GC cell lines. These cellular events were accompanied by ERK activation and c-Jun induction. Downregulation of MCAM suppressed both ERK phosphorylation and c-Jun expression, highlighting the importance of the S100A8/A9‒MCAM‒ERK‒c-Jun axis in promoting GC progression. These findings indicate that S100A8/A9 contributes to GC progression via MCAM, which activates the ERK‒c-Jun pathway. The S100A8/A9‒signaling axis may represent a novel therapeutic target in GC.
en-copyright=
kn-copyright=

en-aut-name=ChenYouyi
en-aut-sei=Chen
en-aut-mei=Youyi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YangXu
en-aut-sei=Yang
en-aut-mei=Xu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KinoshitaRie
en-aut-sei=Kinoshita
en-aut-mei=Rie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TomonobuNahoko
en-aut-sei=Tomonobu
en-aut-mei=Nahoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=PanBo
en-aut-sei=Pan
en-aut-mei=Bo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=WuFangping
en-aut-sei=Wu
en-aut-mei=Fangping
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=ZhangXu
en-aut-sei=Zhang
en-aut-mei=Xu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=SagayamaKazumi
en-aut-sei=Sagayama
en-aut-mei=Kazumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=SunBei
en-aut-sei=Sun
en-aut-mei=Bei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=SakaguchiMasakiyo
en-aut-sei=Sakaguchi
en-aut-mei=Masakiyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of Breast Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine
kn-affil=

affil-num=2
en-affil=Department of Pathology, The First Affiliated Hospital, Zhejiang University School of Medicine
kn-affil=

affil-num=3
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=The First Affiliated Hospital, Zhejiang University School of Medicine
kn-affil=

affil-num=6
en-affil=School of Pharmaceutical Sciences, Zhejiang Chinese Medical University
kn-affil=

affil-num=7
en-affil=Department of Urology, The First Affiliated Hospital, Zhejiang University School of Medicine
kn-affil=

affil-num=8
en-affil=Faculties of Educational and Research Management Field, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Pancreatic and Biliary Surgery, The First Affiliated Hospital of Harbin Medical University
kn-affil=

affil-num=10
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=
en-keyword=Gastric cancer
kn-keyword=Gastric cancer
en-keyword=S100 protein
kn-keyword=S100 protein
en-keyword=MCAM
kn-keyword=MCAM
en-keyword=Inflammation
kn-keyword=Inflammation
en-keyword=Metastasis
kn-keyword=Metastasis
END

start-ver=1.4
cd-journal=joma
no-vol=34
cd-vols=
no-issue=2
article-no=
start-page=67
end-page=73
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240701
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Depletion of Lysyl Oxidase-Like 4 (LOXL4) Attenuates Colony Formation in vitro and Collagen Deposition in vivo Breast Cancer Model
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background:  Lysyl oxidase (LOX) family proteins have recently become a topic in cancer progression. Our recent study found a high expression of LOX-like 4 (LOXL4) in MDA-MB-231 cells. Objective:  To reveal the impact of depleted LOXL4 in both in vitro and in vivo breast cancer models from a histological perspective. Material and Method: Endogenous LOXL4 was depleted using the CRISPR/Cas9 on MDA-MB-231 parental cells. Based on the LOXL4 protein expression, the clone was determined for the next experiment, thus generating MDA-MB-231 LOXL4 KO. Cell assay was conducted using colony formation assay (n=3) followed by crystal violet staining. The indicated cells were inoculated orthotopically to female BALB/c nude mice (n=5). At the end of the experiment, tumors were isolated, fixed, and prepared for Masson Trichrome staining. Result:  CRISPR/Cas9 completely depleted LOXL4 expression on clone number #2-22. Depletion of LOXL4 reduced the colony size formed by MDA-MB-231 cells. MDA-MB-231 LOXL4 KO #2-22 derived tumors showed depressed tumor volume compared to the parental group. Reduced collagen was also observed from the Masson Trichrome staining (p<0.001). Conclusion: Depletion of LOXL4 downregulates the growth of MDA-MB-231 cells in vitro and collagen deposition in vivo.
en-copyright=
kn-copyright=

en-aut-name=Ni Luh Gede Yoni Komalasari
en-aut-sei=Ni Luh Gede Yoni Komalasari
en-aut-mei=
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=I Gde Haryo Ganesha
en-aut-sei=I Gde Haryo Ganesha
en-aut-mei=
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=I Gusti Nyoman Sri Wiryawan
en-aut-sei=I Gusti Nyoman Sri Wiryawan
en-aut-mei=
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TomonobuNahoko
en-aut-sei=Tomonobu
en-aut-mei=Nahoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SakaguchiMasakiyo
en-aut-sei=Sakaguchi
en-aut-mei=Masakiyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Department of Cell Biology, Graduate School of Medicine, Dentistry, and Pharmaceutical Science, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Histology, Faculty of Medicine, Udayana University
kn-affil=

affil-num=3
en-affil=Department of Histology, Faculty of Medicine, Udayana University
kn-affil=

affil-num=4
en-affil=Department of Cell Biology, Graduate School of Medicine, Dentistry, and Pharmaceutical Science, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Cell Biology, Graduate School of Medicine, Dentistry, and Pharmaceutical Science, Okayama University
kn-affil=
en-keyword=Good health
kn-keyword=Good health
en-keyword=Lysyl oxidase
kn-keyword=Lysyl oxidase
en-keyword=Extracellular matrix
kn-keyword=Extracellular matrix
END

start-ver=1.4
cd-journal=joma
no-vol=21
cd-vols=
no-issue=7
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202507
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Animal–chlorophyte photosymbioses: evolutionary origins and ecological diversity
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Photosynthetic symbiosis occurs across diverse animal lineages, including Porifera, Cnidaria, Xenacoelomorpha and Mollusca. These associations between animal hosts and photosynthetic algae often involve the exchange of essential macronutrients, supporting adaptation to a wide range of aquatic environments. A small yet taxonomically widespread subset of animals host photosymbionts from the core chlorophytes, a phylogenetically expansive clade of green algae. These rare instances of ‘plant-like’ animals have arisen independently across distantly related lineages, resulting in striking ecological and physiological diversity. Although such associations provide valuable insights into the evolution of symbiosis and adaptation to novel ecological niches, animal–chlorophyte photosymbioses remain relatively understudied. Here, we present an overview of photosymbioses between animals and chlorophytes, highlighting their independent evolutionary origins, ecological diversity and emerging genomic resources. Focusing on Porifera, Cnidaria and Xenacoelomorpha, we review shared and lineage-specific adaptations underlying these associations. We also contrast them with dinoflagellate-based systems to demonstrate their distinct ecological and cellular features. Our work sets the stage for elucidating the molecular mechanisms underlying these associations, enhancing our understanding of how interspecies interactions drive adaptation to unique ecological niches through animal–chlorophyte symbiosis.
en-copyright=
kn-copyright=

en-aut-name=LiaoIsabel Jiah-Yih
en-aut-sei=Liao
en-aut-mei=Isabel Jiah-Yih
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SakagamiTosuke
en-aut-sei=Sakagami
en-aut-mei=Tosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=LewinThomas D.
en-aut-sei=Lewin
en-aut-mei=Thomas D.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=BaillyXavier
en-aut-sei=Bailly
en-aut-mei=Xavier
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HamadaMayuko
en-aut-sei=Hamada
en-aut-mei=Mayuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=LuoYi-Jyun
en-aut-sei=Luo
en-aut-mei=Yi-Jyun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Biodiversity Research Center, Academia Sinica
kn-affil=

affil-num=2
en-affil=Biodiversity Research Center, Academia Sinica
kn-affil=

affil-num=3
en-affil=Biodiversity Research Center, Academia Sinica
kn-affil=

affil-num=4
en-affil=Laboratoire des Modèles Marins Multicellulaires, Station Biologique de Roscoff
kn-affil=

affil-num=5
en-affil=Ushimado Marine Institute, Okayama University
kn-affil=

affil-num=6
en-affil=Biodiversity Research Center, Academia Sinica
kn-affil=
en-keyword=hydra
kn-keyword=hydra
en-keyword=photosymbiosis
kn-keyword=photosymbiosis
en-keyword=green algae
kn-keyword=green algae
en-keyword=acoels
kn-keyword=acoels
en-keyword=sponges
kn-keyword=sponges
END

start-ver=1.4
cd-journal=joma
no-vol=156
cd-vols=
no-issue=2
article-no=
start-page=473
end-page=479.e1
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202508
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Dried blood spot proteome identifies subclinical interferon signature in neonates with type I interferonopathy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Type I interferonopathy is characterized by aberrant upregulation of type I interferon signaling. The mRNA interferon signature is a useful marker for activation of the interferon pathway and for diagnosis of type I interferonopathy; however, early diagnosis is challenging.<br>
Objective: This study sought to identify the proteomic interferon signature in dried blood spot (DBS) samples. The aim was to evaluate the usefulness of the interferon signature for neonatal screening and to gain insight into presymptomatic state of neonates with inborn errors of immunity (IEIs).<br>
Methods: DBS samples from healthy newborns/adults, patients with type I interferonopathy or other IEIs as well as from neonates with viral infections, including some samples obtained during the presymptomatic neonatal period, were examined by nontargeted proteome analyses. Expression of interferon-stimulated genes (ISGs) was evaluated and a DBS-interferon signature was defined. Differential expression/pathway analysis was also performed.<br>
Results: The ISG products IFIT5, ISG15, and OAS2 were detected. Expression of IFIT5 and ISG15 was upregulated significantly in individuals with type I interferonopathy. We defined the sum of the z scores for these as the DBS-interferon signature, and found that patients with IEIs other than type I interferonopathy, such as chronic granulomatous disease (CGD), also showed significant elevation. Additionally, neonatal samples of type I interferonopathy and CGD patients showed high interferon signatures. Pathway analysis of neonatal CGD samples revealed upregulation of systemic lupus erythematosus–like pathways.<br>
Conclusion: Upregulation of the interferon pathway exists already at birth—not only in neonates with type I interferonopathy but also in other IEIs, including CGD.
en-copyright=
kn-copyright=

en-aut-name=NihiraHiroshi
en-aut-sei=Nihira
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakajimaDaisuke
en-aut-sei=Nakajima
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=IzawaKazushi
en-aut-sei=Izawa
en-aut-mei=Kazushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KawashimaYusuke
en-aut-sei=Kawashima
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ShibataHirofumi
en-aut-sei=Shibata
en-aut-mei=Hirofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KonnoRyo
en-aut-sei=Konno
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=HigashiguchiMotoko
en-aut-sei=Higashiguchi
en-aut-mei=Motoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MiyamotoTakayuki
en-aut-sei=Miyamoto
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=Nishitani-IsaMasahiko
en-aut-sei=Nishitani-Isa
en-aut-mei=Masahiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=HiejimaEitaro
en-aut-sei=Hiejima
en-aut-mei=Eitaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=HondaYoshitaka
en-aut-sei=Honda
en-aut-mei=Yoshitaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=MatsubayashiTadashi
en-aut-sei=Matsubayashi
en-aut-mei=Tadashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=IshiharaTakashi
en-aut-sei=Ishihara
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=YashiroMasato
en-aut-sei=Yashiro
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=IwataNaomi
en-aut-sei=Iwata
en-aut-mei=Naomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=OhwadaYoko
en-aut-sei=Ohwada
en-aut-mei=Yoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=TomotakiSeiichi
en-aut-sei=Tomotaki
en-aut-mei=Seiichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=KawaiMasahiko
en-aut-sei=Kawai
en-aut-mei=Masahiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=MurakamiKosaku
en-aut-sei=Murakami
en-aut-mei=Kosaku
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=OhnishiHidenori
en-aut-sei=Ohnishi
en-aut-mei=Hidenori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

en-aut-name=IshimuraMasataka
en-aut-sei=Ishimura
en-aut-mei=Masataka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=21
ORCID=

en-aut-name=OkadaSatoshi
en-aut-sei=Okada
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=22
ORCID=

en-aut-name=YamashitaMotoi
en-aut-sei=Yamashita
en-aut-mei=Motoi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=23
ORCID=

en-aut-name=MorioTomohiro
en-aut-sei=Morio
en-aut-mei=Tomohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=24
ORCID=

en-aut-name=HoshinoAkihiro
en-aut-sei=Hoshino
en-aut-mei=Akihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=25
ORCID=

en-aut-name=KaneganeHirokazu
en-aut-sei=Kanegane
en-aut-mei=Hirokazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=26
ORCID=

en-aut-name=ImaiKohsuke
en-aut-sei=Imai
en-aut-mei=Kohsuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=27
ORCID=

en-aut-name=NakamuraYasuko
en-aut-sei=Nakamura
en-aut-mei=Yasuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=28
ORCID=

en-aut-name=NonoyamaShigeaki
en-aut-sei=Nonoyama
en-aut-mei=Shigeaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=29
ORCID=

en-aut-name=UchiyamaToru
en-aut-sei=Uchiyama
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=30
ORCID=

en-aut-name=OnoderaMasafumi
en-aut-sei=Onodera
en-aut-mei=Masafumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=31
ORCID=

en-aut-name=IshikawaTakashi
en-aut-sei=Ishikawa
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=32
ORCID=

en-aut-name=KawaiToshinao
en-aut-sei=Kawai
en-aut-mei=Toshinao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=33
ORCID=

en-aut-name=TakitaJunko
en-aut-sei=Takita
en-aut-mei=Junko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=34
ORCID=

en-aut-name=NishikomoriRyuta
en-aut-sei=Nishikomori
en-aut-mei=Ryuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=35
ORCID=

en-aut-name=OharaOsamu
en-aut-sei=Ohara
en-aut-mei=Osamu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=36
ORCID=

en-aut-name=YasumiTakahiro
en-aut-sei=Yasumi
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=37
ORCID=

affil-num=1
en-affil=Department of Pediatrics, Kyoto University Graduate School of Medicine
kn-affil=

affil-num=2
en-affil=Department of Applied Genomics, Kazusa DNA Research Institute
kn-affil=

affil-num=3
en-affil=Department of Pediatrics, Kyoto University Graduate School of Medicine
kn-affil=

affil-num=4
en-affil=Department of Applied Genomics, Kazusa DNA Research Institute
kn-affil=

affil-num=5
en-affil=Department of Pediatrics, Kyoto University Graduate School of Medicine
kn-affil=

affil-num=6
en-affil=Department of Applied Genomics, Kazusa DNA Research Institute
kn-affil=

affil-num=7
en-affil=Department of Pediatrics, Kyoto University Graduate School of Medicine
kn-affil=

affil-num=8
en-affil=Department of Pediatrics, Kyoto University Graduate School of Medicine
kn-affil=

affil-num=9
en-affil=Department of Pediatrics, Kyoto University Graduate School of Medicine
kn-affil=

affil-num=10
en-affil=Department of Pediatrics, Kyoto University Graduate School of Medicine
kn-affil=

affil-num=11
en-affil=Department of Pediatrics, Kyoto University Graduate School of Medicine
kn-affil=

affil-num=12
en-affil=Department of Pediatrics, Seirei Hamamatsu General Hospital
kn-affil=

affil-num=13
en-affil=Department of Pediatrics, Nara Medical University
kn-affil=

affil-num=14
en-affil=Department of Pediatrics, Okayama University
kn-affil=

affil-num=15
en-affil=Department of Infection and Immunology, Aichi Children’s Health and Medical Center
kn-affil=

affil-num=16
en-affil=Department of Pediatrics, Dokkyo Medical University School of Medicine
kn-affil=

affil-num=17
en-affil=Department of Pediatrics, Kyoto University Graduate School of Medicine
kn-affil=

affil-num=18
en-affil=Department of Neonatology, Kyoto University Graduate School of Medicine
kn-affil=

affil-num=19
en-affil=Center for Cancer Immunotherapy and Immunobiology, Kyoto University Graduate School of Medicine
kn-affil=

affil-num=20
en-affil=Department of Pediatrics, Gifu University Graduate School of Medicine
kn-affil=

affil-num=21
en-affil=Department of Pediatrics, Graduate School of Medical Sciences, Kyushu University
kn-affil=

affil-num=22
en-affil=Department of Pediatrics, Hiroshima University Graduate School of Biomedical and Health Sciences
kn-affil=

affil-num=23
en-affil=Department of Pediatrics and Developmental Biology, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo (SCIENCE TOKYO)
kn-affil=

affil-num=24
en-affil=Laboratory of Immunology and Molecular Medicine, Advanced Research Initiative, Institute of Science Tokyo (SCIENCE TOKYO)
kn-affil=

affil-num=25
en-affil=Department of Child Health and Development, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo (SCIENCE TOKYO)
kn-affil=

affil-num=26
en-affil=Department of Child Health and Development, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo (SCIENCE TOKYO)
kn-affil=

affil-num=27
en-affil=Department of Pediatrics, National Defense Medical College
kn-affil=

affil-num=28
en-affil=Department of Pediatrics, National Defense Medical College
kn-affil=

affil-num=29
en-affil=Department of Pediatrics, National Defense Medical College
kn-affil=

affil-num=30
en-affil=Department of Human Genetics, National Center for Child Health and Development
kn-affil=

affil-num=31
en-affil=Department of Human Genetics, National Center for Child Health and Development
kn-affil=

affil-num=32
en-affil=Division of Immunology, National Center for Child Health and Development
kn-affil=

affil-num=33
en-affil=Division of Immunology, National Center for Child Health and Development
kn-affil=

affil-num=34
en-affil=Department of Pediatrics, Kyoto University Graduate School of Medicine
kn-affil=

affil-num=35
en-affil=Department of Pediatrics and Child Health, Kurume University School of Medicine
kn-affil=

affil-num=36
en-affil=Department of Applied Genomics, Kazusa DNA Research Institute
kn-affil=

affil-num=37
en-affil=Department of Pediatrics, Kyoto University Graduate School of Medicine
kn-affil=
en-keyword=Inborn errors of immunity
kn-keyword=Inborn errors of immunity
en-keyword=interferonopathy
kn-keyword=interferonopathy
en-keyword=signature
kn-keyword=signature
en-keyword=proteome
kn-keyword=proteome
en-keyword=dried blood spot
kn-keyword=dried blood spot
en-keyword=CGD
kn-keyword=CGD
en-keyword=WAS
kn-keyword=WAS
en-keyword=newborn
kn-keyword=newborn
en-keyword=neonate
kn-keyword=neonate
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=roaf042
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250603
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Recommendations for the treatment of juvenile idiopathic arthritis with oligoarthritis or polyarthritis from the 2024 update of the Japan College of Rheumatology Clinical Practice Guidelines for the management of rheumatoid arthritis including juvenile idiopathic arthritis with oligoarthritis or polyarthritis – secondary publication
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Objectives: To conduct systematic reviews (SRs) and develop clinical practice guidelines (CPGs) for managing juvenile idiopathic arthritis (JIA) with oligoarthritis or polyarthritis.<br>
Methods: The Grading of Recommendations, Assessment, Development, and Evaluation methodology was employed to carry out SRs and formulate the CPGs. An expert panel, including patients, paediatric and nonpaediatric rheumatologists, guideline specialists, and patient representatives, used the Delphi method to discuss and agree on the recommendations.<br>
Results: Six clinical questions (CQs) on the efficacy and safety of medical treatments were evaluated. These included CQ1 on methotrexate (MTX), CQ2 on non-MTX conventional synthetic disease-modifying antirheumatic drugs, CQ3 on glucocorticoids, CQ4 on tumour necrosis factor inhibitors, CQ5 on interleukin-6 inhibitors, and CQ6 on Janus kinase inhibitors. Two randomized controlled trials were identified for CQ1, three for CQ2, two for CQ3, eight for CQ4, two for CQ5, and two for CQ6. Based on these evaluations, three strong and three conditional recommendations were established. The CPGs have been endorsed by the Japan College of Rheumatology and the Pediatric Rheumatology Association of Japan.<br>
Conclusions: The SRs provided the necessary evidence to develop the CPGs, which are intended to guide not only paediatric but also nonpaediatric rheumatologists, caregivers, patients, and their families in treatment decision-making.
en-copyright=
kn-copyright=

en-aut-name=MiyamaeTakako
en-aut-sei=Miyamae
en-aut-mei=Takako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OkamotoNami
en-aut-sei=Okamoto
en-aut-mei=Nami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=InoueYuzaburo
en-aut-sei=Inoue
en-aut-mei=Yuzaburo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KubotaTomohiro
en-aut-sei=Kubota
en-aut-mei=Tomohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=EbatoTakasuke
en-aut-sei=Ebato
en-aut-mei=Takasuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=IrabuHitoshi
en-aut-sei=Irabu
en-aut-mei=Hitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KamedaHideto
en-aut-sei=Kameda
en-aut-mei=Hideto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KanekoYuko
en-aut-sei=Kaneko
en-aut-mei=Yuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KuboHiroshi
en-aut-sei=Kubo
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=MitsunagaKanako
en-aut-sei=Mitsunaga
en-aut-mei=Kanako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=MoriMasaaki
en-aut-sei=Mori
en-aut-mei=Masaaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=NakajimaAyako
en-aut-sei=Nakajima
en-aut-mei=Ayako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=NishimuraKenichi
en-aut-sei=Nishimura
en-aut-mei=Kenichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=OhkuboNaoaki
en-aut-sei=Ohkubo
en-aut-mei=Naoaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=SatoTomomi
en-aut-sei=Sato
en-aut-mei=Tomomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=SugitaYuko
en-aut-sei=Sugita
en-aut-mei=Yuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=TakanashiSatoshi
en-aut-sei=Takanashi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=TanakaTakayuki
en-aut-sei=Tanaka
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=UmebayashiHiroaki
en-aut-sei=Umebayashi
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=YashiroMasato
en-aut-sei=Yashiro
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

en-aut-name=YamanishiShingo
en-aut-sei=Yamanishi
en-aut-mei=Shingo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=21
ORCID=

en-aut-name=FusamaMie
en-aut-sei=Fusama
en-aut-mei=Mie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=22
ORCID=

en-aut-name=HirataShintaro
en-aut-sei=Hirata
en-aut-mei=Shintaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=23
ORCID=

en-aut-name=KishimotoMitsumasa
en-aut-sei=Kishimoto
en-aut-mei=Mitsumasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=24
ORCID=

en-aut-name=KohnoMasataka
en-aut-sei=Kohno
en-aut-mei=Masataka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=25
ORCID=

en-aut-name=KojimaMasayo
en-aut-sei=Kojima
en-aut-mei=Masayo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=26
ORCID=

en-aut-name=KojimaToshihisa
en-aut-sei=Kojima
en-aut-mei=Toshihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=27
ORCID=

en-aut-name=MorinobuAkio
en-aut-sei=Morinobu
en-aut-mei=Akio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=28
ORCID=

en-aut-name=SugiharaTakahiko
en-aut-sei=Sugihara
en-aut-mei=Takahiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=29
ORCID=

en-aut-name=TanakaEiichi
en-aut-sei=Tanaka
en-aut-mei=Eiichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=30
ORCID=

en-aut-name=YajimaNobuyuki
en-aut-sei=Yajima
en-aut-mei=Nobuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=31
ORCID=

en-aut-name=YanaiRyo
en-aut-sei=Yanai
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=32
ORCID=

en-aut-name=KawahitoYutaka
en-aut-sei=Kawahito
en-aut-mei=Yutaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=33
ORCID=

en-aut-name=HarigaiMasayoshi
en-aut-sei=Harigai
en-aut-mei=Masayoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=34
ORCID=

affil-num=1
en-affil=Department of Pediatric Rheumatology, Institute of Rheumatology, Tokyo Women’s Medical University Hospital
kn-affil=

affil-num=2
en-affil=Department of Pediatrics, Osaka Rosai Hospital, Japan Organization of Occupational Health and Safety
kn-affil=

affil-num=3
en-affil=Department of General Medical Science, Graduate School of Medicine, Chiba University
kn-affil=

affil-num=4
en-affil=Department of Pediatrics, Kagoshima Prefectural Satsunan Hospital
kn-affil=

affil-num=5
en-affil=Department of Pediatrics, Kitasato University
kn-affil=

affil-num=6
en-affil=Department of Pediatrics and Development Biology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University
kn-affil=

affil-num=7
en-affil=Division of Rheumatology, Department of Internal Medicine, Toho University
kn-affil=

affil-num=8
en-affil=Division of Rheumatology, Department of Internal Medicine, Keio University School of Medicine
kn-affil=

affil-num=9
en-affil=Department of Pediatrics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine
kn-affil=

affil-num=10
en-affil=Department of Allergy and Rheumatology, Chiba Children's Hospital
kn-affil=

affil-num=11
en-affil=Department of Lifetime Clinical Immunology, Tokyo Medical and Dental University
kn-affil=

affil-num=12
en-affil=Center for Rheumatic Diseases, Mie University Hospital
kn-affil=

affil-num=13
en-affil=Department of Pediatrics, Yokohama City University Graduate School of Medicine
kn-affil=

affil-num=14
en-affil=Iizuka Hospital
kn-affil=

affil-num=15
en-affil=Clinical Education Center For Physicians, Shiga University of Medical Science
kn-affil=

affil-num=16
en-affil=Department of Pediatrics, School of Medicine, Osaka Medical and Pharmaceutical University
kn-affil=

affil-num=17
en-affil=Division of Rheumatology, Department of Internal Medicine, Keio University School of Medicine
kn-affil=

affil-num=18
en-affil=Department of Pediatrics, Japanese Red Cross Otsu Hospital
kn-affil=

affil-num=19
en-affil=Department of Rheumatology and Infectious Diseases, Miyagi Children’s Hospital
kn-affil=

affil-num=20
en-affil=Department of Pediatrics, Okayama University Hospital
kn-affil=

affil-num=21
en-affil=Department of Pediatrics, Nippon Medical School
kn-affil=

affil-num=22
en-affil=Health Sciences Department of Nursing, Kansai University of International Studies
kn-affil=

affil-num=23
en-affil=Department of Clinical Immunology and Rheumatology, Hiroshima University Hospital
kn-affil=

affil-num=24
en-affil=Department of Nephrology and Rheumatology, Kyorin University School of Medicine
kn-affil=

affil-num=25
en-affil=Inflammation and Immunology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine
kn-affil=

affil-num=26
en-affil=Graduate School of Medical Sciences, Nagoya City University
kn-affil=

affil-num=27
en-affil=Department of Orthopedic Surgery, National Hospital Organization Nagoya Medical Center
kn-affil=

affil-num=28
en-affil=Department of Rheumatology and Clinical Immunology, Graduate School of Medicine, Kyoto University
kn-affil=

affil-num=29
en-affil=Division of Rheumatology, Department of Internal Medicine, Toho University School of Medicine
kn-affil=

affil-num=30
en-affil=Division of Rheumatology, Department of Internal Medicine, School of Medicine, Tokyo Women's Medical University
kn-affil=

affil-num=31
en-affil=Division of Rheumatology, Department of Medicine, Showa University School of Medicine
kn-affil=

affil-num=32
en-affil=Division of Rheumatology, Department of Medicine, Showa University School of Medicine
kn-affil=

affil-num=33
en-affil=Inflammation and Immunology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine
kn-affil=

affil-num=34
en-affil=Division of Rheumatology, Department of Internal Medicine, School of Medicine, Tokyo Women's Medical University
kn-affil=
en-keyword=Clinical practice guidelines
kn-keyword=Clinical practice guidelines
en-keyword=baricitinib
kn-keyword=baricitinib
en-keyword=GRADE (Grading of Recommendations, Assessment, Development, and Evaluation)
kn-keyword=GRADE (Grading of Recommendations, Assessment, Development, and Evaluation)
en-keyword=juvenile idiopathic arthritis
kn-keyword=juvenile idiopathic arthritis
en-keyword=systematic review
kn-keyword=systematic review
END

start-ver=1.4
cd-journal=joma
no-vol=6
cd-vols=
no-issue=S1
article-no=
start-page=7
end-page=12
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202504
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Basic biology is not just “for the birds”: how avian studies have informed us about vertebrate reproduction
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Avian reproductive physiology has been studied for centuries, largely because of the importance of birds as food animals. It is likely that the ubiquity and ease of access to domesticated chickens led to them being used in some of the first experiments on transplantation of endocrine structures—in this case, the testes. Since then, study of seasonal changes in reproductive physiology (photoperiodism) in different orders of bird species has led to advances in the understanding of endocrine regulation of reproductive physiology and behavior. These include mechanisms of adult neuroplasticity, sexual selection, sperm competition, stress physiology, and circadian physiology. Here, we focus mainly on the discovery in birds of a neuropeptide named gonadotropin-inhibitory hormone that mostly has inhibitory effects on reproduction. This hormone has since been shown to exist in all mammals studied to date, including humans (it is known as RFamide-related peptide in mammals). We discuss the history and implications of avian studies on gonadotropin-inhibitory hormone/RFamide-related peptide for human reproductive biology.
en-copyright=
kn-copyright=

en-aut-name=BentleyGeorge E.
en-aut-sei=Bentley
en-aut-mei=George E.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=AizawaSayaka
en-aut-sei=Aizawa
en-aut-mei=Sayaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

affil-num=1
en-affil=Department of Integrative Biology and Helen Wills Neuroscience Institute, University of California at Berkeley
kn-affil=

affil-num=2
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=
en-keyword=GnRH
kn-keyword=GnRH
en-keyword=GnIH
kn-keyword=GnIH
en-keyword=RFamide
kn-keyword=RFamide
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=1
article-no=
start-page=7661
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240916
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Neurotransmitter recognition by human vesicular monoamine transporter 2
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Human vesicular monoamine transporter 2 (VMAT2), a member of the SLC18 family, plays a crucial role in regulating neurotransmitters in the brain by facilitating their uptake and storage within vesicles, preparing them for exocytotic release. Because of its central role in neurotransmitter signalling and neuroprotection, VMAT2 is a target for neurodegenerative diseases and movement disorders, with its inhibitor being used as therapeutics. Despite the importance of VMAT2 in pharmacophysiology, the molecular basis of VMAT2-mediated neurotransmitter transport and its inhibition remains unclear. Here we show the cryo-electron microscopy structure of VMAT2 in the substrate-free state, in complex with the neurotransmitter dopamine, and in complex with the inhibitor tetrabenazine. In addition to these structural determinations, monoamine uptake assays, mutational studies, and pKa value predictions were performed to characterize the dynamic changes in VMAT2 structure. These results provide a structural basis for understanding VMAT2-mediated vesicular transport of neurotransmitters and a platform for modulation of current inhibitor design.
en-copyright=
kn-copyright=

en-aut-name=ImDohyun
en-aut-sei=Im
en-aut-mei=Dohyun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=JormakkaMika
en-aut-sei=Jormakka
en-aut-mei=Mika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=JugeNarinobu
en-aut-sei=Juge
en-aut-mei=Narinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KishikawaJun-ichi
en-aut-sei=Kishikawa
en-aut-mei=Jun-ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KatoTakayuki
en-aut-sei=Kato
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SugitaYukihiko
en-aut-sei=Sugita
en-aut-mei=Yukihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NodaTakeshi
en-aut-sei=Noda
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=UemuraTomoko
en-aut-sei=Uemura
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=ShiimuraYuki
en-aut-sei=Shiimura
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=MiyajiTakaaki
en-aut-sei=Miyaji
en-aut-mei=Takaaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=AsadaHidetsugu
en-aut-sei=Asada
en-aut-mei=Hidetsugu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=IwataSo
en-aut-sei=Iwata
en-aut-mei=So
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

affil-num=1
en-affil=Department of Cell Biology, Graduate School of Medicine, Kyoto University
kn-affil=

affil-num=2
en-affil=Department of Cell Biology, Graduate School of Medicine, Kyoto University
kn-affil=

affil-num=3
en-affil=Department of Genomics and Proteomics, Advanced Science Research Center, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Applied Biology, Kyoto Institute of Technology
kn-affil=

affil-num=5
en-affil=Institute for Protein Research, Osaka University
kn-affil=

affil-num=6
en-affil=Laboratory of Ultrastructural Virology, Institute for Life and Medical Sciences, Kyoto University
kn-affil=

affil-num=7
en-affil=Laboratory of Ultrastructural Virology, Institute for Life and Medical Sciences, Kyoto University
kn-affil=

affil-num=8
en-affil=Department of Cell Biology, Graduate School of Medicine, Kyoto University
kn-affil=

affil-num=9
en-affil=Department of Cell Biology, Graduate School of Medicine, Kyoto University
kn-affil=

affil-num=10
en-affil=Department of Genomics and Proteomics, Advanced Science Research Center, Okayama University
kn-affil=

affil-num=11
en-affil=Department of Cell Biology, Graduate School of Medicine, Kyoto University
kn-affil=

affil-num=12
en-affil=Department of Cell Biology, Graduate School of Medicine, Kyoto University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=32
cd-vols=
no-issue=4
article-no=
start-page=630
end-page=637
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250526
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Immediate breast reconstruction surgery for breast cancer: current status and future directions
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background Immediate breast reconstruction (IBR) has become increasingly recognized in Japan as an important component of breast cancer care, improving patients’ quality of life after mastectomy. While the adoption of IBR is growing, the reconstruction rate in Japan remains lower than in Western countries. To clarify the current practice and challenges, the Japanese Breast Cancer Society (JBCS) conducted a nationwide survey.<br>
Methods We conducted a comprehensive web-based questionnaire survey among all JBCS-certified institutions between December 2020 and February 2021. The survey assessed institutional capabilities, surgical techniques, decision-making criteria for BR, and the integration of adjuvant therapy.<br>
Results A total of 429 institutions responded, with 72.5% offering BR and 61.7% capable of providing immediate reconstruction. Nipple-sparing mastectomy (NSM) was performed at 73.7% of institutions offering reconstruction. Multidisciplinary conferences with plastic surgeons were held at 70.5% of institutions. Approximately 30% of institutions discontinued IBR if sentinel lymph node metastases were detected intraoperatively, and 62.8% avoided recommending IBR for patients likely to require postoperative radiation therapy. In 94% of institutions, BR did not cause delays in the administration of adjuvant chemotherapy. However, 15% of institutions modified their radiation therapy approach in reconstructed patients. Additionally, 27% of physicians still believed that BR could negatively affect prognosis.<br>
Conclusions The survey confirmed that IBR is widely performed and feasible in Japan. However, institutional differences, limited access to plastic surgeons, and persistent misconceptions remain significant barriers. Strengthening multidisciplinary collaboration and establishing standardized guidelines will help improve BR rates and patient outcomes in Japan.
en-copyright=
kn-copyright=

en-aut-name=ShienTadahiko
en-aut-sei=Shien
en-aut-mei=Tadahiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NogiHiroko
en-aut-sei=Nogi
en-aut-mei=Hiroko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OgiyaAkiko
en-aut-sei=Ogiya
en-aut-mei=Akiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=IshitobiMakoto
en-aut-sei=Ishitobi
en-aut-mei=Makoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YamauchiChikako
en-aut-sei=Yamauchi
en-aut-mei=Chikako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ShimoAyaka
en-aut-sei=Shimo
en-aut-mei=Ayaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NaruiKazutaka
en-aut-sei=Narui
en-aut-mei=Kazutaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NaguraNaomi
en-aut-sei=Nagura
en-aut-mei=Naomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=SekiHirohito
en-aut-sei=Seki
en-aut-mei=Hirohito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=TerataKaori
en-aut-sei=Terata
en-aut-mei=Kaori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=SaigaMiho
en-aut-sei=Saiga
en-aut-mei=Miho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=UchidaTatsuya
en-aut-sei=Uchida
en-aut-mei=Tatsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=SasadaShinsuke
en-aut-sei=Sasada
en-aut-mei=Shinsuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=SakuraiTeruhisa
en-aut-sei=Sakurai
en-aut-mei=Teruhisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=NiikuraNaoki
en-aut-sei=Niikura
en-aut-mei=Naoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=MoriHiroki
en-aut-sei=Mori
en-aut-mei=Hiroki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

affil-num=1
en-affil=Department of Breast and Endocrine Surgery, Okayama University Hospital
kn-affil=

affil-num=2
en-affil=Department of Breast and Endocrine Surgery, The Jikei University School of Medicine
kn-affil=

affil-num=3
en-affil=Department of Breast Surgery, Japanese Red Cross Medical Center
kn-affil=

affil-num=4
en-affil=Department of Breast Surgery, Mie University School of Medicine
kn-affil=

affil-num=5
en-affil=Department of Radiation Oncology, Shiga General Hospital
kn-affil=

affil-num=6
en-affil=Department of Breast and Endocrine Surgery, St. Marianna University School of Medicine
kn-affil=

affil-num=7
en-affil=Department of Breast and Thyroid Surgery, Medical Center, Yokohama City University
kn-affil=

affil-num=8
en-affil=Department of Breast Surgical Oncology, St Luke’s International Hospital
kn-affil=

affil-num=9
en-affil=Department of Breast Surgery, Kyorin University School of Medicine
kn-affil=

affil-num=10
en-affil=Department of Breast and Endocrine Surgery, Akita University Hospital
kn-affil=

affil-num=11
en-affil=Department of Plastic Surgery, Okayama University Hospital
kn-affil=

affil-num=12
en-affil=Department of Plastic Surgery, Okayama University Hospital
kn-affil=

affil-num=13
en-affil=Department of Surgical Oncology, Research Institute for Radiation Biology and Medicine, Hiroshima University
kn-affil=

affil-num=14
en-affil=Sakurai Breast Clinic
kn-affil=

affil-num=15
en-affil=Department of Breast Oncology, Tokai University School of Medicine
kn-affil=

affil-num=16
en-affil=Department of Plastic and Reconstructive Surgery, Tokyo Medical and Dental University
kn-affil=
en-keyword=Breast cancer
kn-keyword=Breast cancer
en-keyword=Immediate reconstruction surgery
kn-keyword=Immediate reconstruction surgery
en-keyword=Prognosis
kn-keyword=Prognosis
en-keyword=Complications
kn-keyword=Complications
END

start-ver=1.4
cd-journal=joma
no-vol=12
cd-vols=
no-issue=1
article-no=
start-page=e003250
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202501
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Clinical impact of combined assessment of myocardial inflammation and fibrosis using myocardial biopsy in patients with dilated cardiomyopathy: a multicentre, retrospective cohort study
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background Among patients with dilated cardiomyopathy (DCM), myocardial inflammation and fibrosis are risk factors for poor clinical outcomes. Here, we investigated the combined prognostic value of these two factors, as evaluated using myocardial biopsy samples.<br>
Methods This retrospective and multicentre study included patients with DCM—defined as LVEF of ≤45% and left diastolic diameter of >112% of predicted value, without evidence of secondary or ischaemic cardiomyopathy. In myocardial biopsy samples, inflammatory cells were counted using immunohistochemistry, and Masson’s Trichrome staining was performed to quantify the myocardial fibrosis as collagen area fraction (CAF). Higher myocardial inflammation was defined as leucocytes of ≥14/mm², including ≤4 monocytes/mm², with CD3+ T lymphocytes of≥7/mm². Greater myocardial fibrosis was defined as CAF of>5.9% by the Youden’s index. The primary endpoint was cardiac death or left ventricular assist device implantation.<br>
Results A total of 255 DCM patients were enrolled (average age, 53.1 years; 78% males). Within this cohort, the mean LVEF was 28.0%, mean CAF was 10.7% and median CD3+ cell count was 8.3/mm2. During the median follow-up period of 2688 days, 46 patients met the primary endpoint. Multivariable Cox proportional hazard analyses revealed that CD3+ cell count and CAF were independent determinants of the primary endpoint. Kaplan–Meier analysis showed that patients with both higher myocardial inflammation and greater fibrosis had the worst prognosis (log-rank p<0.001). When myocardial inflammation was graded as one of three degrees: T lymphocytes of <13/mm² (low); 13 of 13.1–23.9/mm² (moderate); and T lymphocytes of ≥24 /mm² (high), patients with moderate inflammation exhibited a superior survival rate when CAF was ≤5.9%, but a worse survival rate when CAF was >5.9%.<br>
Conclusions Having both biopsy-proven higher myocardial inflammation and greater fibrosis predicted the worst clinical prognosis in patients with DCM.
en-copyright=
kn-copyright=

en-aut-name=NakayamaTakafumi
en-aut-sei=Nakayama
en-aut-mei=Takafumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OgoKeiko Ohta
en-aut-sei=Ogo
en-aut-mei=Keiko Ohta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SuganoYasuo
en-aut-sei=Sugano
en-aut-mei=Yasuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YokokawaTetsuro
en-aut-sei=Yokokawa
en-aut-mei=Tetsuro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KanamoriHiromitsu
en-aut-sei=Kanamori
en-aut-mei=Hiromitsu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=IkedaYoshihiko
en-aut-sei=Ikeda
en-aut-mei=Yoshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=HiroeMichiaki
en-aut-sei=Hiroe
en-aut-mei=Michiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=HatakeyamaKinta
en-aut-sei=Hatakeyama
en-aut-mei=Kinta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=Ishibashi-UedaHatsue
en-aut-sei=Ishibashi-Ueda
en-aut-mei=Hatsue
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=DohiKaoru
en-aut-sei=Dohi
en-aut-mei=Kaoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=AnzaiToshihisa
en-aut-sei=Anzai
en-aut-mei=Toshihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=SeoYoshihiro
en-aut-sei=Seo
en-aut-mei=Yoshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=Imanaka-YoshidaKyoko
en-aut-sei=Imanaka-Yoshida
en-aut-mei=Kyoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

affil-num=1
en-affil=Department of Cardiology, Nagoya City University Graduate School of Medical Sciences
kn-affil=

affil-num=2
en-affil=Department of Pathology, National Cerebral and Cardiovascular Center
kn-affil=

affil-num=3
en-affil=Department of Cardiology, Keiyu Hospital
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Fukushima Medical University
kn-affil=

affil-num=5
en-affil=Department of Cardiology, Gifu University Graduate School of Medicine
kn-affil=

affil-num=6
en-affil=Department of Pathology, National Cerebral and Cardiovascular Center
kn-affil=

affil-num=7
en-affil=Department of Cardiology, National Center for Global Health and Medicine
kn-affil=

affil-num=8
en-affil=Department of Pathology, National Cerebral and Cardiovascular Center
kn-affil=

affil-num=9
en-affil=Department of Pathology, National Cerebral and Cardiovascular Center
kn-affil=

affil-num=10
en-affil=Center for Advanced Heart Failure, Okayama University Hospital
kn-affil=

affil-num=11
en-affil=Department of Cardiology and Nephrology, Mie University Graduate School of Medicine
kn-affil=

affil-num=12
en-affil=Department of Cardiovascular Medicine, Hokkaido University Graduate School of Medicine
kn-affil=

affil-num=13
en-affil=Department of Cardiology, Nagoya City University Graduate School of Medical Sciences
kn-affil=

affil-num=14
en-affil=Department of Pathology and Matrix Biology, Mie University Graduate School of Medicine
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=156
cd-vols=
no-issue=2
article-no=
start-page=151
end-page=159.e1
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202502
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The greater palatine nerve and artery both supply the maxillary teeth
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background. It is generally accepted that the greater palatine nerve and artery supply the palatal mucosa, gingiva, and glands, but not the bone or tooth adjacent to those tissues. When the bony palate is observed closely, multiple small foramina are seen on the palatal surface of the alveolar process. The authors hypothesized that the greater palatine nerve and artery might supply the maxillary teeth via the foramina on the palatal surface of the alveolar process and the superior alveolar nerve and artery. The authors aimed to investigate the palatal innervation and blood supply of the maxillary teeth.<br>
Methods. Eight cadaveric maxillae containing most teeth or alveolar sockets were selected. The mean age at the time of death was 82.4 years. The samples were examined with colored water injection, latex injection, microcomputed tomography with contrast dye, gross anatomic dissection, and histologic observation.<br>
Results. Through both injection studies and microcomputed tomographic analysis, the authors found that the small foramina on and around the greater palatine groove connected to the alveolar process and tooth sockets. The small foramina in the greater palatine and incisive canal also continued inside the alveolar process and the tooth sockets.<br>
Conclusions. The alveolar branches of the greater palatine nerve and artery as well as the nasopalatine nerve and sphenopalatine artery supply maxillary teeth, alveolar bone, and periodontal tissue via the palatal alveolar foramina with superior alveolar nerves and arteries.<br>
Practical Implications. This knowledge is essential for dentists when administering local anesthetic to the maxillary teeth and performing an osteotomy. Anatomic and dental textbooks should be updated with this new knowledge for better patient care.
en-copyright=
kn-copyright=

en-aut-name=IwanagaJoe
en-aut-sei=Iwanaga
en-aut-mei=Joe
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakeshitaYohei
en-aut-sei=Takeshita
en-aut-mei=Yohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=AnbalaganMuralidharan
en-aut-sei=Anbalagan
en-aut-mei=Muralidharan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ZouBinghao
en-aut-sei=Zou
en-aut-mei=Binghao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ToriumiTaku
en-aut-sei=Toriumi
en-aut-mei=Taku
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KunisadaYuki
en-aut-sei=Kunisada
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=IbaragiSoichiro
en-aut-sei=Ibaragi
en-aut-mei=Soichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TubbsR. Shane
en-aut-sei=Tubbs
en-aut-mei=R. Shane
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Division of Gross and Clinical Anatomy, Department of Anatomy, School of Medicine, Kurume University
kn-affil=

affil-num=2
en-affil=Department of Oral and Maxillofacial Radiology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Structural and Cellular Biology, School of Medicine, Tulane University
kn-affil=

affil-num=4
en-affil=Department of Structural and Cellular Biology, School of Medicine, Tulane University
kn-affil=

affil-num=5
en-affil=Department of Anatomy, School of Life Dentistry at Niigata, The Nippon Dental University
kn-affil=

affil-num=6
en-affil=Department of Oral and Maxillofacial Surgery, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Oral and Maxillofacial Surgery, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=University of Queensland
kn-affil=
en-keyword=Maxillary teeth
kn-keyword=Maxillary teeth
en-keyword=dental pulp
kn-keyword=dental pulp
en-keyword=anatomy
kn-keyword=anatomy
en-keyword=nerve block
kn-keyword=nerve block
en-keyword=root canal treatment
kn-keyword=root canal treatment
en-keyword=cadaver
kn-keyword=cadaver
END

start-ver=1.4
cd-journal=joma
no-vol=60
cd-vols=
no-issue=10
article-no=
start-page=1151
end-page=1159
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202412
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=NCF-1 plays a pivotal role in the survival of adenocarcinoma cells of pancreatic and gastric origins
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Reactive oxygen species (ROS) play a pivotal biological role in cells, with ROS function differing depending on cellular conditions and the extracellular environment. Notably, ROS act as cytotoxic factors to eliminate infectious pathogens or promote cell death under cellular stress, while also facilitating cell growth (via ROS-sensing pathways) by modifying gene expression. Among ROS-related genes, neutrophil cytosolic factor-1 (NCF-1; p47phox) was identified as a ROS generator in neutrophils. This product is a subunit of a cytosolic NADPH oxidase complex activated in response to pathogens such as bacteria and viruses. NCF-1 has been examined primarily in terms of ROS-production pathways in macrophages and neutrophils; however, the expression of this protein and its biological role in cancer cells remain unclear. Here, we report expression of NCF-1 in pancreatic and gastric cancers, and demonstrate its biological significance in these tumor cells. Abundant expression of NCF-1 was observed in pancreatic adenocarcinoma (PDAC) lines and in patient tissues, as well as in gastric adenocarcinomas. Accumulation of the protein was also detected in the invasive/metastatic foci of these tumors. Unexpectedly, BxPC-3 underwent apoptotic cell death when transfected with a small interfering RNA (siRNA) specific to NCF-1, whereas the cells treated with a control siRNA proliferated in a time-dependent manner. A similar phenomenon was observed in HSC-58, a poorly differentiated gastric adenocarcinoma line. Consequently, the tumor cells highly expressing NCF-1 obtained coincident accumulation of ROS and reduced glutathione (GSH) with expression of glutathione peroxidase 4 (GPX4), a quencher involved in ferroptosis. Unlike the conventional role of ROS as a representative cytotoxic factor, these findings suggest that NCF-1-mediated ROS generation may be required for expansive growth of PDAC and gastric cancers.
en-copyright=
kn-copyright=

en-aut-name=Furuya-IkudeChiemi
en-aut-sei=Furuya-Ikude
en-aut-mei=Chiemi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KittaAkane
en-aut-sei=Kitta
en-aut-mei=Akane
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TomonobuNaoko
en-aut-sei=Tomonobu
en-aut-mei=Naoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KawasakiYoshihiro
en-aut-sei=Kawasaki
en-aut-mei=Yoshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SakaguchiMasakiyo
en-aut-sei=Sakaguchi
en-aut-mei=Masakiyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KondoEisaku
en-aut-sei=Kondo
en-aut-mei=Eisaku
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Division of Tumor Pathology, NIR-PIT Research Institute, Kansai Medical University
kn-affil=

affil-num=2
en-affil=Division of Tumor Pathology, NIR-PIT Research Institute, Kansai Medical University
kn-affil=

affil-num=3
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Division of Tumor Pathology, NIR-PIT Research Institute, Kansai Medical University
kn-affil=

affil-num=5
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Division of Tumor Pathology, NIR-PIT Research Institute, Kansai Medical University
kn-affil=
en-keyword=NCF-1 (p47phox)
kn-keyword=NCF-1 (p47phox)
en-keyword=ROS
kn-keyword=ROS
en-keyword=Cancer
kn-keyword=Cancer
en-keyword=Tumor growth
kn-keyword=Tumor growth
en-keyword=Apoptosis
kn-keyword=Apoptosis
END

start-ver=1.4
cd-journal=joma
no-vol=25
cd-vols=
no-issue=1
article-no=
start-page=1094
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250704
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A cross-sectional interventional study on the effects of periodontal treatment on periodontal inflamed surface area and masticatory efficiency values according to the 2018 periodontal status classification
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background Periodontal inflamed surface area (PISA) and masticatory efficiency have been used to evaluate the relationship between systemic diseases and oral diseases. However, clear standards for PISA values and masticatory efficiency in relation to the severity of periodontitis are lacking. This study aims to evaluate PISA values and masticatory efficiency based on the 2018 periodontal status classification system.<br>
Methods In total, 153 healthy participants diagnosed with periodontitis were included in the study. The diagnosis was based on the 2018 periodontal status classification. PISA values and masticatory efficiency were measured at baseline and after initial periodontal therapy.<br>
Results PISA demonstrated a higher area under the curve for Stage III (0.815) and Grade B (0.85). At baseline, PISA was showed significant negative correlation with masticatory efficiency (B coefficient [95% CI]: -0.02 [-0.03, -0.006], p < 0.01). Following periodontal therapy, both PISA values and masticatory efficiency showed significant improvements, with median PISA values changing from 856 at baseline to 277.5 after treatment, and mean masticatory efficiency increasing from 153.3 to 166.9. After initial periodontal therapy, PISA values were significantly higher in patients classified as Stage IV and Grade C compared to those with other stages and grades. Age exhibited a significant negative correlation with changes in PISA (B coefficient [95%CI]: -11.8 [-20.3, -3.19]), and change in PISA value was significantly positively related to the increase in masticatory efficiency (B coefficient [95%CI], 0.02 [(0.0002, 0.03]). In patients with periodontitis, changes in periodontitis classification were associated with increased PISA values and decreased masticatory efficiency.<br>
Conclusion Periodontal therapy improved PISA and masticatory efficiency values. However, the extent of improvement was less pronounced in patients with higher stages and grades of periodontitis. It is essential to consider the interplay between increased PISA and decreased masticatory efficiency when treating patients with severe periodontitis.
en-copyright=
kn-copyright=

en-aut-name=MatsudaShinji
en-aut-sei=Matsuda
en-aut-mei=Shinji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YumotoHiromichi
en-aut-sei=Yumoto
en-aut-mei=Hiromichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KomatsuYasutaka
en-aut-sei=Komatsu
en-aut-mei=Yasutaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=DewakeNanae
en-aut-sei=Dewake
en-aut-mei=Nanae
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=IwataTakanori
en-aut-sei=Iwata
en-aut-mei=Takanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NaganoTakatoshi
en-aut-sei=Nagano
en-aut-mei=Takatoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MorozumiToshiya
en-aut-sei=Morozumi
en-aut-mei=Toshiya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=GotoRyoma
en-aut-sei=Goto
en-aut-mei=Ryoma
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KatoSatsuki
en-aut-sei=Kato
en-aut-mei=Satsuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=YamashitaMotozo
en-aut-sei=Yamashita
en-aut-mei=Motozo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=HayashiJoichiro
en-aut-sei=Hayashi
en-aut-mei=Joichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=SekinoSatoshi
en-aut-sei=Sekino
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=YamashitaAkiko
en-aut-sei=Yamashita
en-aut-mei=Akiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=YamashitaKeiko
en-aut-sei=Yamashita
en-aut-mei=Keiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=YoshimuraAtsutoshi
en-aut-sei=Yoshimura
en-aut-mei=Atsutoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=SugayaTsutomu
en-aut-sei=Sugaya
en-aut-mei=Tsutomu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=TakashibaShogo
en-aut-sei=Takashiba
en-aut-mei=Shogo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=TaguchiYoichiro
en-aut-sei=Taguchi
en-aut-mei=Yoichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=NemotoEiji
en-aut-sei=Nemoto
en-aut-mei=Eiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=ShintaniTomoaki
en-aut-sei=Shintani
en-aut-mei=Tomoaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

en-aut-name=MiyagawaTsuyoshi
en-aut-sei=Miyagawa
en-aut-mei=Tsuyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=21
ORCID=

en-aut-name=NishiHiromi
en-aut-sei=Nishi
en-aut-mei=Hiromi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=22
ORCID=

en-aut-name=MizunoNoriyoshi
en-aut-sei=Mizuno
en-aut-mei=Noriyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=23
ORCID=

en-aut-name=NumabeYukihiro
en-aut-sei=Numabe
en-aut-mei=Yukihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=24
ORCID=

en-aut-name=KawaguchiHiroyuki
en-aut-sei=Kawaguchi
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=25
ORCID=

affil-num=1
en-affil=Department of Periodontal Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University
kn-affil=

affil-num=2
en-affil=Department of Periodontology and Endodontology, Institute of Biomedical Sciences, Tokushima University Graduate School
kn-affil=

affil-num=3
en-affil=Periodontal Clinic, Medical and Dental Hospital, Niigata University
kn-affil=

affil-num=4
en-affil=Department of Operative Dentistry, Endodontology and Periodontology, School of Dentistry, Matsumoto Dental University
kn-affil=

affil-num=5
en-affil=Department of Periodontology, Tokyo Medical and Dental University
kn-affil=

affil-num=6
en-affil=Department of Periodontology, Tsurumi University School of Dental Medicine
kn-affil=

affil-num=7
en-affil=Department of Periodontology, Faculty of Dentistry, Kanagawa Dental University
kn-affil=

affil-num=8
en-affil=Department of Periodontology, School of Dentistry, Aichi Gakuin University
kn-affil=

affil-num=9
en-affil=School of Dentistry, Division of Periodontology and Endodontology, Department of Oral Rehabilitation, Health Sciences University of Hokkaido
kn-affil=

affil-num=10
en-affil=Department of Periodontology and Regenerative Dentistry, Osaka University Graduate School of Dentistry
kn-affil=

affil-num=11
en-affil=Division of Periodontology, Department of Oral Biology and Tissue Engineering, Meikai University School of Dentistry, Meikai University School of Dentistry
kn-affil=

affil-num=12
en-affil=School of Life Dentistry Department of Periodontology, The Nippon Dental University
kn-affil=

affil-num=13
en-affil=Section of Periodontology, Division of Oral Rehabilitation Faculty of Dental Science, Kyushu University
kn-affil=

affil-num=14
en-affil=Department of Periodontology, Tokyo Dental College
kn-affil=

affil-num=15
en-affil=Department of Periodontology and Endodontology, Nagasaki University Graduate School of Biomedical Sciences
kn-affil=

affil-num=16
en-affil=Department of Periodontology and Endodontology, Faculty of Dental Medicine, Hokkaido University
kn-affil=

affil-num=17
en-affil=Department of Pathophysiology-Periodontal Science, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=18
en-affil=Faculty of Dentistry, Department of Periodontology, Osaka Dental University
kn-affil=

affil-num=19
en-affil=Department of Periodontology and Endodontology, Tohoku University Graduate School of Dentistry
kn-affil=

affil-num=20
en-affil=Center of Oral Clinical Examination, Hiroshima University Hospital
kn-affil=

affil-num=21
en-affil=Clinical Research Center in Hiroshima, Hiroshima University Hospital
kn-affil=

affil-num=22
en-affil=Department of General Dentistry, Hiroshima University Hospital,
kn-affil=

affil-num=23
en-affil=Department of Periodontal Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University
kn-affil=

affil-num=24
en-affil=Department of Periodontology, Tokyo Dental College
kn-affil=

affil-num=25
en-affil=Department of General Dentistry, Hiroshima University Hospital,
kn-affil=
en-keyword=Periodontal diseases
kn-keyword=Periodontal diseases
en-keyword=Masticatory system
kn-keyword=Masticatory system
en-keyword=Nonsurgical periodontal debridement
kn-keyword=Nonsurgical periodontal debridement
END

start-ver=1.4
cd-journal=joma
no-vol=104
cd-vols=
no-issue=2
article-no=
start-page=151495
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202506
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Tri-culture model of intestinal epithelial cell, macrophage, and bacteria for the triggering of inflammatory bowel disease on a microfluidic device
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Inflammatory bowel disease (IBD) involves gastrointestinal inflammation, due to intestinal epithelial barrier destruction caused by excessive immune activation. Conventional cell culture systems do not provide a model system that can recapitulate the complex interactions between epithelial cells, immune cells, and intestinal bacteria. To address this, we developed a microfluidic device that mimics the inflammatory response associated with microbial invasion of the intestinal mucosa. The device consisted of two media channels, an upper and a lower channel, and a porous membrane between these channels on which C2BBe1 intestinal epithelial cells were seeded to form a tight junction layer. Each electrode was placed in contact with both channels to continuously monitor the tight junction state. Fresh medium flow allowed bacterial numbers to be controlled and bacterial toxins to be removed, allowing co-culture of mammalian cells and bacteria. In addition, RAW264 macrophage cells were attached to the bottom of the lower channel. By introducing E. coli into the lower channel, the RAW264 cells were activated and produced TNF-α, successfully recapitulating a culture model of inflammation in which the C2BBe1cell tight junction layer was destroyed. The main structure of the device was initially made of polydimethylsiloxane to facilitate its widespread use, but with a view to introducing anaerobic bacteria in the future, a similar phenomenon was successfully reproduced using polystyrene. When TPCA-1, an IκB kinase 2 inhibitor was added into this IBD culture model, the tight junction destruction was significantly suppressed. The results suggest that this IBD culture model also is useful as a screening system for anti-IBD drugs.
en-copyright=
kn-copyright=

en-aut-name=TamuraShiori
en-aut-sei=Tamura
en-aut-mei=Shiori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=PasangClarissa Ellice Talitha
en-aut-sei=Pasang
en-aut-mei=Clarissa Ellice Talitha
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TsudaMinami
en-aut-sei=Tsuda
en-aut-mei=Minami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MaShilan
en-aut-sei=Ma
en-aut-mei=Shilan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ShindoHiromasa
en-aut-sei=Shindo
en-aut-mei=Hiromasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NagaokaNoriyuki
en-aut-sei=Nagaoka
en-aut-mei=Noriyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=OhkuboTomoki
en-aut-sei=Ohkubo
en-aut-mei=Tomoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=FujiyamaYoichi
en-aut-sei=Fujiyama
en-aut-mei=Yoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TamaiMiho
en-aut-sei=Tamai
en-aut-mei=Miho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=TagawaYoh-ichi
en-aut-sei=Tagawa
en-aut-mei=Yoh-ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=School of Life Science and Technology, Institute of Science Tokyo
kn-affil=

affil-num=2
en-affil=School of Life Science and Technology, Tokyo Institute of Technology
kn-affil=

affil-num=3
en-affil=School of Life Science and Technology, Tokyo Institute of Technology
kn-affil=

affil-num=4
en-affil=School of Life Science and Technology, Institute of Science Tokyo
kn-affil=

affil-num=5
en-affil=School of Life Science and Technology, Tokyo Institute of Technology
kn-affil=

affil-num=6
en-affil=Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Biology-Chemistry Unit, Technology Research Laboratory, Shimadzu Corporation
kn-affil=

affil-num=8
en-affil=Biology-Chemistry Unit, Technology Research Laboratory, Shimadzu Corporation
kn-affil=

affil-num=9
en-affil=School of Life Science and Technology, Tokyo Institute of Technology
kn-affil=

affil-num=10
en-affil=School of Life Science and Technology, Institute of Science Tokyo
kn-affil=
en-keyword=Intestine chip
kn-keyword=Intestine chip
en-keyword=Inflammatory bowel disease
kn-keyword=Inflammatory bowel disease
en-keyword=Co-culture
kn-keyword=Co-culture
en-keyword=Tri-culture
kn-keyword=Tri-culture
en-keyword=Fluidic device
kn-keyword=Fluidic device
en-keyword=Disease model
kn-keyword=Disease model
en-keyword=Macrophage
kn-keyword=Macrophage
en-keyword=Inflammation
kn-keyword=Inflammation
END

start-ver=1.4
cd-journal=joma
no-vol=13
cd-vols=
no-issue=2
article-no=
start-page=159
end-page=161
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A novel de novo disease-causing variant in ATL1 in a pediatric patient with spastic paraplegia
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=NakamuraAyumi
en-aut-sei=Nakamura
en-aut-mei=Ayumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NaruseHiroya
en-aut-sei=Naruse
en-aut-mei=Hiroya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MitsutakeAkihiko
en-aut-sei=Mitsutake
en-aut-mei=Akihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MitsuiJun
en-aut-sei=Mitsui
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MorishitaShinichi
en-aut-sei=Morishita
en-aut-mei=Shinichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=IwakoshiMie
en-aut-sei=Iwakoshi
en-aut-mei=Mie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=IshiuraHiroyuki
en-aut-sei=Ishiura
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TsujiShoji
en-aut-sei=Tsuji
en-aut-mei=Shoji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TodaTatsushi
en-aut-sei=Toda
en-aut-mei=Tatsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=2
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=3
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=4
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=5
en-affil=Department of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo
kn-affil=

affil-num=6
en-affil=Department of Nursing, Faculty of Health Sciences, Kobe Tokiwa University
kn-affil=

affil-num=7
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Institute of Medical Genomics, International University of Health and Welfare
kn-affil=

affil-num=9
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=60
cd-vols=
no-issue=10
article-no=
start-page=1215
end-page=1227
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241121
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Enhanced design of pCMViR-TSC plasmid vector for sustainably high cargo gene expression in mammalian cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The first-generation pCMViR-TSC, implemented through the promoter sandwich rule, yields 10- to 100-fold higher gene expression than the standard plasmid used with the CMV (cytomegalovirus) or CAG promoter. However, the vector’s shortcomings limit its utility to transient expression only, as it is not suitable for establishing stable transformants in mammalian cells. To overcome this weakness, we here introduce the improved plasmid vector pSAKA-4B, derived from pCMViR-TSC as a second-generation chromosome-insertable vector. This vector facilitates the linear entry of the expression unit into the TTAA site of DNA universally with transposase assistance. The vector is helpful for the indefinite expression of our target gene. The new vector system is proven here to be efficient in establishing stable transformants with a high likelihood of positive clones that exhibit significantly elevated expression levels of the delivered foreign gene. This system, alongside the first-generation vector, is therefore instrumental for diverse basic research endeavors concerning genes, proteins, cells, and animals, and potentially for clinical applications such as gene therapy.
en-copyright=
kn-copyright=

en-aut-name=SakaguchiMasakiyo
en-aut-sei=Sakaguchi
en-aut-mei=Masakiyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KinoshitaRie
en-aut-sei=Kinoshita
en-aut-mei=Rie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TomonobuNahoko
en-aut-sei=Tomonobu
en-aut-mei=Nahoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SakaguchiYoshihiko
en-aut-sei=Sakaguchi
en-aut-mei=Yoshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=FutamiJunichiro
en-aut-sei=Futami
en-aut-mei=Junichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YamauchiAkira
en-aut-sei=Yamauchi
en-aut-mei=Akira
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MurataHitoshi
en-aut-sei=Murata
en-aut-mei=Hitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YamamotoKen-ichi
en-aut-sei=Yamamoto
en-aut-mei=Ken-ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TakahashiTetta
en-aut-sei=Takahashi
en-aut-mei=Tetta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=GoharaYuma
en-aut-sei=Gohara
en-aut-mei=Yuma
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=OchiToshiki
en-aut-sei=Ochi
en-aut-mei=Toshiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=JiangFan
en-aut-sei=Jiang
en-aut-mei=Fan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=KomalasariNi Luh Gede Yoni
en-aut-sei=Komalasari
en-aut-mei=Ni Luh Gede Yoni
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=ChenYouyi
en-aut-sei=Chen
en-aut-mei=Youyi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=RumaI Made Winarsa
en-aut-sei=Ruma
en-aut-mei=I Made Winarsa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=SumardikaI Wayan
en-aut-sei=Sumardika
en-aut-mei=I Wayan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=ZhouJin
en-aut-sei=Zhou
en-aut-mei=Jin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=HonjoTomoko
en-aut-sei=Honjo
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=KuribayashiFutoshi
en-aut-sei=Kuribayashi
en-aut-mei=Futoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=SagayamaKazumi
en-aut-sei=Sagayama
en-aut-mei=Kazumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

en-aut-name=ToyookaShinichi
en-aut-sei=Toyooka
en-aut-mei=Shinichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=21
ORCID=

en-aut-name=KondoEisaku
en-aut-sei=Kondo
en-aut-mei=Eisaku
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=22
ORCID=

en-aut-name=InoueYusuke
en-aut-sei=Inoue
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=23
ORCID=

affil-num=1
en-affil=Department of Cell Biology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=2
en-affil=Department of Cell Biology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=3
en-affil=Department of Cell Biology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=4
en-affil=Department of Microbiology, Tokushima Bunri University
kn-affil=

affil-num=5
en-affil=Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Biochemistry, Kawasaki Medical School
kn-affil=

affil-num=7
en-affil=Department of Cell Biology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=8
en-affil=Department of Cell Biology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=9
en-affil=Department of Cell Biology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=10
en-affil=Department of Cell Biology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=11
en-affil=Department of Cell Biology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=12
en-affil=Department of Cell Biology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=13
en-affil=Faculty of Medicine, Udayana University
kn-affil=

affil-num=14
en-affil=Department of Breast Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine
kn-affil=

affil-num=15
en-affil=Faculty of Medicine, Udayana University
kn-affil=

affil-num=16
en-affil=Faculty of Medicine, Udayana University
kn-affil=

affil-num=17
en-affil=Medical Oncology Department of Gastrointestinal Tumors, Liaoning Cancer Hospital & Institute, Cancer Hospital of the Dalian University of Technology
kn-affil=

affil-num=18
en-affil=Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=19
en-affil=Department of Biochemistry, Kawasaki Medical School
kn-affil=

affil-num=20
en-affil=Organization for Research and Innovation Strategy, Okayama University
kn-affil=

affil-num=21
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=22
en-affil=Division of Tumor Pathology, Near InfraRed Photo-Immuno-Therapy Research Institute, Kansai Medical University
kn-affil=

affil-num=23
en-affil=Faculty of Science and Technology, Division of Molecular Science, Gunma University
kn-affil=
en-keyword=Plasmid
kn-keyword=Plasmid
en-keyword=Gene engineering
kn-keyword=Gene engineering
en-keyword=Cancer
kn-keyword=Cancer
en-keyword=Cell culture
kn-keyword=Cell culture
END

start-ver=1.4
cd-journal=joma
no-vol=77
cd-vols=
no-issue=8
article-no=
start-page=522
end-page=532
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240625
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Synthesis and biochemical characterization of naphthoquinone derivatives targeting bacterial histidine kinases
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Waldiomycin is an inhibitor of histidine kinases (HKs). Although most HK inhibitors target the ATP-binding region, waldiomycin binds to the intracellular dimerization domain (DHp domain) with its naphthoquinone moiety presumed to interact with the conserved H-box region. To further develop inhibitors targeting the H-box, various 2-aminonaphthoquinones with cyclic, aliphatic, or aromatic amino groups and naphtho [2,3-d] isoxazole-4,9-diones were synthesized. These compounds were tested for their inhibitory activity (IC50) against WalK, an essential HK for Bacillus subtilis growth, and their minimum inhibitory concentrations (MIC) against B. subtilis. As a result, 11 novel HK inhibitors were obtained as naphthoquinone derivatives (IC50: 12.6–305 µM, MIC: 0.5–128 µg ml−1). The effect of representative compounds on the expression of WalK/WalR regulated genes in B. subtilis was investigated. Four naphthoquinone derivatives induced the expression of iseA (formerly yoeB), whose expression is negatively regulated by the WalK/WalR system. This suggests that these compounds inhibit WalK in B. subtilis cells, resulting in antibacterial activity. Affinity selection/mass spectrometry analysis was performed to identify whether these naphthoquinone derivatives interact with WalK in a manner similar to waldiomycin. Three compounds were found to competitively inhibit the binding of waldiomycin to WalK, suggesting that they bind to the H-box region conserved in HKs and inhibit HK activity.
en-copyright=
kn-copyright=

en-aut-name=IshikawaTeruhiko
en-aut-sei=Ishikawa
en-aut-mei=Teruhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=EguchiYoko
en-aut-sei=Eguchi
en-aut-mei=Yoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=IgarashiMasayuki
en-aut-sei=Igarashi
en-aut-mei=Masayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OkajimaToshihide
en-aut-sei=Okajima
en-aut-mei=Toshihide
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MitaKohei
en-aut-sei=Mita
en-aut-mei=Kohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YamasakiYuri
en-aut-sei=Yamasaki
en-aut-mei=Yuri
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SumikuraKaho
en-aut-sei=Sumikura
en-aut-mei=Kaho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=OkumuraTaisei
en-aut-sei=Okumura
en-aut-mei=Taisei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TabuchiYuna
en-aut-sei=Tabuchi
en-aut-mei=Yuna
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=HayashiChigusa
en-aut-sei=Hayashi
en-aut-mei=Chigusa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=PasquaMartina
en-aut-sei=Pasqua
en-aut-mei=Martina
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=ColucciaMarco
en-aut-sei=Coluccia
en-aut-mei=Marco
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=ProssedaGianni
en-aut-sei=Prosseda
en-aut-mei=Gianni
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=ColonnaBianca
en-aut-sei=Colonna
en-aut-mei=Bianca
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=KohayakawaChie
en-aut-sei=Kohayakawa
en-aut-mei=Chie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=TaniAkiyoshi
en-aut-sei=Tani
en-aut-mei=Akiyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=HarutaJun-ichi
en-aut-sei=Haruta
en-aut-mei=Jun-ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=UtsumiRyutaro
en-aut-sei=Utsumi
en-aut-mei=Ryutaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

affil-num=1
en-affil=Graduate School of Education, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Science and Technology on Food Safety, Faculty of Biology-Oriented Science and Technology, Kindai University
kn-affil=

affil-num=3
en-affil=Institute of Microbial Chemistry (BIKAKEN)
kn-affil=

affil-num=4
en-affil=SANKEN (The Institute of Scientific and Industrial Research), Osaka University
kn-affil=

affil-num=5
en-affil=Graduate School of Education, Okayama University
kn-affil=

affil-num=6
en-affil=Graduate School of Education, Okayama University
kn-affil=

affil-num=7
en-affil=Graduate School of Education, Okayama University
kn-affil=

affil-num=8
en-affil=Graduate School of Education, Okayama University
kn-affil=

affil-num=9
en-affil=Graduate School of Education, Okayama University
kn-affil=

affil-num=10
en-affil=Institute of Microbial Chemistry (BIKAKEN)
kn-affil=

affil-num=11
en-affil=Istituto Pasteur Italy, Department of Biology and Biotechnology, “C. Darwin”, Sapienza University of Rome
kn-affil=

affil-num=12
en-affil=Istituto Pasteur Italy, Department of Biology and Biotechnology, “C. Darwin”, Sapienza University of Rome
kn-affil=

affil-num=13
en-affil=Istituto Pasteur Italy, Department of Biology and Biotechnology, “C. Darwin”, Sapienza University of Rome
kn-affil=

affil-num=14
en-affil=Istituto Pasteur Italy, Department of Biology and Biotechnology, “C. Darwin”, Sapienza University of Rome
kn-affil=

affil-num=15
en-affil=Department of Lead Exploration Units, Graduate School of Pharmaceutical Sciences, Osaka University
kn-affil=

affil-num=16
en-affil=Compound Library Screening Center, Graduate School of Pharmaceutical Sciences, Osaka University
kn-affil=

affil-num=17
en-affil=Department of Lead Exploration Units, Graduate School of Pharmaceutical Sciences, Osaka University
kn-affil=

affil-num=18
en-affil=SANKEN (The Institute of Scientific and Industrial Research), Osaka University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=33
cd-vols=
no-issue=3
article-no=
start-page=99
end-page=117
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240429
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Generation and characterization of cerebellar granule neurons specific knockout mice of Golli-MBP
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Golli–myelin basic proteins, encoded by the myelin basic protein gene, are widely expressed in neurons and oligodendrocytes in the central nervous system. Further, prior research has shown that Golli–myelin basic protein is necessary for myelination and neuronal maturation during central nervous system development. In this study, we established Golli–myelin basic protein-floxed mice to elucidate the cell-type-specific effects of Golli–myelin basic protein knockout through the generation of conditional knockout mice (Golli–myelin basic proteinsfl/fl; E3CreN), in which Golli–myelin basic proteins were specifically deleted in cerebellar granule neurons, where Golli–myelin basic proteins are expressed abundantly in wild-type mice. To investigate the role of Golli–myelin basic proteins in cerebellar granule neurons, we further performed histopathological analyses of these mice, with results indicating no morphological changes or degeneration of the major cellular components of the cerebellum. Furthermore, behavioral analysis showed that Golli–myelin basic proteinsfl/fl; E3CreN mice were healthy and did not display any abnormal behavior. These results suggest that the loss of Golli–myelin basic proteins in cerebellar granule neurons does not lead to cerebellar perturbations or behavioral abnormalities. This mouse model could therefore be employed to analyze the effect of Golli–myelin basic protein deletion in specific cell types of the central nervous system, such as other neuronal cells and oligodendrocytes, or in lymphocytes of the immune system.
en-copyright=
kn-copyright=

en-aut-name=MiyazakiHaruko
en-aut-sei=Miyazaki
en-aut-mei=Haruko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NishiokaSaki
en-aut-sei=Nishioka
en-aut-mei=Saki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YamanakaTomoyuki
en-aut-sei=Yamanaka
en-aut-mei=Tomoyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=AbeManabu
en-aut-sei=Abe
en-aut-mei=Manabu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ImamuraYukio
en-aut-sei=Imamura
en-aut-mei=Yukio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MiyasakaTomohiro
en-aut-sei=Miyasaka
en-aut-mei=Tomohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KakudaNobuto
en-aut-sei=Kakuda
en-aut-mei=Nobuto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=OohashiToshitaka
en-aut-sei=Oohashi
en-aut-mei=Toshitaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=ShimogoriTomomi
en-aut-sei=Shimogori
en-aut-mei=Tomomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=YamakawaKazuhiro
en-aut-sei=Yamakawa
en-aut-mei=Kazuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=IkawaMasahito
en-aut-sei=Ikawa
en-aut-mei=Masahito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=NukinaNobuyuki
en-aut-sei=Nukina
en-aut-mei=Nobuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

affil-num=1
en-affil=Department of Molecular Biology and Biochemistry, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=2
en-affil=Department of Experimental Genome Research, Research Institute for Microbial Diseases, Osaka University
kn-affil=

affil-num=3
en-affil=Laboratory of Structural Neuropathology, Graduate School of Brain Science, Doshisha University
kn-affil=

affil-num=4
en-affil=Department of Animal Model Development, Brain Research Institute, Niigata University
kn-affil=

affil-num=5
en-affil=Laboratory of Structural Neuropathology, Graduate School of Brain Science, Doshisha University
kn-affil=

affil-num=6
en-affil=Faculty of Life and Medical Sciences, Doshisha University
kn-affil=

affil-num=7
en-affil=Faculty of Life and Medical Sciences, Doshisha University
kn-affil=

affil-num=8
en-affil=Department of Molecular Biology and Biochemistry, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=9
en-affil=Laboratory for Molecular Mechanisms of Brain Development, RIKEN Center for Brain Science
kn-affil=

affil-num=10
en-affil=Laboratory for Neurogenetics, RIKEN Center for Brain Science
kn-affil=

affil-num=11
en-affil=Department of Experimental Genome Research, Research Institute for Microbial Diseases, Osaka University
kn-affil=

affil-num=12
en-affil=Laboratory of Structural Neuropathology, Graduate School of Brain Science, Doshisha University
kn-affil=
en-keyword=Golli-MBP
kn-keyword=Golli-MBP
en-keyword=Cerebellar granule neuron
kn-keyword=Cerebellar granule neuron
en-keyword=CRISPR/Cas9
kn-keyword=CRISPR/Cas9
en-keyword=Conditional knockout
kn-keyword=Conditional knockout
END

start-ver=1.4
cd-journal=joma
no-vol=218
cd-vols=
no-issue=
article-no=
start-page=104922
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202509
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Alteration of perineuronal nets and parvalbumin interneurons in prefrontal cortex and hippocampus, and correlation with blood corticosterone in activity-based anorexia model mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Anorexia nervosa (AN) is an eating disorder characterized by restricted energy intake, severely underweight status, and frequent hyperactivity. Previous research has shown structural and functional alterations in the medial prefrontal cortex (mPFC) and hippocampus of AN patients. To investigate the pathological mechanism of AN, we analyzed the expression and distribution of parvalbumin (PV) interneurons and perineuronal nets (PNNs), which are implicated in the pathology of neuropsychiatric disorders, in the mPFC and hippocampus dorsal (HPCd) and ventral (HPCv) using an activity-based anorexia (ABA) mouse model. We found that PNN expression and density increased in the mPFC, with minor alterations in the HPCd and HPCv of ABA mice. The expression and distribution of PV neurons were unchanged in the brains of ABA mice, except for a regional decrease in PV-expressing neuron density in the HPCd. Co-localization analysis showed an increased number of PNNs enwrapping PV-negative neurons in the mPFC of ABA mice. Furthermore, the upregulation of PNN expression in the mPFC was positively correlated with elevated blood corticosterone levels, a well-known stress indicator, in ABA mice. Our findings suggest that the increased expression and distribution of PNNs surrounding PV-negative neurons in the mPFC may indicate the pathological mechanisms of AN.
en-copyright=
kn-copyright=

en-aut-name=NguyenHoang Duy
en-aut-sei=Nguyen
en-aut-mei=Hoang Duy
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MiyazakiHaruko
en-aut-sei=Miyazaki
en-aut-mei=Haruko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KawaiHiroki
en-aut-sei=Kawai
en-aut-mei=Hiroki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=WangZiyi
en-aut-sei=Wang
en-aut-mei=Ziyi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SakamotoShinji
en-aut-sei=Sakamoto
en-aut-mei=Shinji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TakakiManabu
en-aut-sei=Takaki
en-aut-mei=Manabu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=OohashiToshitaka
en-aut-sei=Oohashi
en-aut-mei=Toshitaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Neuropsychiatry, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Neuropsychiatry, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=anorexia nervosa
kn-keyword=anorexia nervosa
en-keyword=activity-based anorexia
kn-keyword=activity-based anorexia
en-keyword=perineuronal nets
kn-keyword=perineuronal nets
en-keyword=parvalbumin
kn-keyword=parvalbumin
en-keyword=corticosterone
kn-keyword=corticosterone
en-keyword=prefrontal cortex
kn-keyword=prefrontal cortex
en-keyword=hippocampus
kn-keyword=hippocampus
END

start-ver=1.4
cd-journal=joma
no-vol=106
cd-vols=
no-issue=7
article-no=
start-page=002112
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250725
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Summary of taxonomy changes ratified by the International Committee on Taxonomy of Viruses (ICTV) from the Animal dsRNA and ssRNA(−) Viruses Subcommittee, 2025
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=RNA viruses are ubiquitous in the environment and are important pathogens of humans, animals and plants. In 2024, the International Committee on Taxonomy of Viruses Animal dsRNA and ssRNA(−) Viruses Subcommittee submitted 18 taxonomic proposals for consideration. These proposals expanded the known virosphere by classifying 9 new genera and 88 species for newly detected virus genomes. Of note, newly established species expand the large family of Rhabdoviridae to 580 species. A new species in the family Arenaviridae includes a virus detected in Antarctic fish with a unique split nucleoprotein ORF. Additionally, four new species were established for historically isolated viruses with previously unsequenced genomes. Furthermore, three species were abolished due to incomplete genome sequence information, and one family was moved from being unassigned in the phylum Negarnaviricota into a subphylum and order. Herein, we summarize the 18 ratified taxonomic proposals and the general features of the current taxonomy, thereby supporting public and animal health responses.
en-copyright=
kn-copyright=

en-aut-name=HughesHolly R.
en-aut-sei=Hughes
en-aut-mei=Holly R.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=BallingerMatthew J.
en-aut-sei=Ballinger
en-aut-mei=Matthew J.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=BaoYiming
en-aut-sei=Bao
en-aut-mei=Yiming
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=BejermanNicolas
en-aut-sei=Bejerman
en-aut-mei=Nicolas
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=BlasdellKim R.
en-aut-sei=Blasdell
en-aut-mei=Kim R.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=BrieseThomas
en-aut-sei=Briese
en-aut-mei=Thomas
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=BrignoneJulia
en-aut-sei=Brignone
en-aut-mei=Julia
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=CarreraJean Paul
en-aut-sei=Carrera
en-aut-mei=Jean Paul
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=De ConinckLander
en-aut-sei=De Coninck
en-aut-mei=Lander
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=de SouzaWilliam Marciel
en-aut-sei=de Souza
en-aut-mei=William Marciel
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=DebatHumberto
en-aut-sei=Debat
en-aut-mei=Humberto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=DietzgenRalf G.
en-aut-sei=Dietzgen
en-aut-mei=Ralf G.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=DürrwaldRalf
en-aut-sei=Dürrwald
en-aut-mei=Ralf
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=ErdinMert
en-aut-sei=Erdin
en-aut-mei=Mert
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=FooksAnthony R.
en-aut-sei=Fooks
en-aut-mei=Anthony R.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=ForbesKristian M.
en-aut-sei=Forbes
en-aut-mei=Kristian M.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=Freitas-AstúaJuliana
en-aut-sei=Freitas-Astúa
en-aut-mei=Juliana
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=GarciaJorge B.
en-aut-sei=Garcia
en-aut-mei=Jorge B.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=GeogheganJemma L.
en-aut-sei=Geoghegan
en-aut-mei=Jemma L.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=GrimwoodRebecca M.
en-aut-sei=Grimwood
en-aut-mei=Rebecca M.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

en-aut-name=HorieMasayuki
en-aut-sei=Horie
en-aut-mei=Masayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=21
ORCID=

en-aut-name=HyndmanTimothy H.
en-aut-sei=Hyndman
en-aut-mei=Timothy H.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=22
ORCID=

en-aut-name=JohneReimar
en-aut-sei=Johne
en-aut-mei=Reimar
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=23
ORCID=

en-aut-name=KlenaJohn D.
en-aut-sei=Klena
en-aut-mei=John D.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=24
ORCID=

en-aut-name=KondoHideki
en-aut-sei=Kondo
en-aut-mei=Hideki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=25
ORCID=

en-aut-name=KooninEugene V.
en-aut-sei=Koonin
en-aut-mei=Eugene V.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=26
ORCID=

en-aut-name=KostygovAlexei Y.
en-aut-sei=Kostygov
en-aut-mei=Alexei Y.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=27
ORCID=

en-aut-name=KrupovicMart
en-aut-sei=Krupovic
en-aut-mei=Mart
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=28
ORCID=

en-aut-name=KuhnJens H.
en-aut-sei=Kuhn
en-aut-mei=Jens H.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=29
ORCID=

en-aut-name=LetkoMichael
en-aut-sei=Letko
en-aut-mei=Michael
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=30
ORCID=

en-aut-name=LiJun-Min
en-aut-sei=Li
en-aut-mei=Jun-Min
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=31
ORCID=

en-aut-name=LiuYiyun
en-aut-sei=Liu
en-aut-mei=Yiyun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=32
ORCID=

en-aut-name=MartinMaria Laura
en-aut-sei=Martin
en-aut-mei=Maria Laura
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=33
ORCID=

en-aut-name=MullNathaniel
en-aut-sei=Mull
en-aut-mei=Nathaniel
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=34
ORCID=

en-aut-name=NazarYael
en-aut-sei=Nazar
en-aut-mei=Yael
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=35
ORCID=

en-aut-name=NowotnyNorbert
en-aut-sei=Nowotny
en-aut-mei=Norbert
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=36
ORCID=

en-aut-name=NunesMárcio Roberto Teixeira
en-aut-sei=Nunes
en-aut-mei=Márcio Roberto Teixeira
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=37
ORCID=

en-aut-name=ØklandArnfinn Lodden
en-aut-sei=Økland
en-aut-mei=Arnfinn Lodden
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=38
ORCID=

en-aut-name=RubbenstrothDennis
en-aut-sei=Rubbenstroth
en-aut-mei=Dennis
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=39
ORCID=

en-aut-name=RussellBrandy J.
en-aut-sei=Russell
en-aut-mei=Brandy J.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=40
ORCID=

en-aut-name=SchottEric
en-aut-sei=Schott
en-aut-mei=Eric
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
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affil-num=2
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affil-num=3
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affil-num=4
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affil-num=5
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kn-affil=

affil-num=6
en-affil=Center for Infection and Immunity, and Department of Epidemiology, Mailman School of Public Health, Columbia University
kn-affil=

affil-num=7
en-affil=Instituto Nacional de Enfermedades Virales Humanas Dr. Julio I. Maiztegui. INEVH -ANLIS
kn-affil=

affil-num=8
en-affil=Instituto Conmemorativo Gorgas de Estudios de la Salud
kn-affil=

affil-num=9
en-affil=Division of Clinical and Epidemiological Virology, KU Leuven
kn-affil=

affil-num=10
en-affil=Department of Microbiology, Immunology and Molecular Genetics, University of Kentucky
kn-affil=

affil-num=11
en-affil=Instituto Nacional de Tecnología Agropecuaria (INTA)
kn-affil=

affil-num=12
en-affil=QAAFI, The University of Queensland
kn-affil=

affil-num=13
en-affil=Robert Koch Institut
kn-affil=

affil-num=14
en-affil=Department of Virology, University of Helsinki
kn-affil=

affil-num=15
en-affil=Animal and Plant Health Agency (APHA)
kn-affil=

affil-num=16
en-affil=Department of Biological Sciences, University of Arkansas
kn-affil=

affil-num=17
en-affil=Embrapa Cassava and Fruits
kn-affil=

affil-num=18
en-affil=Instituto Nacional de Enfermedades Virales Humanas Dr. Julio I. Maiztegui. INEVH -ANLIS
kn-affil=

affil-num=19
en-affil=Department of Microbiology and Immunology, University of Otago
kn-affil=

affil-num=20
en-affil=Department of Microbiology and Immunology, University of Otago
kn-affil=

affil-num=21
en-affil=Osaka International Research Center for Infectious Diseases, Osaka Metropolitan University
kn-affil=

affil-num=22
en-affil=School of Veterinary Medicine, Murdoch University
kn-affil=

affil-num=23
en-affil=German Federal Institute for Risk Assessment
kn-affil=

affil-num=24
en-affil=Viral Special Pathogens Branch, The Centers for Disease Control and Prevention
kn-affil=

affil-num=25
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=26
en-affil=Computational Biology Branch, Division of Intramural Research National Library of Medicine, National Institutes of Health
kn-affil=

affil-num=27
en-affil=University of Ostrava
kn-affil=

affil-num=28
en-affil=Institut Pasteur, Université Paris Cité, CNRS UMR6047, Archaeal Virology Unit
kn-affil=

affil-num=29
en-affil=Integrated Research Facility at Fort Detrick, National Institute of Allergy and Infectious Diseases, National Institutes of Health
kn-affil=

affil-num=30
en-affil=Paul G. Allen School for Global Health, Washington State University
kn-affil=

affil-num=31
en-affil=Institute of Plant Virology, Ningbo University
kn-affil=

affil-num=32
en-affil=National Genomics Data Center, China National Center for Bioinformation; Beijing Institute of Genomics, Chinese Academy of Sciences; University of Chinese Academy of Sciences
kn-affil=

affil-num=33
en-affil=Instituto Nacional de Enfermedades Virales Humanas Dr. Julio I. Maiztegui. INEVH -ANLIS
kn-affil=

affil-num=34
en-affil=Department of Natural Sciences, Shawnee State University
kn-affil=

affil-num=35
en-affil=Instituto Nacional de Enfermedades Virales Humanas Dr. Julio I. Maiztegui. INEVH -ANLIS
kn-affil=

affil-num=36
en-affil=College of Medicine, Mohammed Bin Rashid University of Medicine and Health Sciences, Dubai Health
kn-affil=

affil-num=37
en-affil=Universidade Federal do Pará
kn-affil=

affil-num=38
en-affil=Pharmaq Analytiq
kn-affil=

affil-num=39
en-affil=Institute of Diagnostic Virology, Friedrich-Loeffler-Institut
kn-affil=

affil-num=40
en-affil=Centers for Disease Control and Prevention
kn-affil=

affil-num=41
en-affil=Institute of Marine and Environmental Technology, University of Maryland Center for Environmental Science
kn-affil=

affil-num=42
en-affil=Paul G. Allen School for Global Health, Washington State University
kn-affil=

affil-num=43
en-affil=Instituto Nacional de Enfermedades Virales Humanas Dr. Julio I. Maiztegui. INEVH -ANLIS
kn-affil=

affil-num=44
en-affil=Viral Special Pathogens Branch, The Centers for Disease Control and Prevention
kn-affil=

affil-num=45
en-affil=Department of Virology, University of Helsinki
kn-affil=

affil-num=46
en-affil=Department of Virology, University of Helsinki
kn-affil=

affil-num=47
en-affil=Integrated Group of Aquaculture and Environmental Studies, Federal University of Paraná
kn-affil=

affil-num=48
en-affil=Department of Pathology, The University of Texas Medical Branch
kn-affil=

affil-num=49
en-affil=Department of Microbiology and Immunology, Indiana University School of Medicine
kn-affil=

affil-num=50
en-affil=Institut Pasteur
kn-affil=

affil-num=51
en-affil=Department of Pathology, The University of Texas Medical Branch
kn-affil=

affil-num=52
en-affil=University of Queensland
kn-affil=

affil-num=53
en-affil=Wuhan Institute of Virology, Chinese Academy of Sciences
kn-affil=

affil-num=54
en-affil=North Carolina State University
kn-affil=

affil-num=55
en-affil=Viral Special Pathogens Branch, The Centers for Disease Control and Prevention
kn-affil=

affil-num=56
en-affil=Computational Biology Branch, Division of Intramural Research National Library of Medicine, National Institutes of Health
kn-affil=

affil-num=57
en-affil=Wuhan Institute of Virology, Chinese Academy of Sciences
kn-affil=

affil-num=58
en-affil=Institute of Insect Sciences, Zhejiang University
kn-affil=

affil-num=59
en-affil=Institute of Plant Virology, Ningbo University
kn-affil=

affil-num=60
en-affil=University of Ostrava
kn-affil=

affil-num=61
en-affil=Department of Pathobiology and Population Sciences, Royal Veterinary College
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=106
cd-vols=
no-issue=7
article-no=
start-page=002114
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250725
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Summary of taxonomy changes ratified by the International Committee on Taxonomy of Viruses from the Plant Viruses Subcommittee, 2025
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=In March 2025, following the annual International Committee on Taxonomy of Viruses (ICTV) ratification vote, newly proposed taxa were added to those under the mandate of the Plant Viruses Subcommittee. In brief, 1 new order, 3 new families, 6 new genera, 2 new subgenera and 206 new species were created. Some taxa were reorganized. Genus Cytorhabdovirus in the family Rhabdoviridae was abolished and its taxa were redistributed into three new genera Alphacytorhabdovirus, Betacytorhabdovirus and Gammacytorhabdovirus. Genus Waikavirus in the family Secoviridae was reorganized into two subgenera (Actinidivirus and Ritunrivirus). One family and four previously unaffiliated genera were moved to the newly established order Tombendovirales. Twelve species not assigned to a genus were abolished. To comply with the ICTV mandate of a binomial format for virus species, eight species were renamed. Demarcation criteria in the absence of biological information were defined in the genus Ilarvirus (family Bromoviridae). This article presents the updated taxonomy put forth by the Plant Viruses Subcommittee and ratified by the ICTV.
en-copyright=
kn-copyright=

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kn-aut-name=
kn-aut-sei=
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aut-affil-num=50
ORCID=

en-aut-name=Lopez-MoyaJuan J.
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kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=51
ORCID=

en-aut-name=MaclotFrancois
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aut-affil-num=52
ORCID=

en-aut-name=MäkinenKristiina
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aut-affil-num=53
ORCID=

en-aut-name=MartinDarren
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kn-aut-name=
kn-aut-sei=
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aut-affil-num=54
ORCID=

en-aut-name=MassartSebastien
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kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=55
ORCID=

en-aut-name=MillerW. Allen
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kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=56
ORCID=

en-aut-name=MohammadiMusa
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aut-affil-num=57
ORCID=

en-aut-name=MollovDimitre
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aut-affil-num=58
ORCID=

en-aut-name=MullerEmmanuelle
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kn-aut-name=
kn-aut-sei=
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aut-affil-num=59
ORCID=

en-aut-name=NagataTatsuya
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aut-affil-num=60
ORCID=

en-aut-name=Navas-CastilloJesús
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aut-affil-num=61
ORCID=

en-aut-name=NeriyaYutaro
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kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=62
ORCID=

en-aut-name=Ochoa-CoronaFrancisco M.
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en-aut-mei=Francisco M.
kn-aut-name=
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kn-aut-mei=
aut-affil-num=63
ORCID=

en-aut-name=OhshimaKazusato
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aut-affil-num=64
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en-aut-name=PallásVicente
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kn-aut-name=
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aut-affil-num=65
ORCID=

en-aut-name=PappuHanu
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aut-affil-num=66
ORCID=

en-aut-name=PetrzikKarel
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en-aut-mei=Karel
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=67
ORCID=

en-aut-name=PoogginMikhail
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en-aut-mei=Mikhail
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=68
ORCID=

en-aut-name=PrigigalloMaria Isabella
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en-aut-mei=Maria Isabella
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=69
ORCID=

en-aut-name=Ramos-GonzálezPedro L.
en-aut-sei=Ramos-González
en-aut-mei=Pedro L.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=70
ORCID=

en-aut-name=RibeiroSimone
en-aut-sei=Ribeiro
en-aut-mei=Simone
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=71
ORCID=

en-aut-name=Richert-PöggelerKatja R.
en-aut-sei=Richert-Pöggeler
en-aut-mei=Katja R.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=72
ORCID=

en-aut-name=RoumagnacPhilippe
en-aut-sei=Roumagnac
en-aut-mei=Philippe
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=73
ORCID=

en-aut-name=RoyAvijit
en-aut-sei=Roy
en-aut-mei=Avijit
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=74
ORCID=

en-aut-name=SabanadzovicSead
en-aut-sei=Sabanadzovic
en-aut-mei=Sead
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=75
ORCID=

en-aut-name=ŠafářováDana
en-aut-sei=Šafářová
en-aut-mei=Dana
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=76
ORCID=

en-aut-name=SaldarelliPasquale
en-aut-sei=Saldarelli
en-aut-mei=Pasquale
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=77
ORCID=

en-aut-name=SanfaçonHélène
en-aut-sei=Sanfaçon
en-aut-mei=Hélène
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=78
ORCID=

en-aut-name=SarmientoCecilia
en-aut-sei=Sarmiento
en-aut-mei=Cecilia
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=79
ORCID=

en-aut-name=SasayaTakahide
en-aut-sei=Sasaya
en-aut-mei=Takahide
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=80
ORCID=

en-aut-name=ScheetsKay
en-aut-sei=Scheets
en-aut-mei=Kay
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=81
ORCID=

en-aut-name=SchravesandeWillem E.W.
en-aut-sei=Schravesande
en-aut-mei=Willem E.W.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=82
ORCID=

en-aut-name=SealSusan
en-aut-sei=Seal
en-aut-mei=Susan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=83
ORCID=

en-aut-name=ShimomotoYoshifumi
en-aut-sei=Shimomoto
en-aut-mei=Yoshifumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=84
ORCID=

en-aut-name=SõmeraMerike
en-aut-sei=Sõmera
en-aut-mei=Merike
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=85
ORCID=

en-aut-name=StavoloneLivia
en-aut-sei=Stavolone
en-aut-mei=Livia
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=86
ORCID=

en-aut-name=StewartLucy R.
en-aut-sei=Stewart
en-aut-mei=Lucy R.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=87
ORCID=

en-aut-name=TeycheneyPierre-Yves
en-aut-sei=Teycheney
en-aut-mei=Pierre-Yves
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=88
ORCID=

en-aut-name=ThomasJohn E.
en-aut-sei=Thomas
en-aut-mei=John E.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=89
ORCID=

en-aut-name=ThompsonJeremy R.
en-aut-sei=Thompson
en-aut-mei=Jeremy R.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=90
ORCID=

en-aut-name=TiberiniAntonio
en-aut-sei=Tiberini
en-aut-mei=Antonio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=91
ORCID=

en-aut-name=TomitakaYasuhiro
en-aut-sei=Tomitaka
en-aut-mei=Yasuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=92
ORCID=

en-aut-name=TzanetakisIoannis
en-aut-sei=Tzanetakis
en-aut-mei=Ioannis
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=93
ORCID=

en-aut-name=UmberMarie
en-aut-sei=Umber
en-aut-mei=Marie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=94
ORCID=

en-aut-name=UrbinoCica
en-aut-sei=Urbino
en-aut-mei=Cica
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=95
ORCID=

en-aut-name=van den BurgHarrold A.
en-aut-sei=van den Burg
en-aut-mei=Harrold A.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=96
ORCID=

en-aut-name=Van der VlugtRené A.A.
en-aut-sei=Van der Vlugt
en-aut-mei=René A.A.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=97
ORCID=

en-aut-name=VarsaniArvind
en-aut-sei=Varsani
en-aut-mei=Arvind
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=98
ORCID=

en-aut-name=VerhageAdriaan
en-aut-sei=Verhage
en-aut-mei=Adriaan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=99
ORCID=

en-aut-name=VillamorDan
en-aut-sei=Villamor
en-aut-mei=Dan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=100
ORCID=

en-aut-name=von BargenSusanne
en-aut-sei=von Bargen
en-aut-mei=Susanne
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=101
ORCID=

en-aut-name=WalkerPeter J.
en-aut-sei=Walker
en-aut-mei=Peter J.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=102
ORCID=

en-aut-name=WetzelThierry
en-aut-sei=Wetzel
en-aut-mei=Thierry
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=103
ORCID=

en-aut-name=WhitfieldAnna E.
en-aut-sei=Whitfield
en-aut-mei=Anna E.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=104
ORCID=

en-aut-name=WylieStephen J.
en-aut-sei=Wylie
en-aut-mei=Stephen J.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=105
ORCID=

en-aut-name=YangCaixia
en-aut-sei=Yang
en-aut-mei=Caixia
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=106
ORCID=

en-aut-name=ZerbiniF. Murilo
en-aut-sei=Zerbini
en-aut-mei=F. Murilo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=107
ORCID=

en-aut-name=ZhangSong
en-aut-sei=Zhang
en-aut-mei=Song
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=108
ORCID=

affil-num=1
en-affil=Istituto per la Protezione Sostenibile delle Piante, CNR
kn-affil=

affil-num=2
en-affil=USDA-ARS, BARC, National Germplasm Resources Laboratory
kn-affil=

affil-num=3
en-affil=Liaoning Key Laboratory of Urban Integrated Pest Management and Ecological Security, Shenyang University
kn-affil=

affil-num=4
en-affil=Centro de Edafología y Biología Aplicada del Segura-CSIC
kn-affil=

affil-num=5
en-affil=Department of Molecular and Structural Biochemistry, North Carolina State University
kn-affil=

affil-num=6
en-affil=Unidad de Fitopatología y Modelización Agrícola (UFYMA) INTA-CONICET
kn-affil=

affil-num=7
en-affil=Plant Protection Department
kn-affil=

affil-num=8
en-affil=UMR 1332 Biologie du Fruit et Pathologie, University of Bordeaux, INRAE
kn-affil=

affil-num=9
en-affil=Margarita Salas Center for Biological Research (CIB-CSIC) Spanish Council for Scientific Research (CSIC)
kn-affil=

affil-num=10
en-affil=National Citrus Engineering and Technology Research Center, Integrative Science Center of Germplasm Creation in Western China (CHONGQING) Science City, Citrus Research Institute, Southwest University
kn-affil=

affil-num=11
en-affil=Department of Plant Sciences, University of Cambridge
kn-affil=

affil-num=12
en-affil=Agriculture and Life Sciences Research Institute, Kangwon National University
kn-affil=

affil-num=13
en-affil=Agriculture Victoria Research, Department of Energy, Environment and Climate Action and School of Applied Systems Biology, La Trobe University
kn-affil=

affil-num=14
en-affil=University of Delhi South Campu
kn-affil=

affil-num=15
en-affil=Unidad de Fitopatología y Modelización Agrícola (UFYMA) INTA-CONICET
kn-affil=

affil-num=16
en-affil=Queensland Alliance for Agriculture and Food Innovation, The University of Queensland
kn-affil=

affil-num=17
en-affil=CIHEAM, Istituto Agronomico Mediterraneo of Bari
kn-affil=

affil-num=18
en-affil=Centro de Edafología y Biología Aplicada del Segura-CSIC
kn-affil=

affil-num=19
en-affil=CIHEAM, Istituto Agronomico Mediterraneo of Bari
kn-affil=

affil-num=20
en-affil=Virus South Data
kn-affil=

affil-num=21
en-affil=Queensland Department of Primary Industries
kn-affil=

affil-num=22
en-affil=Max Planck Institute for Marine Microbiology
kn-affil=

affil-num=23
en-affil=Plant Protection Department
kn-affil=

affil-num=24
en-affil=Fera Science Ltd (Fera), York Biotech Campus
kn-affil=

affil-num=25
en-affil=Embrapa Cassava and Fruits, Brazilian Agricultural Research Corporation
kn-affil=

affil-num=26
en-affil=Plant Pathology, Cornell University
kn-affil=

affil-num=27
en-affil=Queensland Alliance for Agriculture and Food Innovation, The University of Queensland
kn-affil=

affil-num=28
en-affil=Department of Biology, University of Oxford
kn-affil=

affil-num=29
en-affil=Swedish University of Agriculture
kn-affil=

affil-num=30
en-affil=USDA-ARS, USNA, Floral and Nursery Plants Research Unit
kn-affil=

affil-num=31
en-affil=USDA-ARS, BARC, Molecular Plant Pathology Laboratory
kn-affil=

affil-num=32
en-affil=Institute of Plant Protection-NRI
kn-affil=

affil-num=33
en-affil=PHIM Plant Health Institute, University of Montpellier, INRAE, CIRAD, IRD, Institute Agro
kn-affil=

affil-num=34
en-affil=Instituto de Biología Molecular y Celular de Plantas (IBMCP), Universitat Politècnica de Valencia-CSIC
kn-affil=

affil-num=35
en-affil=Institut Français de la Vigne et du Vin
kn-affil=

affil-num=36
en-affil=Vali-e-Asr University of Rafsanjan, Department of Plant Protection
kn-affil=

affil-num=37
en-affil=Retired from John Innes Centre
kn-affil=

affil-num=38
en-affil=Embrapa Hortaliças
kn-affil=

affil-num=39
en-affil=USDA-ARS, USNA, Floral and Nursery Plants Research Unit
kn-affil=

affil-num=40
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=41
en-affil=International Potato Center (CIP)
kn-affil=

affil-num=42
en-affil=Institut Pasteur, Université Paris Cité, CNRS UMR6047, Archaeal Virology Unit
kn-affil=

affil-num=43
en-affil=Institute for Plant Protection, NARO
kn-affil=

affil-num=44
en-affil=Integrated Research Facility at Fort Detrick, National Institute of Allergy and Infectious Diseases, National Institutes of Health
kn-affil=

affil-num=45
en-affil=Department of Biological Sciences, University of Toledo
kn-affil=

affil-num=46
en-affil=CIRAD, UMR PVBMT
kn-affil=

affil-num=47
en-affil=Liaoning Key Laboratory of Urban Integrated Pest Management and Ecological Security, Shenyang University
kn-affil=

affil-num=48
en-affil=State Key Laboratory for Conservation and Utilization of Bio-Resources in Yunnan, Yunnan Agricultural University
kn-affil=

affil-num=49
en-affil=Institute of Plant Virology, Ningbo University
kn-affil=

affil-num=50
en-affil=Instituto de Patología Vegetal (IPAVE), INTA, Unidad de Fitopatología y Modelización Agrícola (UFYMA) INTA-CONICET
kn-affil=

affil-num=51
en-affil=Centre for Research in Agricultural Genomics, CRAG (CSIC-IRTA-UAB-UB)
kn-affil=

affil-num=52
en-affil=UMR 1332 Biologie du Fruit et Pathologie, University of Bordeaux, INRAE
kn-affil=

affil-num=53
en-affil=Department of Agricultural Sciences, University of Helsinki
kn-affil=

affil-num=54
en-affil=Institute of Infectious Disease and Molecular Medicine, University of Cape Town
kn-affil=

affil-num=55
en-affil=Plant Pathology Laboratory, TERRA Gembloux Agro-Bio Tech, University of Liege
kn-affil=

affil-num=56
en-affil=Department of Plant Pathology, Entomology and Microbiology, Iowa State University
kn-affil=

affil-num=57
en-affil=Department of Plant Protection, Gorgan University of Agricultural Sciences and Natural Resources
kn-affil=

affil-num=58
en-affil=USDA-APHIS, Plant Protection and Quarantine
kn-affil=

affil-num=59
en-affil=CIRAD, AGAP Institut; AGAP Institut, University of Montpellier; CIRAD, INRAE
kn-affil=

affil-num=60
en-affil=Instituto de Ciências Biológicas, Universidade de Brasília
kn-affil=

affil-num=61
en-affil=Instituto de Hortofruticultura Subtropical y Mediterránea “La Mayora” (IHSM-UMA-CSIC), Consejo Superior de Investigaciones Científicas
kn-affil=

affil-num=62
en-affil=Utsunomiya University
kn-affil=

affil-num=63
en-affil=Oklahoma State University, Institute for Biosecurity & Microbial Forensics
kn-affil=

affil-num=64
en-affil=Saga University
kn-affil=

affil-num=65
en-affil=Instituto de Biología Molecular y Celular de Plantas (IBMCP), Universitat Politècnica de Valencia-CSIC
kn-affil=

affil-num=66
en-affil=Department of Plant Pathology, Washington State University
kn-affil=

affil-num=67
en-affil=Institute of Plant Molecular Biology
kn-affil=

affil-num=68
en-affil=PHIM Plant Health Institute, University of Montpellier, INRAE, CIRAD, IRD
kn-affil=

affil-num=69
en-affil=Istituto per la Protezione Sostenibile delle Piante, CNR
kn-affil=

affil-num=70
en-affil=Applied Molecular Biology Laboratory, Instituto Biológico de São Paulo
kn-affil=

affil-num=71
en-affil=Embrapa Recursos Genéticos e Biotecnologia
kn-affil=

affil-num=72
en-affil=Julius Kühn Institute, Federal Research Centre for Cultivated Plants, Institute for Epidemiology and Pathogen Diagnostics
kn-affil=

affil-num=73
en-affil=CIRAD, UMR PHIM
kn-affil=

affil-num=74
en-affil=USDA-ARS, BARC, Molecular Plant Pathology Laboratory, Beltsville, MD, USA
kn-affil=

affil-num=75
en-affil=Department of Agricultural Science and Plant Protection, Mississippi State University
kn-affil=

affil-num=76
en-affil=Department of Cell Biology and Genetics, Faculty of Science, Palacký University Olomouc
kn-affil=

affil-num=77
en-affil=Istituto per la Protezione Sostenibile delle Piante, CNR
kn-affil=

affil-num=78
en-affil=Summerland Research and Development Centre, Agriculture and Agri-Food Canada
kn-affil=

affil-num=79
en-affil=Department of Chemistry and Biotechnology, Tallinn University of Technology
kn-affil=

affil-num=80
en-affil=Strategic Planning Headquarters, NARO
kn-affil=

affil-num=81
en-affil=Department of Plant Pathology, Ecology and Evolution, Oklahoma State University
kn-affil=

affil-num=82
en-affil=Molecular Plant Pathology, University of Amsterdam
kn-affil=

affil-num=83
en-affil=Natural Resources Institute, University of Greenwich
kn-affil=

affil-num=84
en-affil=Kochi Agricultural Research Center
kn-affil=

affil-num=85
en-affil=Department of Chemistry and Biotechnology, Tallinn University of Technology
kn-affil=

affil-num=86
en-affil=Istituto per la Protezione Sostenibile delle Piante, CNR
kn-affil=

affil-num=87
en-affil=Currently unaffiliated
kn-affil=

affil-num=88
en-affil=CIRAD, UMR PVBMT & UMR PVBMT, Université de la Réunion
kn-affil=

affil-num=89
en-affil=Queensland Alliance for Agriculture and Food Innovation, The University of Queensland
kn-affil=

affil-num=90
en-affil=Plant Health and Environment Laboratory
kn-affil=

affil-num=91
en-affil=Council for Agricultural Research and Economics, Research Centre for Plant Protection and Certification
kn-affil=

affil-num=92
en-affil=Institute for Plant Protection, NARO
kn-affil=

affil-num=93
en-affil=Department of Entomology and Plant Pathology, Division of Agriculture, University of Arkansas System
kn-affil=

affil-num=94
en-affil=INRAE, UR ASTRO
kn-affil=

affil-num=95
en-affil=PHIM Plant Health Institute, University of Montpellier, INRAE, CIRAD, IRD, Institute Agro
kn-affil=

affil-num=96
en-affil=Molecular Plant Pathology, University of Amsterdam
kn-affil=

affil-num=97
en-affil=Wageningen University and Research
kn-affil=

affil-num=98
en-affil=The Biodesign Center for Fundamental and Applied Microbiomics, Center for Evolution and Medicine, School of Life Sciences, Arizona State University
kn-affil=

affil-num=99
en-affil=Rijk Zwaan Breeding B.V.
kn-affil=

affil-num=100
en-affil=Department of Entomology and Plant Pathology, Division of Agriculture, University of Arkansas System
kn-affil=

affil-num=101
en-affil=Humboldt-Universität zu Berlin, Thaer-Institute of Agricultural and Horticultural Sciences
kn-affil=

affil-num=102
en-affil=The University of Queensland
kn-affil=

affil-num=103
en-affil=Dienstleistungszentrum Ländlicher Raum Rheinpfalz
kn-affil=

affil-num=104
en-affil=North Carolina State University
kn-affil=

affil-num=105
en-affil=Food Futures Institute, Murdoch University
kn-affil=

affil-num=106
en-affil=Liaoning Key Laboratory of Urban Integrated Pest Management and Ecological Security, Shenyang University
kn-affil=

affil-num=107
en-affil=Dep. de Fitopatologia/BIOAGRO, Universidade Federal de Viçosa
kn-affil=

affil-num=108
en-affil=National Citrus Engineering and Technology Research Center, Integrative Science Center of Germplasm Creation in Western China (CHONGQING) Science City, Citrus Research Institute, Southwest University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=19
cd-vols=
no-issue=12
article-no=
start-page=2429
end-page=2437
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241112
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Discovery of a Compound That Inhibits IRE1α S-Nitrosylation and Preserves the Endoplasmic Reticulum Stress Response under Nitrosative Stress
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Inositol-requiring enzyme 1α (IRE1α) is a sensor of endoplasmic reticulum (ER) stress and drives ER stress response pathways. Activated IRE1α exhibits RNase activity and cleaves mRNA encoding X-box binding protein 1, a transcription factor that induces the expression of genes that maintain ER proteostasis for cell survival. Previously, we showed that IRE1α undergoes S-nitrosylation, a post-translational modification induced by nitric oxide (NO), resulting in reduced RNase activity. Therefore, S-nitrosylation of IRE1α compromises the response to ER stress, making cells more vulnerable. We conducted virtual screening and cell-based validation experiments to identify compounds that inhibit the S-nitrosylation of IRE1α by targeting nitrosylated cysteine residues. We ultimately identified a compound (1ACTA) that selectively inhibits the S-nitrosylation of IRE1α and prevents the NO-induced reduction of RNase activity. Furthermore, 1ACTA reduces the rate of NO-induced cell death. Our research identified S-nitrosylation as a novel target for drug development for IRE1α and provides a suitable screening strategy.
en-copyright=
kn-copyright=

en-aut-name=KurogiHaruna
en-aut-sei=Kurogi
en-aut-mei=Haruna
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakasugiNobumasa
en-aut-sei=Takasugi
en-aut-mei=Nobumasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KubotaSho
en-aut-sei=Kubota
en-aut-mei=Sho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KumarAshutosh
en-aut-sei=Kumar
en-aut-mei=Ashutosh
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SuzukiTakehiro
en-aut-sei=Suzuki
en-aut-mei=Takehiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=DohmaeNaoshi
en-aut-sei=Dohmae
en-aut-mei=Naoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SawadaDaisuke
en-aut-sei=Sawada
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=ZhangKam Y.J.
en-aut-sei=Zhang
en-aut-mei=Kam Y.J.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=UeharaTakashi
en-aut-sei=Uehara
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Laboratory for Structural Bioinformatics, Center for Biosystems Dynamics Research, RIKEN
kn-affil=

affil-num=5
en-affil=Biomolecular Characterization Unit, Technology Platform Division, RIKEN Center for Sustainable Resource Science
kn-affil=

affil-num=6
en-affil=Biomolecular Characterization Unit, Technology Platform Division, RIKEN Center for Sustainable Resource Science
kn-affil=

affil-num=7
en-affil=Department of Fine Organic Synthesis, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Laboratory for Structural Bioinformatics, Center for Biosystems Dynamics Research, RIKEN
kn-affil=

affil-num=9
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=26
cd-vols=
no-issue=2
article-no=
start-page=294
end-page=300
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240104
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Evaluating the Patterns of FAPI Uptake in the Shoulder Joint: a Preliminary Study Comparing with FDG Uptake in Oncological Studies
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background Fibroblast activation protein inhibitor (FAPI) targeting PET has been introduced as a novel molecular imaging modality for visualizing cancer-associated fibroblasts. There have also been reports suggesting incidental findings of localized accumulation in the shoulder joints. However, further characterization in a larger patient cohort is still lacking.<br>
Methods 77 consecutive patients (28 females; mean age, 63.1 ± 11.6) who underwent Ga-68 FAPI-04 PET/CT for diagnosis of solid tumors were included. The incidence and localization of tracer uptake in shoulder joints were investigated and compared with available F-18 FDG scans serving as reference.<br>
Results Ga-68 FAPI-04 uptake was evaluated in 77 patients (154 shoulder joints), of whom 54 subjects (108 shoulder joints) also had available F-18 FDG scans for head-to-head comparison. On FAPI-targeted imaging, 67/154 shoulders (43.5%) demonstrated increased radiotracer accumulation in target lesions, which were distributed as follows: acromioclavicular (AC) joints in 25/67 (37.3%), followed by glenohumeral and subacromial (GH + SA) joints in 23/67 (34.3%), or both (AC and GH + SA joints) in the remaining 19/67 (28.4%). Ga-68 FAPI-04 correlated with quantified F-18 FDG uptake (r = 0.69, p < 0.0001). Relative to the latter radiotracer, however, in-vivo FAP expression in the shoulders was significantly increased (Ga-68 FAPI-04, 4.7 ± 3.2 vs F-18 FDG, 3.6 ± 1.3, p < 0.001).<br>
Conclusion Our study revealed focal accumulation of Ga-68 FAPI-04 in the shoulders, particularly in the AC joints, with higher uptake compared to the inflammatory-directed PET radiotracer F-18 FDG in oncological studies. As a result, further trials are warranted to investigate the potential of FAPI-directed molecular imaging in identifying chronic remodeling in shoulder joints. This could have implications for initiating anti-FAP targeted photodynamic therapy based on PET signal strength.
en-copyright=
kn-copyright=

en-aut-name=MatsusakaYohji
en-aut-sei=Matsusaka
en-aut-mei=Yohji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=WernerRudolf A.
en-aut-sei=Werner
en-aut-mei=Rudolf A.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SerflingSebastian E.
en-aut-sei=Serfling
en-aut-mei=Sebastian E.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=BuckAndreas K.
en-aut-sei=Buck
en-aut-mei=Andreas K.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KosmalaAleksander
en-aut-sei=Kosmala
en-aut-mei=Aleksander
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SasakiTakanori
en-aut-sei=Sasaki
en-aut-mei=Takanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=WeichAlexander
en-aut-sei=Weich
en-aut-mei=Alexander
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=HiguchiTakahiro
en-aut-sei=Higuchi
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Nuclear Medicine and Comprehensive Heart Failure Center (CHFC), Molecular Imaging of the Heart, University Hospital of Würzburg
kn-affil=

affil-num=2
en-affil=Department of Nuclear Medicine and Comprehensive Heart Failure Center (CHFC), Molecular Imaging of the Heart, University Hospital of Würzburg
kn-affil=

affil-num=3
en-affil=Department of Nuclear Medicine and Comprehensive Heart Failure Center (CHFC), Molecular Imaging of the Heart, University Hospital of Würzburg
kn-affil=

affil-num=4
en-affil=Department of Nuclear Medicine and Comprehensive Heart Failure Center (CHFC), Molecular Imaging of the Heart, University Hospital of Würzburg
kn-affil=

affil-num=5
en-affil=Department of Nuclear Medicine and Comprehensive Heart Failure Center (CHFC), Molecular Imaging of the Heart, University Hospital of Würzburg
kn-affil=

affil-num=6
en-affil=Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Nuclear Medicine and Comprehensive Heart Failure Center (CHFC), Molecular Imaging of the Heart, University Hospital of Würzburg
kn-affil=

affil-num=8
en-affil=Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Fibroblast activation inhibitor
kn-keyword=Fibroblast activation inhibitor
en-keyword=Shoulder
kn-keyword=Shoulder
en-keyword=Acromioclavicular joints
kn-keyword=Acromioclavicular joints
en-keyword=F-18 fluorodeoxyglucose
kn-keyword=F-18 fluorodeoxyglucose
en-keyword=Positron emission tomography
kn-keyword=Positron emission tomography
en-keyword=FAP
kn-keyword=FAP
en-keyword=Ga-68 FAPI-04
kn-keyword=Ga-68 FAPI-04
en-keyword=Rheumatoid arthritis
kn-keyword=Rheumatoid arthritis
en-keyword=Osteoarthritis
kn-keyword=Osteoarthritis
END

start-ver=1.4
cd-journal=joma
no-vol=47
cd-vols=
no-issue=6
article-no=
start-page=466
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250617
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Artificial Intelligence Approach in Machine Learning-Based Modeling and Networking of the Coronavirus Pathogenesis Pathway
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The coronavirus pathogenesis pathway, which consists of severe acute respiratory syndrome (SARS) coronavirus infection and signaling pathways, including the interferon pathway, the transforming growth factor beta pathway, the mitogen-activated protein kinase pathway, the apoptosis pathway, and the inflammation pathway, is activated upon coronaviral infection. An artificial intelligence approach based on machine learning was utilized to develop models with images of the coronavirus pathogenesis pathway to predict the activation states. Data on coronaviral infection held in a database were analyzed with Ingenuity Pathway Analysis (IPA), a network pathway analysis tool. Data related to SARS coronavirus 2 (SARS-CoV-2) were extracted from more than 100,000 analyses and datasets in the IPA database. A total of 27 analyses, including nine analyses of SARS-CoV-2-infected human-induced pluripotent stem cells (iPSCs) and iPSC-derived cardiomyocytes and fibroblasts, and a total of 22 analyses of SARS-CoV-2-infected lung adenocarcinoma (LUAD), were identified as being related to “human” and “SARS coronavirus 2” in the database. The coronavirus pathogenesis pathway was activated in SARS-CoV-2-infected iPSC-derived cells and LUAD cells. A prediction model was developed in Python 3.11 using images of the coronavirus pathogenesis pathway under different conditions. The prediction model of activation states of the coronavirus pathogenesis pathway may aid in treatment identification.
en-copyright=
kn-copyright=

en-aut-name=TanabeShihori
en-aut-sei=Tanabe
en-aut-mei=Shihori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=QuaderSabina
en-aut-sei=Quader
en-aut-mei=Sabina
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OnoRyuichi
en-aut-sei=Ono
en-aut-mei=Ryuichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TanakaHiroyoshi Y.
en-aut-sei=Tanaka
en-aut-mei=Hiroyoshi Y.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YamamotoAkihisa
en-aut-sei=Yamamoto
en-aut-mei=Akihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KojimaMotohiro
en-aut-sei=Kojima
en-aut-mei=Motohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=PerkinsEdward J.
en-aut-sei=Perkins
en-aut-mei=Edward J.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=CabralHoracio
en-aut-sei=Cabral
en-aut-mei=Horacio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Division of Risk Assessment, Center for Biological Safety and Research, National Institute of Health Sciences
kn-affil=

affil-num=2
en-affil=Innovation Centre of NanoMedicine (iCONM), Kawasaki Institute of Industrial Promotion
kn-affil=

affil-num=3
en-affil=Division of Cellular and Molecular Toxicology, Center for Biological Safety and Research, National Institute of Health Sciences
kn-affil=

affil-num=4
en-affil=Department of Pharmaceutical Biomedicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Mechanical Systems Engineering, Graduate School of Systems Design Tokyo Metropolitan University
kn-affil=

affil-num=6
en-affil=Department of Surgical Pathology, Kyoto Prefecture University of Medicine
kn-affil=

affil-num=7
en-affil=US Army Engineer Research and Development Center
kn-affil=

affil-num=8
en-affil=Department of Bioengineering, Graduate School of Engineering, The University of Tokyo
kn-affil=
en-keyword=artificial intelligence
kn-keyword=artificial intelligence
en-keyword=coronavirus
kn-keyword=coronavirus
en-keyword=coronaviral infection
kn-keyword=coronaviral infection
en-keyword=machine learning
kn-keyword=machine learning
en-keyword=pathway analysis
kn-keyword=pathway analysis
en-keyword=predictionmodel
kn-keyword=predictionmodel
en-keyword=molecular network
kn-keyword=molecular network
en-keyword=molecular pathway image
kn-keyword=molecular pathway image
en-keyword=network analysis
kn-keyword=network analysis
END

start-ver=1.4
cd-journal=joma
no-vol=144-145
cd-vols=
no-issue=
article-no=
start-page=109001
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202505
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Investigating the fate of Zirconium-89 labelled antibody in cynomolgus macaques
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Preclinical pharmacokinetic studies of therapeutic antibodies in non-human primates are desired because of the difficulty in extrapolating ADME data from animal models to humans. We evaluated the pharmacokinetics of 89Zr (Zirconium-89) -labelled anti-KLH human IgG and its metabolites to confirm their non-specific/physiological accumulation in healthy cynomolgus macaques. The anti-KLH antibody was used as a negative control, ensuring that the observed distribution reflected general IgG behavior rather than antigen-specific accumulation. This provides a valuable reference for comparing the biodistribution of targeted antibodies.<br>
Methods: Selected IgG was conjugated to desferrioxamine (DFO), labelled with 89Zr, and injected into healthy cynomolgus macaques. PET/CT images at the whole-body level were acquired at different time points, and standard uptake values (SUV) in regions of interest, such as the heart, liver, spleen, kidneys, bone, and muscles, were calculated. The distribution of a shortened antibody variant, 89Zr-labelled Fab, as well as that of [89Zr]Zr-DFO and [89Zr]Zr-oxalate, the expected metabolites of 89Zr- labelled IgG, was also assessed.<br>
Results: After 89Zr-labelled IgG injection, the SUV in the heart, vertebral body, and muscle decreased, in line with the 89Zr concentration decrease in the circulation, whereas radioactivity increased over time in the kidneys and liver. Autoradiography of the renal sections indicated that most of the 89Zr- labelled IgG radioactivity accumulated in the renal cortex. Relatively high accumulation in the kidneys was also observed in 89Zr- labelled Fab-injected macaques, and renal autoradiographs of these animals showed that the renal cortex was the preferred accumulation site. However, [89Zr]Zr-DFO was rapidly excreted into the urine, whereas [89Zr]Zr-oxalate was highly accumulated in the epiphysis of the long bones and vertebral body.<br>
Conclusion: In the non-human primate cynomolgus macaque, 89Zr- labelled IgG accumulated in the kidneys and the liver. However, [89Zr]Zr-DFO and 89Zr did not accumulate in these organs. This preclinical pharmacokinetic study performed with human IgG in a non-human primate model using PET is of great significance as it sheds light on the basic fate and distribution of 89Zr- labelled IgG.
en-copyright=
kn-copyright=

en-aut-name=SasakiTakanori
en-aut-sei=Sasaki
en-aut-mei=Takanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KimuraSadaaki
en-aut-sei=Kimura
en-aut-mei=Sadaaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NodaAkihiro
en-aut-sei=Noda
en-aut-mei=Akihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MurakamiYoshihiro
en-aut-sei=Murakami
en-aut-mei=Yoshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MiyoshiSosuke
en-aut-sei=Miyoshi
en-aut-mei=Sosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=AkehiMasaru
en-aut-sei=Akehi
en-aut-mei=Masaru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=OchiaiKazuhiko
en-aut-sei=Ochiai
en-aut-mei=Kazuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=WatanabeMasami
en-aut-sei=Watanabe
en-aut-mei=Masami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=HiguchiTakahiro
en-aut-sei=Higuchi
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=MatsuuraEiji
en-aut-sei=Matsuura
en-aut-mei=Eiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Faculty of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Astellas Pharma Inc.
kn-affil=

affil-num=3
en-affil=Astellas Pharma Inc.
kn-affil=

affil-num=4
en-affil=Astellas Pharma Inc.
kn-affil=

affil-num=5
en-affil=Astellas Pharma Inc.
kn-affil=

affil-num=6
en-affil=Faculty of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=School of Veterinary Nursing and Technology, Faculty of Veterinary Science, Nippon Veterinary and Life Science University
kn-affil=

affil-num=8
en-affil=Faculty of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Faculty of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=10
en-affil=Faculty of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=PET imaging
kn-keyword=PET imaging
en-keyword=Zirconium-89
kn-keyword=Zirconium-89
en-keyword=Therapeutic antibodies
kn-keyword=Therapeutic antibodies
en-keyword=Non-human primates
kn-keyword=Non-human primates
END

start-ver=1.4
cd-journal=joma
no-vol=36
cd-vols=
no-issue=12
article-no=
start-page=4932
end-page=4951
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241021
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The leucine-rich repeat receptor kinase QSK1 regulates PRR-RBOHD complexes targeted by the bacterial effector HopF2Pto
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Plants detect pathogens using cell-surface pattern recognition receptors (PRRs) such as ELONGATION Factor-TU (EF-TU) RECEPTOR (EFR) and FLAGELLIN SENSING 2 (FLS2), which recognize bacterial EF-Tu and flagellin, respectively. These PRRs belong to the leucine-rich repeat receptor kinase (LRR-RK) family and activate the production of reactive oxygen species via the NADPH oxidase RESPIRATORY BURST OXIDASE HOMOLOG D (RBOHD). The PRR-RBOHD complex is tightly regulated to prevent unwarranted or exaggerated immune responses. However, certain pathogen effectors can subvert these regulatory mechanisms, thereby suppressing plant immunity. To elucidate the intricate dynamics of the PRR-RBOHD complex, we conducted a comparative coimmunoprecipitation analysis using EFR, FLS2, and RBOHD in Arabidopsis thaliana. We identified QIAN SHOU KINASE 1 (QSK1), an LRR-RK, as a PRR-RBOHD complex-associated protein. QSK1 downregulated FLS2 and EFR abundance, functioning as a negative regulator of PRR-triggered immunity (PTI). QSK1 was targeted by the bacterial effector HopF2Pto, a mono-ADP ribosyltransferase, reducing FLS2 and EFR levels through both transcriptional and transcription-independent pathways, thereby inhibiting PTI. Furthermore, HopF2Pto transcriptionally downregulated PROSCOOP genes encoding important stress-regulated phytocytokines and their receptor MALE DISCOVERER 1-INTERACTING RECEPTOR-LIKE KINASE 2. Importantly, HopF2Pto requires QSK1 for its accumulation and virulence functions within plants. In summary, our results provide insights into the mechanism by which HopF2Pto employs QSK1 to desensitize plants to pathogen attack.
en-copyright=
kn-copyright=

en-aut-name=GotoYukihisa
en-aut-sei=Goto
en-aut-mei=Yukihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KadotaYasuhiro
en-aut-sei=Kadota
en-aut-mei=Yasuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MbengueMalick
en-aut-sei=Mbengue
en-aut-mei=Malick
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=LewisJennifer D
en-aut-sei=Lewis
en-aut-mei=Jennifer D
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MatsuiHidenori
en-aut-sei=Matsui
en-aut-mei=Hidenori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MakiNoriko
en-aut-sei=Maki
en-aut-mei=Noriko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NgouBruno Pok Man
en-aut-sei=Ngou
en-aut-mei=Bruno Pok Man
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=SklenarJan
en-aut-sei=Sklenar
en-aut-mei=Jan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=DerbyshirePaul
en-aut-sei=Derbyshire
en-aut-mei=Paul
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=ShibataArisa
en-aut-sei=Shibata
en-aut-mei=Arisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=IchihashiYasunori
en-aut-sei=Ichihashi
en-aut-mei=Yasunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=GuttmanDavid S
en-aut-sei=Guttman
en-aut-mei=David S
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=NakagamiHirofumi
en-aut-sei=Nakagami
en-aut-mei=Hirofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=SuzukiTakamasa
en-aut-sei=Suzuki
en-aut-mei=Takamasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=MenkeFrank L H
en-aut-sei=Menke
en-aut-mei=Frank L H
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=RobatzekSilke
en-aut-sei=Robatzek
en-aut-mei=Silke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=DesveauxDarrell
en-aut-sei=Desveaux
en-aut-mei=Darrell
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=ZipfelCyril
en-aut-sei=Zipfel
en-aut-mei=Cyril
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=ShirasuKen
en-aut-sei=Shirasu
en-aut-mei=Ken
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

affil-num=1
en-affil=Plant Immunity Research Group, RIKEN Center for Sustainable Resource Science (CSRS) 
kn-affil=

affil-num=2
en-affil=Plant Immunity Research Group, RIKEN Center for Sustainable Resource Science (CSRS) 
kn-affil=

affil-num=3
en-affil=The Sainsbury Laboratory, University of East Anglia
kn-affil=

affil-num=4
en-affil=Department of Cell and System Biology, Centre for the Analysis of Genome Function and Evolution, University of Toronto
kn-affil=

affil-num=5
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=6
en-affil=Plant Immunity Research Group, RIKEN Center for Sustainable Resource Science (CSRS) 
kn-affil=

affil-num=7
en-affil=Plant Immunity Research Group, RIKEN Center for Sustainable Resource Science (CSRS) 
kn-affil=

affil-num=8
en-affil=The Sainsbury Laboratory, University of East Anglia
kn-affil=

affil-num=9
en-affil=The Sainsbury Laboratory, University of East Anglia
kn-affil=

affil-num=10
en-affil=Plant Immunity Research Group, RIKEN Center for Sustainable Resource Science (CSRS) 
kn-affil=

affil-num=11
en-affil=Plant Immunity Research Group, RIKEN Center for Sustainable Resource Science (CSRS) 
kn-affil=

affil-num=12
en-affil=Department of Cell and System Biology, Centre for the Analysis of Genome Function and Evolution, University of Toronto
kn-affil=

affil-num=13
en-affil=Plant Proteomics Research Unit, RIKEN CSRS
kn-affil=

affil-num=14
en-affil=College of Bioscience and Biotechnology, Chubu University
kn-affil=

affil-num=15
en-affil=The Sainsbury Laboratory, University of East Anglia
kn-affil=

affil-num=16
en-affil=The Sainsbury Laboratory, University of East Anglia
kn-affil=

affil-num=17
en-affil=Department of Cell and System Biology, Centre for the Analysis of Genome Function and Evolution, University of Toronto
kn-affil=

affil-num=18
en-affil=Institute of Plant and Microbial Biology, Zurich-Basel Plant Science Center, University of Zurich
kn-affil=

affil-num=19
en-affil=Plant Immunity Research Group, RIKEN Center for Sustainable Resource Science (CSRS) 
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=121
cd-vols=
no-issue=5
article-no=
start-page=e70046
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250304
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Spider mite tetranins elicit different defense responses in different host habitats
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Spider mites (Tetranychus urticae) are a major threat to economically important crops. Here, we investigated the potential of tetranins, in particular Tet3 and Tet4, as T. urticae protein-type elicitors that stimulate plant defense. Truncated Tet3 and Tet4 proteins showed efficacy in activating the defense gene pathogenesis-related 1 (PR1) and inducing phytohormone production in leaves of Phaseolus vulgaris. In particular, Tet3 caused a drastically higher Ca2+ influx in leaves, but a lower reactive oxygen species (ROS) generation compared to other tetranins, whereas Tet4 caused a low Ca2+ influx and a high ROS generation in the host plants. Such specific and non-specific elicitor activities were examined by knockdown of Tet3 and Tet4 expressions in mites, confirming their respective activities and in particular showing that they function additively or synergistically to induce defense responses. Of great interest is the fact that Tet3 and Tet4 expression levels were higher in mites on their preferred host, P. vulgaris, compared to the levels in mites on the less-preferred host, Cucumis sativus, whereas Tet1 and Tet2 were constitutively expressed regardless of their host. Furthermore, mites that had been hosted on C. sativus induced lower levels of PR1 expression, Ca2+ influx and ROS generation, i.e., Tet3- and Tet4-responsive defense responses, in both P. vulgaris and C. sativus leaves compared to the levels induced by mites that had been hosted on P. vulgaris. Taken together, these findings show that selected tetranins respond to variable host cues that may optimize herbivore fitness by altering the anti-mite response of the host plant.
en-copyright=
kn-copyright=

en-aut-name=EndoYukiko
en-aut-sei=Endo
en-aut-mei=Yukiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TanakaMiku
en-aut-sei=Tanaka
en-aut-mei=Miku
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=UemuraTakuya
en-aut-sei=Uemura
en-aut-mei=Takuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TanimuraKaori
en-aut-sei=Tanimura
en-aut-mei=Kaori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=DesakiYoshitake
en-aut-sei=Desaki
en-aut-mei=Yoshitake
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OzawaRika
en-aut-sei=Ozawa
en-aut-mei=Rika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=BonzanoSara
en-aut-sei=Bonzano
en-aut-mei=Sara
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MaffeiMassimo E.
en-aut-sei=Maffei
en-aut-mei=Massimo E.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=ShinyaTomonori
en-aut-sei=Shinya
en-aut-mei=Tomonori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=GalisIvan
en-aut-sei=Galis
en-aut-mei=Ivan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=ArimuraGen‐ichiro
en-aut-sei=Arimura
en-aut-mei=Gen‐ichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

affil-num=1
en-affil=Department of Biological Science and Technology, Faculty of Advanced Engineering, Tokyo University of Science
kn-affil=

affil-num=2
en-affil=Department of Biological Science and Technology, Faculty of Advanced Engineering, Tokyo University of Science
kn-affil=

affil-num=3
en-affil=Department of Biological Science and Technology, Faculty of Advanced Engineering, Tokyo University of Science
kn-affil=

affil-num=4
en-affil=Department of Biological Science and Technology, Faculty of Advanced Engineering, Tokyo University of Science
kn-affil=

affil-num=5
en-affil=Department of Biological Science and Technology, Faculty of Advanced Engineering, Tokyo University of Science
kn-affil=

affil-num=6
en-affil=Center for Ecological Research, Kyoto University
kn-affil=

affil-num=7
en-affil=Department of Life Sciences and Systems Biology, Plant Physiology Unit, University of Turin
kn-affil=

affil-num=8
en-affil=Department of Life Sciences and Systems Biology, Plant Physiology Unit, University of Turin
kn-affil=

affil-num=9
en-affil=Institute of Plant Science and Resources (IPSR), Okayama University
kn-affil=

affil-num=10
en-affil=Institute of Plant Science and Resources (IPSR), Okayama University
kn-affil=

affil-num=11
en-affil=Department of Biological Science and Technology, Faculty of Advanced Engineering, Tokyo University of Science
kn-affil=
en-keyword=Cucumis sativus
kn-keyword=Cucumis sativus
en-keyword=elicitor
kn-keyword=elicitor
en-keyword=Phaseolus vulgaris
kn-keyword=Phaseolus vulgaris
en-keyword=spider mite (Tetranychus urticae)
kn-keyword=spider mite (Tetranychus urticae)
en-keyword=tetranin
kn-keyword=tetranin
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=1
article-no=
start-page=12857
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250414
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=OsPIP2;4 aquaporin water channel primarily expressed in roots of rice mediates both water and nonselective Na+ and K+ conductance
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Aquaporin (AQP)-dependent water transport across membranes is indispensable in plants. Recent evidence shows that several AQPs, including plasma membrane intrinsic proteins (PIPs), facilitate the electrogenic transport of ions as well as water transport and are referred to as ion-conducting aquaporins (icAQPs). The present study attempted to identify icAQPs that exhibit cation transport activity among PIPs from rice. Electrophysiological experiments on 11 OsPIPs using Xenopus laevis oocytes revealed that OsPIP2;4 mediated the electrogenic transport of alkali monovalent cations with the selectivity sequence of Na+ ≈ K+ > Rb+ > Cs+ > Li+, suggesting non-selective cation conductance for Na+ and K+. Transcripts of OsPIP2;4 were abundant in the elongation and mature zones of roots with similar expression levels between the root stelar and remaining outer parts in the cultivar Nipponbare. Immunostaining using sections of the crown roots of Nipponbare plants revealed the expression of OsPIP2;4 in the exodermis and sclerenchyma of the surface region and in the endodermis and pericycle of the stelar region. The present results provide novel insights into OsPIP2;4-dependent non-selective Na+ and K+ transport and its physiological roles in rice.
en-copyright=
kn-copyright=

en-aut-name=TranSen Thi Huong
en-aut-sei=Tran
en-aut-mei=Sen Thi Huong
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KatsuharaMaki
en-aut-sei=Katsuhara
en-aut-mei=Maki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MitoYunosuke
en-aut-sei=Mito
en-aut-mei=Yunosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OnishiAya
en-aut-sei=Onishi
en-aut-mei=Aya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HigaAyaka
en-aut-sei=Higa
en-aut-mei=Ayaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OnoShuntaro
en-aut-sei=Ono
en-aut-mei=Shuntaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=PaulNewton Chandra
en-aut-sei=Paul
en-aut-mei=Newton Chandra
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=HorieRie
en-aut-sei=Horie
en-aut-mei=Rie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=HaradaYoshihiko
en-aut-sei=Harada
en-aut-mei=Yoshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=HorieTomoaki
en-aut-sei=Horie
en-aut-mei=Tomoaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=2
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=3
en-affil=Division of Applied Biology, Faculty of Textile Science and Technology, Shinshu University
kn-affil=

affil-num=4
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=5
en-affil=Division of Applied Biology, Faculty of Textile Science and Technology, Shinshu University
kn-affil=

affil-num=6
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=7
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=8
en-affil=Division of Applied Biology, Faculty of Textile Science and Technology, Shinshu University
kn-affil=

affil-num=9
en-affil=Division of Applied Biology, Faculty of Textile Science and Technology, Shinshu University
kn-affil=

affil-num=10
en-affil=Division of Applied Biology, Faculty of Textile Science and Technology, Shinshu University
kn-affil=
en-keyword=Ion-conducting Aquaporins
kn-keyword=Ion-conducting Aquaporins
en-keyword=Non-selective cation channel
kn-keyword=Non-selective cation channel
en-keyword=Rice
kn-keyword=Rice
en-keyword=Roots
kn-keyword=Roots
END

start-ver=1.4
cd-journal=joma
no-vol=262
cd-vols=
no-issue=2
article-no=
start-page=385
end-page=395
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241023
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Analysis of the effect of permeant solutes on the hydraulic resistance of the plasma membrane in cells of Chara corallina
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=In the cells of Chara corallina, permeant monohydric alcohols including methanol, ethanol and 1-propanol increased the hydraulic resistance of the membrane (Lpm−1). We found that the relative value of the hydraulic resistance (rLpm−1) was linearly dependent on the concentration (Cs) of the alcohol. The relationship is expressed in the equation: rLpm−1 = ρmCs + 1, where ρm is the hydraulic resistance modifier coefficient of the membrane. Ye et al. (2004) showed that membrane-permeant glycol ethers also increased Lp−1. We used their data to estimate Lpm−1 and rLpm−1. The values of rLpm−1 fit the above relation we found for alcohols. When we plotted the ρm values of all the permeant alcohols and glycol ethers against their molecular weights (MW), we obtained a linear curve with a slope of 0.014 M−1/MW and with a correlation coefficient of 0.99. We analyzed the influence of the permeant solutes on the relative hydraulic resistance of the membrane (rLpm−1) as a function of the external (π0) and internal (πi) osmotic pressures. The analysis showed that the hydraulic resistance modifier coefficients (ρm) were linearly related to the MW of the permeant solutes with a slope of 0.012 M−1/MW and with a correlation coefficient of 0.84. The linear relationship between the effects of permeating solutes on the hydraulic resistance modifier coefficient (ρm) and the MW can be explained in terms of the effect of the effective osmotic pressure on the hydraulic conductivity of water channels. The result of the analysis suggests that the osmotic pressure and not the size of the permeant solute as proposed by (Ye et al., J Exp Bot 55:449–461, 2004) is the decisive factor in a solute’s influence on hydraulic conductivity. Thus, characean water channels (aquaporins) respond to permeant solutes with essentially the same mechanism as to impermeant solutes.
en-copyright=
kn-copyright=

en-aut-name=TazawaMasashi
en-aut-sei=Tazawa
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=WayneRandy
en-aut-sei=Wayne
en-aut-mei=Randy
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KatsuharaMaki
en-aut-sei=Katsuhara
en-aut-mei=Maki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Yoshida Biological Laboratory
kn-affil=

affil-num=2
en-affil=Laboratory of Natural Philosophy, Plant Biology Section, Cornell University
kn-affil=

affil-num=3
en-affil=Institute of Plant Science and Resources (IPSR), Okayama University
kn-affil=
en-keyword=Chara corallina
kn-keyword=Chara corallina
en-keyword=Effective osmotic pressure
kn-keyword=Effective osmotic pressure
en-keyword=Hydraulic resistance
kn-keyword=Hydraulic resistance
en-keyword=Plasma membrane
kn-keyword=Plasma membrane
en-keyword=Reflection coefficient
kn-keyword=Reflection coefficient
END

start-ver=1.4
cd-journal=joma
no-vol=599
cd-vols=
no-issue=13
article-no=
start-page=1914
end-page=1924
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250525
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Characterization of molecular mechanisms of CaMKKα/1 oligomerization
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Calcium/calmodulin-dependent protein kinase kinase (CaMKK) is an activating kinase for calcium/calmodulin-dependent protein kinase type 1 (CaMKI), calcium/calmodulin-dependent protein kinase type IV (CaMKIV), RAC-alpha serine/threonine-protein kinase (PKB), and AMP-activated protein kinase (AMPK) that has been reported to form an active oligomer in cells. Glutathione S-transferase (GST) pulldown assay from the extracts of COS-7 cells expressing GST- and His6-CaMKKα/1 mutants showed that the C-terminal region containing the autoinhibitory and calmodulin (CaM)-binding sequence (residues 438–463) is required for CaMKKα/1 homo-oligomerization. This was confirmed by the fact that the GST-CaMKKα/1 C-terminal domain (residues 435–505) directly interacted with EGFP-CaMKKα/1 residues 435–505 as well as with wild-type CaMKKα/1. Notably, once oligomerized in cells, CaMKKα/1 is neither exchangeable between the oligomeric complexes nor dissociated by Ca2+/CaM binding. These results support stable oligomerization of CaMKK in the cells by intermolecular self-association of its C-terminal region containing a regulatory domain.
en-copyright=
kn-copyright=

en-aut-name=UenoyamaShun
en-aut-sei=Uenoyama
en-aut-mei=Shun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NittaHayato
en-aut-sei=Nitta
en-aut-mei=Hayato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OhtsukaSatomi
en-aut-sei=Ohtsuka
en-aut-mei=Satomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MagariMasaki
en-aut-sei=Magari
en-aut-mei=Masaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SuizuFutoshi
en-aut-sei=Suizu
en-aut-mei=Futoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TokumitsuHiroshi
en-aut-sei=Tokumitsu
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Applied Cell Biology, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Applied Chemistry and Biotechnology, Faculty of Engineering, Okayama University
kn-affil=

affil-num=3
en-affil=Applied Cell Biology, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=4
en-affil=Applied Cell Biology, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Medical Technology, Kagawa Prefectural University of Health Sciences
kn-affil=

affil-num=6
en-affil=
kn-affil=
en-keyword=calmodulin
kn-keyword=calmodulin
en-keyword=calmodulin-kinase cascade
kn-keyword=calmodulin-kinase cascade
en-keyword=CaMKKa/
kn-keyword=CaMKKa/
en-keyword=oligomerization
kn-keyword=oligomerization
en-keyword=protein–protein interaction
kn-keyword=protein–protein interaction
en-keyword=regulatory domain
kn-keyword=regulatory domain
END

start-ver=1.4
cd-journal=joma
no-vol=16
cd-vols=
no-issue=26
article-no=
start-page=12024
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=2025
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Collective motions in the primary coordination sphere: a critical functional framework for catalytic activity of the oxygen-evolving complex of photosystem II
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Photosynthetic water oxidation, vital for dioxygen production and light energy conversion, is catalyzed by the oxygen-evolving complex of photosystem II, where the inorganic Mn4CaO5 cluster acts as the catalytic core. In this study, we investigate the functional significance of collective motions of amino acid side chains within the primary coordination sphere of the Mn cluster, focusing on their role in modulating the energetic demands for catalytic transformations in the S3 state. We applied regularized canonical correlation analysis to quantitatively correlate the three-dimensional arrangement of coordinating atoms with catalytic driving forces computed via density functional theory. Our analysis reveals that distinct collective side chain motions profoundly influence the energetic requirements for structural reconfigurations of the Mn cluster, achieved through expansion and contraction of the ligand cavity while fine-tuning its geometry to stabilize key intermediates. Complementary predictions from a neural network-based machine learning model indicate that the coordination sphere exerts a variable energetic impact on the catalytic transformations of the Mn cluster, depending on the S-state environment. Integrated computational analyses suggest that the extended lifetime of the S3YZ˙ state, consistently observed after three flash illuminations, may result from slow, progressive protein dynamics that continuously reshape the energy landscape, thereby shifting the equilibrium positions of rapid, reversible chemical processes over time. Overall, our findings demonstrate that collective motions in the primary coordination sphere constitute an active, dynamic framework essential for the efficient execution of multi-electron catalysis under ambient conditions, while simultaneously achieving a high selectivity with irreversible nature required for effective 3O2 evolution.
en-copyright=
kn-copyright=

en-aut-name=IsobeHiroshi
en-aut-sei=Isobe
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SuzukiTakayoshi
en-aut-sei=Suzuki
en-aut-mei=Takayoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SugaMichihiro
en-aut-sei=Suga
en-aut-mei=Michihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ShenJian-Ren
en-aut-sei=Shen
en-aut-mei=Jian-Ren
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YamaguchiKizashi
en-aut-sei=Yamaguchi
en-aut-mei=Kizashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=
kn-affil=

affil-num=2
en-affil=Research Institute for Interdisciplinary Science, Okayama University
kn-affil=

affil-num=3
en-affil=Research Institute for Interdisciplinary Science, Okayama University
kn-affil=

affil-num=4
en-affil=Research Institute for Interdisciplinary Science, Okayama University
kn-affil=

affil-num=5
en-affil=Center for Quantum Information and Quantum Biology, Osaka University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=14
cd-vols=
no-issue=5
article-no=
start-page=489
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250430
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Mutagenesis Targeting the S153 Residue Within the Transmembrane β-Hairpin of Mosquito-Larvicidal Mpp46Ab Affects Its Toxicity and the Synergistic Toxicity with Cry4Aa
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=We constructed a library of Mpp46Ab mutants, in which S153 within the transmembrane β-hairpin was randomly replaced by other amino acids. Mutagenesis and subsequent primary screening yielded 10 different Mpp46Ab mutants in addition to the wild type. Remarkably, S153 was replaced with a more hydrophobic amino acid in most of the mutants, and the S153I mutant in particular exhibited significantly increased toxicity. Electrophysiologic analysis using artificial lipid bilayers revealed that the single-channel conductance and PK/PCl permeability ratio were significantly increased for S153I pores. This suggests that the formation of highly ion-permeable and highly cation-selective toxin pores increases the influx of cations and water into cells, thereby facilitating osmotic shock. In addition, the S153F, S153L, and S153I mutants exhibited significantly reduced synergistic toxicity with Cry4Aa. Electrophysiologic analysis showed that the S153F, S153L, and S153I mutants form toxin pores with a significantly reduced PK/PNa permeability ratio and a significantly increased PK/PCa permeability ratio compared to wild-type pores. Thus, our results suggest that pore formation is central to the insecticidal activity of Mpp46Ab and that the ion permeability of toxin pores is a potential indicator correlated with both toxicity and synergistic toxicity with other toxins.
en-copyright=
kn-copyright=

en-aut-name=HayakawaTohru
en-aut-sei=Hayakawa
en-aut-mei=Tohru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YamaokaSyun
en-aut-sei=Yamaoka
en-aut-mei=Syun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=AsakuraMami
en-aut-sei=Asakura
en-aut-mei=Mami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HiranoMinako
en-aut-sei=Hirano
en-aut-mei=Minako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=IdeToru
en-aut-sei=Ide
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=4
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=5
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
en-keyword=Bacillus thuringiensis
kn-keyword=Bacillus thuringiensis
en-keyword=mosquito-larvicidal proteins
kn-keyword=mosquito-larvicidal proteins
en-keyword=synergistic toxicity
kn-keyword=synergistic toxicity
en-keyword=Culex pipiens mosquito larvae
kn-keyword=Culex pipiens mosquito larvae
en-keyword=side-directed mutagenesis
kn-keyword=side-directed mutagenesis
en-keyword=electrophysiologic analysis
kn-keyword=electrophysiologic analysis
END

start-ver=1.4
cd-journal=joma
no-vol=35
cd-vols=
no-issue=12
article-no=
start-page=2916
end-page=2926.e3
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202506
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Oxytocin facilitates human touch-induced play behavior in rats
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Pleasant touch sensations play a fundamental role in social bonding, yet the neural mechanisms underlying affinity-like behaviors remain poorly understood. Here, we demonstrate that juvenile-adolescent rats, which naturally engage in social play with peers characterized by rough-and-tumble interactions and 50 kHz ultrasonic vocalizations indicating pleasant sensations, develop a strong affinity for human hands through similar playful contact achieved by repeated tickling with human hands. Using this rat with tickling-induced high affinity for human hands, we discovered that repeated tickling mimicking rough-and-tumble play led to increased oxytocin receptor (OTR) expression in the ventrolateral part of the ventromedial hypothalamus (VMHvl). Inhibition of oxytocin signaling in the VMHvl reduced affinity-like behaviors from rats to human hands. These findings suggest that OTR neurons in VMHvl play an important role in the increase in affinity for human hands induced by pleasant touch sensation with human touch-induced play behavior. Based on retrograde and anterograde tracing studies examining the supraoptic nucleus (SON) and the paraventricular nucleus (PVN) as primary sources of oxytocin, we demonstrate that a subset of oxytocin fibers in the VMHvl originate from the SON, suggesting that affinity-like behavior from rats to human hands may be controlled by oxytocin signaling from magnocellular neurons. Together, this work advances our understanding of how oxytocin shapes social behavior and may inform the development of therapeutic strategies to promote positive social interactions.
en-copyright=
kn-copyright=

en-aut-name=HayashiHimeka
en-aut-sei=Hayashi
en-aut-mei=Himeka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TateishiSayaka
en-aut-sei=Tateishi
en-aut-mei=Sayaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=InutsukaAyumu
en-aut-sei=Inutsuka
en-aut-mei=Ayumu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MaejimaSho
en-aut-sei=Maejima
en-aut-mei=Sho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HagiwaraDaisuke
en-aut-sei=Hagiwara
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SakumaYasuo
en-aut-sei=Sakuma
en-aut-mei=Yasuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=OnakaTatsushi
en-aut-sei=Onaka
en-aut-mei=Tatsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=GrinevichValery
en-aut-sei=Grinevich
en-aut-mei=Valery
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=SakamotoHirotaka
en-aut-sei=Sakamoto
en-aut-mei=Hirotaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Biology, Faculty of Environmental, Life, Natural Science and Technology, Okayama University,
kn-affil=

affil-num=2
en-affil=Ushimado Marine Institute (UMI), Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=3
en-affil=Division of Brain and Neurophysiology, Department of Physiology, Jichi Medical University
kn-affil=

affil-num=4
en-affil=Ushimado Marine Institute (UMI), Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Neuropeptide Research in Psychiatry, Central Institute of Mental Health, German Center for Psychiatry (DZPG), Medical Faculty Mannheim, University of Heidelberg
kn-affil=

affil-num=6
en-affil=Department of Anatomy and Neurobiology, Graduate School of Medical Sciences, Nippon Medical School
kn-affil=

affil-num=7
en-affil=Division of Brain and Neurophysiology, Department of Physiology, Jichi Medical University
kn-affil=

affil-num=8
en-affil=Department of Neuropeptide Research in Psychiatry, Central Institute of Mental Health, German Center for Psychiatry (DZPG), Medical Faculty Mannheim, University of Heidelberg
kn-affil=

affil-num=9
en-affil=Department of Biology, Faculty of Environmental, Life, Natural Science and Technology, Okayama University,
kn-affil=
en-keyword=tickling
kn-keyword=tickling
en-keyword=oxytocin
kn-keyword=oxytocin
en-keyword=oxytocin receptor
kn-keyword=oxytocin receptor
en-keyword=ventrolateral part of the ventromedial hypothalamus
kn-keyword=ventrolateral part of the ventromedial hypothalamus
en-keyword=affinity-like behaviors
kn-keyword=affinity-like behaviors
END

start-ver=1.4
cd-journal=joma
no-vol=14
cd-vols=
no-issue=7
article-no=
start-page=808
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250630
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Carnosol, a Rosemary Ingredient Discovered in a Screen for Inhibitors of SARM1-NAD+ Cleavage Activity, Ameliorates Symptoms of Peripheral Neuropathy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Sterile alpha and Toll/interleukin receptor motif-containing protein 1 (SARM1) is a nicotinamide adenine dinucleotide (NAD+) hydrolase involved in axonal degeneration and neuronal cell death. SARM1 plays a pivotal role in triggering the neurodegenerative processes that underlie peripheral neuropathies, traumatic brain injury, and neurodegenerative diseases. Importantly, SARM1 knockdown or knockout prevents the degeneration; as a result, SARM1 has been attracting attention as a potent therapeutic target. In recent years, the development of several SARM1 inhibitors derived from synthetic chemical compounds has been reported; however, no dietary ingredients with SARM1 inhibitory activity have been identified. Therefore, we here focused on dietary ingredients and found that carnosol, an antioxidant contained in rosemary, inhibits the NAD+-cleavage activity of SARM1. Purified carnosol inhibited the enzymatic activity of SARM1 and suppressed neurite degeneration and cell death induced by the anti-cancer medicine vincristine (VCR). Carnosol also inhibited VCR-induced hyperalgesia symptoms, suppressed the loss of intra-epidermal nerve fibers in vivo, and reduced the blood fluid level of phosphorylated neurofilament-H caused by an axonal degeneration event. These results indicate that carnosol has a neuroprotective effect via SARM1 inhibition in addition to its previously known antioxidant effect via NF-E2-related factor 2 and thus suppresses neurotoxin-induced peripheral neuropathy.
en-copyright=
kn-copyright=

en-aut-name=MurataHitoshi
en-aut-sei=Murata
en-aut-mei=Hitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OgawaKazuki
en-aut-sei=Ogawa
en-aut-mei=Kazuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YasuiYu
en-aut-sei=Yasui
en-aut-mei=Yu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OchiToshiki
en-aut-sei=Ochi
en-aut-mei=Toshiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TomonobuNahoko
en-aut-sei=Tomonobu
en-aut-mei=Nahoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YamamotoKen-Ichi
en-aut-sei=Yamamoto
en-aut-mei=Ken-Ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KinoshitaRie
en-aut-sei=Kinoshita
en-aut-mei=Rie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=WadaYoji
en-aut-sei=Wada
en-aut-mei=Yoji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=NakamuraHiromichi
en-aut-sei=Nakamura
en-aut-mei=Hiromichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=NishiboriMasahiro
en-aut-sei=Nishibori
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=SakaguchiMasakiyo
en-aut-sei=Sakaguchi
en-aut-mei=Masakiyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

affil-num=1
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Tama Biochemical Co., Ltd.
kn-affil=

affil-num=3
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Tama Biochemical Co., Ltd.
kn-affil=

affil-num=9
en-affil=Tama Biochemical Co., Ltd.
kn-affil=

affil-num=10
en-affil=Department of Translational Research and Drug Development, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=SARM1
kn-keyword=SARM1
en-keyword=carnosol
kn-keyword=carnosol
en-keyword=NAD+
kn-keyword=NAD+
en-keyword=axon degeneration
kn-keyword=axon degeneration
en-keyword=peripheral neuropathy
kn-keyword=peripheral neuropathy
END

start-ver=1.4
cd-journal=joma
no-vol=227
cd-vols=
no-issue=
article-no=
start-page=110168
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202510
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The hidden cation-selective pore in ion-conducting aquaporin OsPIP2;4 from rice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Ion-conducting aquaporins (icAQPs) transport ions as well as water. Although the molecular mechanism of how AQPs establish selective permeability for water molecules is well understood, the ion-transporting mechanism in icAQPs has not yet been fully elucidated. In this study, we investigated the molecular mechanism of cation transport in OsPIP2;4, an icAQP in rice, by homology modeling and the electrophysiological analysis using Xenopus laevis oocytes. Water and ion transport assays using OsPIP2;4 T227M and G278K mutants strongly suggested that water- and cation-transporting pathways are independent of each other. Data from amino acid substitutions V54I and A143G in OsPIP2;4 led to the identification of a novel hidden pathway for cation transport located on the side surfaces of the tetramer channel, where two protomers are in contact, which is distinct from conventional monomeric pores and the tetrameric central pore in AQPs. Moreover, the present results provide the possibility that this hypothetical hidden pore also functions in the barley icAQP HvPIP2;8. The overall structure of this novel pathway appears to differ from the structure of general cation channels. However, the arrangement of hydrophilic amino acids at the entrance of the pathway of OsPIP2;4 was found to be comparable to that of some cation channels, which implies that the molecular mechanism of dehydration of hydrated ions might resemble that of the channels. Although direct structural evidence is needed to confirm the proposed pathway, the present study can be a stepping stone toward unraveling the mechanism of dual water and ion transport through icAQPs in plants.
en-copyright=
kn-copyright=

en-aut-name=OnoShuntaro
en-aut-sei=Ono
en-aut-mei=Shuntaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TranSen Thi Huong
en-aut-sei=Tran
en-aut-mei=Sen Thi Huong
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SaitohYasunori
en-aut-sei=Saitoh
en-aut-mei=Yasunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=UtsugiShigeko
en-aut-sei=Utsugi
en-aut-mei=Shigeko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HorieTomoaki
en-aut-sei=Horie
en-aut-mei=Tomoaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KatsuharaMaki
en-aut-sei=Katsuhara
en-aut-mei=Maki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=2
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=3
en-affil=Research Institute for Interdisciplinary Science, Okayama University
kn-affil=

affil-num=4
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=5
en-affil=Division of Applied Biology, Faculty of Textile Science and Technology, Shinshu University
kn-affil=

affil-num=6
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=
en-keyword=Rice
kn-keyword=Rice
en-keyword=Barley
kn-keyword=Barley
en-keyword=Ion transport
kn-keyword=Ion transport
en-keyword=Ion-conducting aquaporin (icAQP)
kn-keyword=Ion-conducting aquaporin (icAQP)
en-keyword=Plasma membrane intrinsic protein (PIP)
kn-keyword=Plasma membrane intrinsic protein (PIP)
END

start-ver=1.4
cd-journal=joma
no-vol=301
cd-vols=
no-issue=7
article-no=
start-page=110291
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202507
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A repertoire of visible light–sensitive opsins in the deep-sea hydrothermal vent shrimp Rimicaris hybisae
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Unlike terrestrial environments, where humans reside, there is no sunlight in the deep sea. Instead, dim visible light from black-body radiation and bioluminescence illuminates hydrothermal vent areas in the deep sea. A deep-sea hydrothermal vent shrimp, Rimicaris hybisae, is thought to detect this dim light using its enlarged dorsal eye; however, the molecular basis of its photoreception remains unexplored. Here, we characterized the molecular properties of opsins, universal photoreceptive proteins in animals, found in R. hybisae. Transcriptomic analysis identified six opsins: three Gq-coupled opsins, one Opn3, one Opn5, and one peropsin. Functional analysis revealed that five of these opsins exhibited light-dependent G protein activity, whereas peropsin exhibited the ability to convert all-trans-retinal to 11-cis-retinal like photoisomerases. Notably, all the R. hybisae opsins, including Opn5, convergently show visible light sensitivity (around 457–517 nm), whereas most opsins categorized as Opn5 have been demonstrated to be UV sensitive. Mutational analysis revealed that the unique visible light sensitivity of R. hybisae Opn5 is achieved through the stabilization of a protonated Schiff base by a counterion residue at position 83 (Asp83), which differs from the position identified in other opsins. These findings suggest that the vent shrimp R. hybisae has adapted its photoreceptive devices to dim deep-sea hydrothermal light by selectively maintaining a repertoire of visible light–sensitive opsins, including the uniquely tuned Opn5.
en-copyright=
kn-copyright=

en-aut-name=NagataYuya
en-aut-sei=Nagata
en-aut-mei=Yuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MiyamotoNorio
en-aut-sei=Miyamoto
en-aut-mei=Norio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SatoKeita
en-aut-sei=Sato
en-aut-mei=Keita
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NishimuraYosuke
en-aut-sei=Nishimura
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TaniokaYuki
en-aut-sei=Tanioka
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YamanakaYuji
en-aut-sei=Yamanaka
en-aut-mei=Yuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YoshizawaSusumu
en-aut-sei=Yoshizawa
en-aut-mei=Susumu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TakahashiKuto
en-aut-sei=Takahashi
en-aut-mei=Kuto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=ObayashiKohei
en-aut-sei=Obayashi
en-aut-mei=Kohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=TsukamotoHisao
en-aut-sei=Tsukamoto
en-aut-mei=Hisao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=TakaiKen
en-aut-sei=Takai
en-aut-mei=Ken
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=OhuchiHideyo
en-aut-sei=Ohuchi
en-aut-mei=Hideyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=YamashitaTakahiro
en-aut-sei=Yamashita
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=SudoYuki
en-aut-sei=Sudo
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=KojimaKeiichi
en-aut-sei=Kojima
en-aut-mei=Keiichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

affil-num=1
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Institute for Extra-Cutting-Edge Science and Technology Avant-Garde Research (X-Star), Japan Agency for Marine-Earth Science and Technology (JAMSTEC)
kn-affil=

affil-num=3
en-affil=Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Research Center for Bioscience and Nanoscience (CeBN), Research Institute for Marine Resources Utilization, Japan Agency for Marine-Earth Science and Technology (JAMSTEC)
kn-affil=

affil-num=5
en-affil=School of Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=School of Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Atmosphere and Ocean Research Institute, The University of Tokyo
kn-affil=

affil-num=8
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Biology, Graduate School of Science, Kobe University
kn-affil=

affil-num=10
en-affil=Department of Biology, Graduate School of Science, Kobe University
kn-affil=

affil-num=11
en-affil=Institute for Extra-Cutting-Edge Science and Technology Avant-Garde Research (X-Star), Japan Agency for Marine-Earth Science and Technology (JAMSTEC)
kn-affil=

affil-num=12
en-affil=Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=13
en-affil=Department of Biophysics, Graduate School of Science, Kyoto University
kn-affil=

affil-num=14
en-affil=Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=15
en-affil=Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=rhodopsin
kn-keyword=rhodopsin
en-keyword=opsin
kn-keyword=opsin
en-keyword=G protein–coupled receptor
kn-keyword=G protein–coupled receptor
en-keyword=signal transduction
kn-keyword=signal transduction
en-keyword=photoreceptor
kn-keyword=photoreceptor
en-keyword=vision
kn-keyword=vision
en-keyword=photobiology
kn-keyword=photobiology
en-keyword=vent shrimp
kn-keyword=vent shrimp
en-keyword=deep sea
kn-keyword=deep sea
en-keyword=molecular evolution
kn-keyword=molecular evolution
END

start-ver=1.4
cd-journal=joma
no-vol=166
cd-vols=
no-issue=8
article-no=
start-page=bqaf102
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250605
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Neuromedin U Deficiency Disrupts Daily Testosterone Fluctuation and Reduces Wheel-running Activity in Rats
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The objective of this study was to elucidate the role of endogenous Neuromedin U (NMU) in rats by performing NMU knockout (KO). Male, but not female NMU KO rats exhibited decreased wheel-running activity vs wildtype (WT), although overall home cage activity was not affected. Plasma testosterone in WT rats varied significantly over the course of a day, with a peak at ZT1 and a nadir at ZT18, whereas in NMU KO rats testosterone remained stable throughout the day. Chronic administration of testosterone restored wheel-running activity in NMU KO rats to the same level as in WT rats, suggesting that the decrease in wheel-running activity in NMU KO rats is due to the disruption of the diurnal change of testosterone. Accordingly, expression of the luteinizing hormone beta subunit (Lhb) mRNA in the pars distalis of anterior pituitary was significantly lower in NMU KO rats; immunostaining revealed that the size of luteinizing hormone (LH)–expressing cells was also relatively small in those animals. In the brain of male WT rats, Nmu was highly expressed in the pars tuberalis, and the NMU receptor Nmur2 was highly expressed in the ependymal cell layer of the third ventricle. This study reveals a novel function of NMU and indicates that endogenous NMU in rats plays a role in the regulation of motivated activity via regulation of testosterone.
en-copyright=
kn-copyright=

en-aut-name=OtsukaMai
en-aut-sei=Otsuka
en-aut-mei=Mai
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakeuchiYu
en-aut-sei=Takeuchi
en-aut-mei=Yu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MoriyamaMaho
en-aut-sei=Moriyama
en-aut-mei=Maho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=EgoshiSakura
en-aut-sei=Egoshi
en-aut-mei=Sakura
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=GotoYuki
en-aut-sei=Goto
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=GuTingting
en-aut-sei=Gu
en-aut-mei=Tingting
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KimuraAtsushi P
en-aut-sei=Kimura
en-aut-mei=Atsushi P
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=HaraguchiShogo
en-aut-sei=Haraguchi
en-aut-mei=Shogo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=YoshiiTaishi
en-aut-sei=Yoshii
en-aut-mei=Taishi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=TakeuchiSakae
en-aut-sei=Takeuchi
en-aut-mei=Sakae
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=MatsuyamaMakoto
en-aut-sei=Matsuyama
en-aut-mei=Makoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=BentleyGeorge E
en-aut-sei=Bentley
en-aut-mei=George E
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=AizawaSayaka
en-aut-sei=Aizawa
en-aut-mei=Sayaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

affil-num=1
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Biology, Faculty of Science, Okayama University
kn-affil=

affil-num=5
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=6
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Biological Sciences, Faculty of Science, Hokkaido University
kn-affil=

affil-num=8
en-affil=Department of Biochemistry, Showa University School of Medicine
kn-affil=

affil-num=9
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=10
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=11
en-affil=Division of Molecular Genetics, Shigei Medical Research Institute
kn-affil=

affil-num=12
en-affil=Department of Integrative Biology and Helen Wills Neuroscience Institute, University of California at Berkeley
kn-affil=

affil-num=13
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=
en-keyword=Neuromedin U
kn-keyword=Neuromedin U
en-keyword=rat
kn-keyword=rat
en-keyword=motivation
kn-keyword=motivation
en-keyword=activity
kn-keyword=activity
en-keyword=testosterone
kn-keyword=testosterone
en-keyword=wheel-running
kn-keyword=wheel-running
END

start-ver=1.4
cd-journal=joma
no-vol=64
cd-vols=
no-issue=5
article-no=
start-page=759
end-page=762
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250301
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A Novel De Novo Variant in KCNH5 in a Patient with Refractory Epileptic Encephalopathy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=We herein report a novel de novo KCNH5 variant in a patient with refractory epileptic encephalopathy. The patient exhibited seizures at 1 year and 7 months old, which gradually worsened, leading to a bedridden status. Brain magnetic resonance imaging (MRI) showed cerebral atrophy and cerebellar hypoplasia. A trio whole-exome sequence analysis identified a de novo heterozygous c.640A>C, p.Lys214Gln variant in KCNH5 that was predicted to be deleterious. Recent studies have linked KCNH5 to various epileptic encephalopathies, with many patients showing normal MRI findings. The present case expands the clinical spectrum of the disease, as it is characterized by severe neurological prognosis, cerebral atrophy, and cerebellar hypoplasia.
en-copyright=
kn-copyright=

en-aut-name=MitsutakeAkihiko
en-aut-sei=Mitsutake
en-aut-mei=Akihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MatsukawaTakashi
en-aut-sei=Matsukawa
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NaitoTatsuhiko
en-aut-sei=Naito
en-aut-mei=Tatsuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=IshiuraHiroyuki
en-aut-sei=Ishiura
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MitsuiJun
en-aut-sei=Mitsui
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=HaradaHiroaki
en-aut-sei=Harada
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=FujioKeishi
en-aut-sei=Fujio
en-aut-mei=Keishi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=FujishiroJun
en-aut-sei=Fujishiro
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MoriHarushi
en-aut-sei=Mori
en-aut-mei=Harushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=MorishitaShinichi
en-aut-sei=Morishita
en-aut-mei=Shinichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=TsujiShoji
en-aut-sei=Tsuji
en-aut-mei=Shoji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=TodaTatsushi
en-aut-sei=Toda
en-aut-mei=Tatsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

affil-num=1
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=2
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=3
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=4
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=6
en-affil=Department of Rheumatology and Allergy, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=7
en-affil=Department of Rheumatology and Allergy, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=8
en-affil=Department of Pediatric Surgery, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=9
en-affil=Department of Radiology, School of Medicine, Jichi Medical University
kn-affil=

affil-num=10
en-affil=Department of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo
kn-affil=

affil-num=11
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=12
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=
en-keyword=epileptic encephalopathy
kn-keyword=epileptic encephalopathy
en-keyword=whole-exome sequencing
kn-keyword=whole-exome sequencing
en-keyword=KCNH5
kn-keyword=KCNH5
en-keyword=de novo variant
kn-keyword=de novo variant
END

start-ver=1.4
cd-journal=joma
no-vol=58
cd-vols=
no-issue=2
article-no=
start-page=145
end-page=148
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250630
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The trochlea for the intermediate tendon of the digastric muscle: a review
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=This review explores the novel perspective that the intermediate tendon of the digastric muscle may function as an anatomical trochlear pulley system within the human body, challenging the traditional understanding of trochlear systems. While widely recognized trochlear units include structures like the medial part of the humerus and the superior oblique muscle of the orbit, the review focuses on the unique anatomical arrangement of the intermediate tendon of the digastric muscle in connection with the anterior and posterior bellies of the digastric muscles. Despite current debates within the anatomical community about labeling the digastric muscles as having a trochlea, this paper delves into the scientific definition of a trochlear pulley system, presenting the intermediate tendon of the digastric muscle as a potential trochlea.
en-copyright=
kn-copyright=

en-aut-name=du PlooyXander
en-aut-sei=du Plooy
en-aut-mei=Xander
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KunisadaYuki
en-aut-sei=Kunisada
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=CardonaJuan J.
en-aut-sei=Cardona
en-aut-mei=Juan J.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TabiraYoko
en-aut-sei=Tabira
en-aut-mei=Yoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=BubbKathleen Carol
en-aut-sei=Bubb
en-aut-mei=Kathleen Carol
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=RaeburnKazzara
en-aut-sei=Raeburn
en-aut-mei=Kazzara
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=IbaragiSoichiro
en-aut-sei=Ibaragi
en-aut-mei=Soichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=IwanagaJoe
en-aut-sei=Iwanaga
en-aut-mei=Joe
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TubbsR. Shane
en-aut-sei=Tubbs
en-aut-mei=R. Shane
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Tulane University School of Medicine
kn-affil=

affil-num=2
en-affil=Department of Oral and Maxillofacial Surgery, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Neurosurgery, Tulane Center for Clinical Neurosciences, Tulane University School of Medicine
kn-affil=

affil-num=4
en-affil=Division of Gross and Clinical Anatomy, Department of Anatomy, Kurume University School of Medicine
kn-affil=

affil-num=5
en-affil=Anatomy Division, Department of Radiology, Weill Cornell Medical College
kn-affil=

affil-num=6
en-affil=Department of Anatomical Sciences, St. George’s University
kn-affil=

affil-num=7
en-affil=Department of Oral and Maxillofacial Surgery, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Neurosurgery, Tulane Center for Clinical Neurosciences, Tulane University School of Medicine
kn-affil=

affil-num=9
en-affil=Department of Neurosurgery, Tulane Center for Clinical Neurosciences, Tulane University School of Medicine
kn-affil=
en-keyword=Digastric muscles
kn-keyword=Digastric muscles
en-keyword=Intermediate tendon
kn-keyword=Intermediate tendon
en-keyword=Trochlea
kn-keyword=Trochlea
en-keyword=Anatomy
kn-keyword=Anatomy
en-keyword=Fascia
kn-keyword=Fascia
END

start-ver=1.4
cd-journal=joma
no-vol=12
cd-vols=
no-issue=1
article-no=
start-page=5
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250228
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=In-frame deletion variant of ABCD1 in a sporadic case of adrenoleukodystrophy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Adrenoleukodystrophy (ALD), an X-linked leukodystrophy caused by pathogenic variants in ABCD1, exhibits a broad range of phenotypes from childhood-onset cerebral forms to adult-onset adrenomyeloneuropathy (AMN). We report a rare in-frame ABCD1 deletion c.1469_71delTGG (p.Val490del) in a man with AMN. Although this variant has been interpreted as ‘uncertain significance’ in ClinVar, biochemical analysis along with clinical evaluation confirmed the pathogenicity of this variant, underscoring the importance of functional assessment of in-frame deletions.
en-copyright=
kn-copyright=

en-aut-name=MatsukawaTakashi
en-aut-sei=Matsukawa
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SudoAtsushi
en-aut-sei=Sudo
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KakumotoToshiyuki
en-aut-sei=Kakumoto
en-aut-mei=Toshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HaoAkihito
en-aut-sei=Hao
en-aut-mei=Akihito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KainagaMitsuhiro
en-aut-sei=Kainaga
en-aut-mei=Mitsuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ChangHyangri
en-aut-sei=Chang
en-aut-mei=Hyangri
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=ManoTatsuo
en-aut-sei=Mano
en-aut-mei=Tatsuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=IshiuraHiroyuki
en-aut-sei=Ishiura
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MitsuiJun
en-aut-sei=Mitsui
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=HayashiToshihiro
en-aut-sei=Hayashi
en-aut-mei=Toshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=MorishitaShinichi
en-aut-sei=Morishita
en-aut-mei=Shinichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=TsujiShoji
en-aut-sei=Tsuji
en-aut-mei=Shoji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=TodaTatsushi
en-aut-sei=Toda
en-aut-mei=Tatsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

affil-num=1
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=2
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=3
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=4
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=5
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=6
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=7
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=8
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Precision Medicine Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=10
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=11
en-affil=Department of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo
kn-affil=

affil-num=12
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=13
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250616
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Leg-biting fights reduce the number of sperm transferred by the loser and in draws in Zophobas atratus
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Intra-sexual selection has been observed across a wide range of species. Male-male combat can not only determine the winner and loser but also affect subsequent reproductive success. The effects of combat outcomes on reproduction are thought to depend on the reproductive ecology of the target species. However, to our knowledge, studies examining the impact of combat outcomes on sperm competition and fitness remain limited. In the giant mealworm (Zophobas atratus), male’s combat involves biting each other's hind legs. Females mated to the losers of leg-biting contests had significantly fewer eggs and fewer offspring than females mated to males that were not in a contest. Possible explanations for this fitness reduction include the inability of males to transfer sperm effectively due to the combat outcome or the inability of their sperm to fertilize eggs due to female cryptic sperm choice, and the mechanisms underlying this reduction remain unclear. Previous studies have observed distorted mating postures in losing males, leading us to hypothesize that leg-biting during combat might affect sperm transfer. To test this, we allowed uncontested males, winners, losers, and males with a draw outcome to mate with females and compared the number of sperm within the female’s spermatheca. Additionally, we examined the correlation between combat duration and sperm count. Results showed that losers and males with draw transferred fewer sperm than non-combat males. Moreover, the longer the combat duration, the fewer sperm males were able to transfer. These findings suggest that the reduction in sperm transferred was affected by both losing in combat and prolonged combat duration in leg-biting encounters.
en-copyright=
kn-copyright=

en-aut-name=MatsuuraTeruhisa
en-aut-sei=Matsuura
en-aut-mei=Teruhisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MiyatakeTakahisa
en-aut-sei=Miyatake
en-aut-mei=Takahisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

affil-num=1
en-affil=Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=
en-keyword=Male combat
kn-keyword=Male combat
en-keyword=Male-male competition
kn-keyword=Male-male competition
en-keyword=Sperm transfer
kn-keyword=Sperm transfer
en-keyword=Sperm biology
kn-keyword=Sperm biology
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250609
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The maxillary vein: an anatomical narrative review with clinical implications for oral and maxillofacial surgeons
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The maxillary vein, despite its clinical significance, remains underexplored in anatomical literature. It plays a crucial role in venous drainage of the maxillofacial region and is closely associated with surgical procedures such as sagittal split ramus osteotomy, mandibuloplasty, and condylar or parotid surgeries. Due to its variable anatomy and proximity to critical structures, the maxillary vein poses a risk of significant hemorrhage if injured. Its small size and deep location make preoperative identification challenging, especially without contrast-enhanced imaging. Embryologically, the maxillary vein originates from the primitive maxillary vein and develops through complex anastomoses with other craniofacial veins. Anatomical studies have revealed several variations, including the presence of accessory mandibular foramina and unusual venous connections, which may increase surgical risk. Understanding the detailed anatomy and potential variations of the maxillary vein is essential for minimizing complications and improving surgical outcomes. Despite its importance, more anatomical and clinical research is needed to better define its course, variations, and implications in oral and maxillofacial surgery.
en-copyright=
kn-copyright=

en-aut-name=RaeburnKazzara
en-aut-sei=Raeburn
en-aut-mei=Kazzara
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakeshitaYohei
en-aut-sei=Takeshita
en-aut-mei=Yohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TakakuraHiroaki
en-aut-sei=Takakura
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KikutaShogo
en-aut-sei=Kikuta
en-aut-mei=Shogo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KunisadaYuki
en-aut-sei=Kunisada
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=IbaragiSoichiro
en-aut-sei=Ibaragi
en-aut-mei=Soichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SamridRarinthorn
en-aut-sei=Samrid
en-aut-mei=Rarinthorn
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=LoukasMarios
en-aut-sei=Loukas
en-aut-mei=Marios
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TubbsR. Shane
en-aut-sei=Tubbs
en-aut-mei=R. Shane
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=IwanagaJoe
en-aut-sei=Iwanaga
en-aut-mei=Joe
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of Anatomical Sciences, St. George’s University
kn-affil=

affil-num=2
en-affil=Department of Oral and Maxillofacial Radiology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Oral and Maxillofacial Surgery, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Dental and Oral Medical Center, Kurume University School of Medicine
kn-affil=

affil-num=5
en-affil=Department of Oral and Maxillofacial Surgery, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Oral and Maxillofacial Surgery, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=
kn-affil=

affil-num=8
en-affil=Department of Anatomical Sciences, St. George’s University
kn-affil=

affil-num=9
en-affil=Department of Anatomical Sciences, St. George’s University
kn-affil=

affil-num=10
en-affil=Dental and Oral Medical Center, Kurume University School of Medicine
kn-affil=
en-keyword=Embryology
kn-keyword=Embryology
en-keyword=Anatomy
kn-keyword=Anatomy
en-keyword=Radiology
kn-keyword=Radiology
en-keyword=Cadaver
kn-keyword=Cadaver
en-keyword=Mandible
kn-keyword=Mandible
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250526
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Lytic Transglycosylase Deficiency Increases Susceptibility to β-lactam Antibiotics But Reduces Susceptibility to Vancomycin in Escherichia coli
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=In Staphylococcus aureus, a gram-positive pathogen, vancomycin-resistant strains become susceptible to β-lactam antibiotics, referred to as the “seesaw effect.” However, in gram-negative bacteria, the phenomenon is less clear. Here, we analyzed the gene-knockout effects of eight lytic transglycosylases (slt, mltA, mltB, mltC, mltD, mltE, mltF, mltG) on antibiotic sensitivity in Escherichia coli. Knockout of both slt and mltG increased sensitivity to β-lactam antibiotics and reduced sensitivity to vancomycin. The β-lactam antibiotic sensitivity and vancomycin resistance of the slt-knockout mutant were abolished by the introduction of the wild-type slt gene but remained unchanged by the introduction of the mutant slt gene encoding an amino acid substitution variant of the transglycosylase catalytic centre. The double-knockout strain for slt and mltB was more sensitive to ampicillin and more resistant to vancomycin than each single-knockout strain. The double-knockout strain for slt and mltG was more sensitive to ampicillin and more resistant to vancomycin than each single-knockout strain. These results suggest that loss of lytic transglycosylase activity causes β-lactam antibiotic sensitivity and vancomycin resistance in E. coli.
en-copyright=
kn-copyright=

en-aut-name=KimuraTakahiko
en-aut-sei=Kimura
en-aut-mei=Takahiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=IshikawaKazuya
en-aut-sei=Ishikawa
en-aut-mei=Kazuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NakagawaRyosuke
en-aut-sei=Nakagawa
en-aut-mei=Ryosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=FurutaKazuyuki
en-aut-sei=Furuta
en-aut-mei=Kazuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KaitoChikara
en-aut-sei=Kaito
en-aut-mei=Chikara
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Laboratory of Molecular Biology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Laboratory of Molecular Biology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Laboratory of Molecular Biology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Laboratory of Molecular Biology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Laboratory of Molecular Biology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Escherichia coli
kn-keyword=Escherichia coli
en-keyword=lytic transglycosylase
kn-keyword=lytic transglycosylase
en-keyword=seesaw effect
kn-keyword=seesaw effect
en-keyword=vancomycin
kn-keyword=vancomycin
en-keyword=β‐lactam antibiotics
kn-keyword=β‐lactam antibiotics
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=上顎洞に認められた扁平上皮癌および非扁平上皮癌のCT画像の評価
kn-title=Evaluation of CT Findings in Squamous and Non-Squamous Cell Carcinomas of the Maxillary Sinus
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=ASAUMIYuka
en-aut-sei=ASAUMI
en-aut-mei=Yuka
kn-aut-name=浅海結華
kn-aut-sei=浅海
kn-aut-mei=結華
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=岡山大学大学院医歯薬学総合研究科
END

start-ver=1.4
cd-journal=joma
no-vol=79
cd-vols=
no-issue=3
article-no=
start-page=157
end-page=166
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202506
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Continuous Stimulation with Glycolaldehyde-derived Advanced Glycation End Product Reduces Aggrecan and COL2A1 Production via RAGE in Human OUMS-27 Chondrosarcoma Cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Chondrocytes are responsible for the production of extracellular matrix (ECM) components such as collagen type II alpha-1 (COL2A1) and aggrecan, which are loosely distributed in articular cartilage. Chondrocyte dysfunction has been implicated in the pathogenesis of rheumatic diseases such as osteoarthritis (OA) and rheumatoid arthritis (RA). With age, advanced glycation end products (AGEs) accumulate in all tissues and body fluids, including cartilage and synovial fluid, causing and accelerating pathological changes associated with chronic diseases such as OA. Glycolaldehyde-derived AGE (AGE3), which is toxic to a variety of cell types, have a stronger effect on cartilage compared with other AGEs. To understand the long-term effects of AGE3 on cartilage, we stimulated a human chondrosarcoma cell line (OUMS-27), which exhibits a chondrocytic phenotype, with 10 μg/ml AGE3 for 4 weeks. As a result, the expressions of COL2A1 and aggrecan were significantly downregulated in the OUMS-27 cells without inducing cell death, but the expressions of proteases that play an important role in cartilage destruction were not affected. Inhibition of the receptor for advanced glycation end products (RAGE) suppressed the AGE3-induced reduction in cartilage component production, suggesting the involvement of RAGE in the action of AGE3.
en-copyright=
kn-copyright=

en-aut-name=HatipogluOmer Faruk
en-aut-sei=Hatipoglu
en-aut-mei=Omer Faruk
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NishinakaTakashi
en-aut-sei=Nishinaka
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YaykasliKursat Oguz
en-aut-sei=Yaykasli
en-aut-mei=Kursat Oguz
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MoriShuji
en-aut-sei=Mori
en-aut-mei=Shuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=WatanabeMasahiro
en-aut-sei=Watanabe
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ToyomuraTakao
en-aut-sei=Toyomura
en-aut-mei=Takao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NishiboriMasahiro
en-aut-sei=Nishibori
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=HirohataSatoshi
en-aut-sei=Hirohata
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TakahashiHideo
en-aut-sei=Takahashi
en-aut-mei=Hideo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=WakeHidenori
en-aut-sei=Wake
en-aut-mei=Hidenori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of Pharmacology, Faculty of Medicine, Kindai University
kn-affil=

affil-num=2
en-affil=Department of Pharmacology, Faculty of Medicine, Kindai University
kn-affil=

affil-num=3
en-affil=Department of Internal Medicine 3-Rheumatology and Immunology, Friedrich-Alexander-University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen
kn-affil=

affil-num=4
en-affil=Department of Pharmacology, School of Pharmacy, Shujitsu University
kn-affil=

affil-num=5
en-affil=Department of Pharmacology, School of Pharmacy, Shujitsu University
kn-affil=

affil-num=6
en-affil=Department of Pharmacology, School of Pharmacy, Shujitsu University
kn-affil=

affil-num=7
en-affil=Department of Translational Research & Dug Development, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Medical Technology, Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Pharmacology, Faculty of Medicine, Kindai University
kn-affil=

affil-num=10
en-affil=Department of Pharmacology, Faculty of Medicine, Kindai University
kn-affil=
en-keyword=advanced glycation end product
kn-keyword=advanced glycation end product
en-keyword=aging
kn-keyword=aging
en-keyword=cartilage
kn-keyword=cartilage
en-keyword=collagen
kn-keyword=collagen
en-keyword=aggrecan
kn-keyword=aggrecan
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250501
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Xenopus laevis as an infection model for human pathogenic bacteria
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Animal infection models are essential for understanding bacterial pathogenicity and corresponding host immune responses. In this study, we investigated whether juvenile Xenopus laevis could be used as an infection model for human pathogenic bacteria. Xenopus frogs succumbed to intraperitoneal injection containing the human pathogenic bacteria Staphylococcus aureus, Pseudomonas aeruginosa, and Listeria monocytogenes. In contrast, non-pathogenic bacteria Bacillus subtilis and Escherichia coli did not induce mortality in Xenopus frogs. The administration of appropriate antibiotics suppressed mortality caused by S. aureus and P. aeruginosa. Strains lacking the agr locus, cvfA (rny) gene, or hemolysin genes in S. aureus, LIPI-1-deleted mutant of L. monocytogenes, which attenuate virulence within mammals, exhibited reduced virulence in Xenopus frogs compared with their respective wild-type counterparts. Bacterial distribution analysis revealed that S. aureus persisted in the blood, liver, heart, and muscles of Xenopus frogs until death. These results suggested that intraperitoneal injection of human pathogenic bacteria induces sepsis-like symptoms in Xenopus frogs, supporting their use as a valuable animal model for evaluating antimicrobial efficacy and identifying virulence genes in various human pathogenic bacteria.
en-copyright=
kn-copyright=

en-aut-name=KuriuAyano
en-aut-sei=Kuriu
en-aut-mei=Ayano
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=IshikawaKazuya
en-aut-sei=Ishikawa
en-aut-mei=Kazuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TsuchiyaKohsuke
en-aut-sei=Tsuchiya
en-aut-mei=Kohsuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=FurutaKazuyuki
en-aut-sei=Furuta
en-aut-mei=Kazuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KaitoChikara
en-aut-sei=Kaito
en-aut-mei=Chikara
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Division of Molecular Biology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Division of Molecular Biology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Division of Immunology and Molecular Biology, Cancer Research Institute, Kanazawa University
kn-affil=

affil-num=4
en-affil=Division of Molecular Biology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Division of Molecular Biology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=animal infection model
kn-keyword=animal infection model
en-keyword=Staphylococcus aureus
kn-keyword=Staphylococcus aureus
en-keyword=Listeria monocytogenes
kn-keyword=Listeria monocytogenes
en-keyword=Pseudomonas aeruginosa
kn-keyword=Pseudomonas aeruginosa
en-keyword=antibiotics efficacy
kn-keyword=antibiotics efficacy
en-keyword=virulence genes
kn-keyword=virulence genes
en-keyword=hemolysin
kn-keyword=hemolysin
END

start-ver=1.4
cd-journal=joma
no-vol=8
cd-vols=
no-issue=1
article-no=
start-page=715
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250508
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=TRPV2 mediates stress resilience in mouse cardiomyocytes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The heart dynamically compensates for haemodynamic stress, but how this resilience forms during cardiac growth is not clear. Using a temporally inducible, cardiac-specific knockout in mice we show that the Transient receptor potential vanilloid family 2 (TRPV2) channel is crucial for the maturation of cardiomyocyte stress resilience. TRPV2 defects in growing hearts lead to small morphology, abnormal intercalated discs, weak contractility, and low expression of serum response factor and Insulin-like growth factor-1 (IGF-1) signalling. Individual cardiomyocytes of TRPV2-deficient hearts show reduced contractility with abnormal Ca2+ handling. In cultured neonatal cardiomyocytes, mechanical Ca2+ response, excitation-contraction coupling, sarcoplasmic reticulum Ca2+ content, actin formation, nuclear localisation of Myocyte enhancer factor 2c, and IGF-1 expression require TRPV2. TRPV2-deficient hearts show a defective response to dobutamine stress and no compensatory hypertrophic response to phenylephrine administration, but no stress response to pressure overload. These data suggest TRPV2 mediates the maturation of cardiomyocyte stress resilience, and will advance therapeutic interventions and drug discovery for heart disease.
en-copyright=
kn-copyright=

en-aut-name=DongYubing
en-aut-sei=Dong
en-aut-mei=Yubing
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=WangGuohao
en-aut-sei=Wang
en-aut-mei=Guohao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=UjiharaYoshihiro
en-aut-sei=Ujihara
en-aut-mei=Yoshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ChenYanzhu
en-aut-sei=Chen
en-aut-mei=Yanzhu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YoshidaMasashi
en-aut-sei=Yoshida
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KatanosakaKimiaki
en-aut-sei=Katanosaka
en-aut-mei=Kimiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NaruseKeiji
en-aut-sei=Naruse
en-aut-mei=Keiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KatanosakaYuki
en-aut-sei=Katanosaka
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Electrical and Mechanical Engineering, Graduate School of Engineering, Nagoya Institute of Technology
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Chronic Kidney Disease and Cardiovascular Disease, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Medicine, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Biomedical Sciences, College of Life and Health Sciences, Chubu University
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=1
article-no=
start-page=10462
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250326
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Gingipain regulates isoform switches of PD-L1 in macrophages infected with Porphyromonas gingivalis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Periodontal pathogen Porphyromonas gingivalis (P. gingivalis) is believed to possess immune evasion capabilities, but it remains unclear whether this immune evasion is related to host gene alternative splicing (AS). In this study, RNA-sequencing revealed significant changes in both AS landscape and transcriptomic profile of macrophages following P. gingivalis infection with/without knockout of gingipain (a unique toxic protease of P. gingivalis). P. gingivalis infection increased the PD-L1 transcripts expression and selectively upregulated a specific coding isoform that more effectively binds to PD-1 on T cells, thereby inhibiting immune function. Biological experiments also detected AS switch of PD-L1 in P. gingivalis-infected or gingipain-treated macrophages. AlphaFold 3 predictions indicated that the protein docking compatibility between PD-1 and P. gingivalis-upregulated PD-L1 isoform was over 80% higher than another coding isoform. These findings suggest that P. gingivalis employs gingipain to modulate the AS of PD-L1, facilitating immune evasion.
en-copyright=
kn-copyright=

en-aut-name=ZhengYilin
en-aut-sei=Zheng
en-aut-mei=Yilin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=WangZiyi
en-aut-sei=Wang
en-aut-mei=Ziyi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=WengYao
en-aut-sei=Weng
en-aut-mei=Yao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SitosariHeriati
en-aut-sei=Sitosari
en-aut-mei=Heriati
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HeYuhan
en-aut-sei=He
en-aut-mei=Yuhan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ZhangXiu
en-aut-sei=Zhang
en-aut-mei=Xiu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=ShiotsuNoriko
en-aut-sei=Shiotsu
en-aut-mei=Noriko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=FukuharaYoko
en-aut-sei=Fukuhara
en-aut-mei=Yoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=IkegameMika
en-aut-sei=Ikegame
en-aut-mei=Mika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=OkamuraHirohiko
en-aut-sei=Okamura
en-aut-mei=Hirohiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of Oral Morphology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Hospital, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Molecular Biology and Biochemistry, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Oral Morphology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Hospital, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Oral Morphology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Hospital, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Oral Morphology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Hospital, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Oral Morphology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Hospital, Okayama University
kn-affil=

affil-num=7
en-affil=Comprehensive Dental Clinic, Okayama University Hospital, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Oral Morphology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Hospital, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Oral Morphology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Hospital, Okayama University
kn-affil=

affil-num=10
en-affil=Department of Oral Morphology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Hospital, Okayama University
kn-affil=
en-keyword=Porphyromonas gingivalis
kn-keyword=Porphyromonas gingivalis
en-keyword=Gingipain
kn-keyword=Gingipain
en-keyword=Macrophage
kn-keyword=Macrophage
en-keyword=Alternative splicing
kn-keyword=Alternative splicing
en-keyword=PD-L1
kn-keyword=PD-L1
en-keyword=Immune evasion
kn-keyword=Immune evasion
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=6
article-no=
start-page=790
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250320
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Improving Diagnostic Performance for Head and Neck Tumors with Simple Diffusion Kurtosis Imaging and Machine Learning Bi-Parameter Analysis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background/Objectives: Mean kurtosis (MK) values in simple diffusion kurtosis imaging (SDI)-a type of diffusion kurtosis imaging (DKI)-have been reported to be useful in the diagnosis of head and neck malignancies, for which pre-processing with smoothing filters has been reported to improve the diagnostic accuracy. Multi-parameter analysis using DKI in combination with other image types has recently been reported to improve the diagnostic performance. The purpose of this study was to evaluate the usefulness of machine learning (ML)-based multi-parameter analysis using the MK and apparent diffusion coefficient (ADC) values-which can be acquired simultaneously through SDI-for the differential diagnosis of benign and malignant head and neck tumors, which is important for determining the treatment strategy, as well as examining the usefulness of filter pre-processing. Methods: A total of 32 pathologically diagnosed head and neck tumors were included in the study, and a Gaussian filter was used for image pre-processing. MK and ADC values were extracted from pixels within the tumor area and used as explanatory variables. Five ML algorithms were used to create models for the prediction of tumor status (benign or malignant), which were evaluated through ROC analysis. Results: Bi-parameter analysis with gradient boosting achieved the best diagnostic performance, with an AUC of 0.81. Conclusions: The usefulness of bi-parameter analysis with ML methods for the differential diagnosis of benign and malignant head and neck tumors using SDI data were demonstrated.
en-copyright=
kn-copyright=

en-aut-name=YoshidaSuzuka
en-aut-sei=Yoshida
en-aut-mei=Suzuka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KurodaMasahiro
en-aut-sei=Kuroda
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NakamuraYoshihide
en-aut-sei=Nakamura
en-aut-mei=Yoshihide
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=FukumuraYuka
en-aut-sei=Fukumura
en-aut-mei=Yuka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NakamitsuYuki
en-aut-sei=Nakamitsu
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=Al-HammadWlla E.
en-aut-sei=Al-Hammad
en-aut-mei=Wlla E.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KurodaKazuhiro
en-aut-sei=Kuroda
en-aut-mei=Kazuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=ShimizuYudai
en-aut-sei=Shimizu
en-aut-mei=Yudai
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TanabeYoshinori
en-aut-sei=Tanabe
en-aut-mei=Yoshinori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=OitaMasataka
en-aut-sei=Oita
en-aut-mei=Masataka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=SugiantoIrfan
en-aut-sei=Sugianto
en-aut-mei=Irfan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=BarhamMajd
en-aut-sei=Barham
en-aut-mei=Majd
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=TekikiNouha
en-aut-sei=Tekiki
en-aut-mei=Nouha
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=KamaruddinNurul N.
en-aut-sei=Kamaruddin
en-aut-mei=Nurul N.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=HisatomiMiki
en-aut-sei=Hisatomi
en-aut-mei=Miki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=YanagiYoshinobu
en-aut-sei=Yanagi
en-aut-mei=Yoshinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=AsaumiJunichi
en-aut-sei=Asaumi
en-aut-mei=Junichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

affil-num=1
en-affil=Department of Oral and Maxillofacial Radiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Radiological Technology, Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Oral and Maxillofacial Radiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Oral and Maxillofacial Radiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Radiological Technology, Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Oral and Maxillofacial Radiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Radiological Technology, Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Oral and Maxillofacial Radiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Radiological Technology, Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=10
en-affil=Graduate School of Interdisciplinary Sciences and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=11
en-affil=Department of Oral Radiology, Faculty of Dentistry, Hasanuddin University
kn-affil=

affil-num=12
en-affil=Department of Dentistry and Dental Surgery, College of Medicine and Health Sciences, An-Najah National University
kn-affil=

affil-num=13
en-affil=Department of Oral and Maxillofacial Radiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=14
en-affil=Department of Oral Rehabilitation and Regenerative Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=15
en-affil=Department of Oral and Maxillofacial Radiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=16
en-affil=Department of Oral and Maxillofacial Radiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=17
en-affil=Department of Oral and Maxillofacial Radiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=head and neck tumors
kn-keyword=head and neck tumors
en-keyword=mean kurtosis
kn-keyword=mean kurtosis
en-keyword=simple diffusion kurtosis imaging
kn-keyword=simple diffusion kurtosis imaging
en-keyword=magnetic resonance imaging
kn-keyword=magnetic resonance imaging
en-keyword=apparent diffusion coefficient value
kn-keyword=apparent diffusion coefficient value
en-keyword=diffusion kurtosis imaging
kn-keyword=diffusion kurtosis imaging
en-keyword=machine learning
kn-keyword=machine learning
en-keyword=bi-parameter analysis
kn-keyword=bi-parameter analysis
en-keyword=gradient boosting
kn-keyword=gradient boosting
en-keyword=differential diagnosis of benign and malignant
kn-keyword=differential diagnosis of benign and malignant
END

start-ver=1.4
cd-journal=joma
no-vol=85
cd-vols=
no-issue=6
article-no=
start-page=1082
end-page=1096
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250314
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Myeloid Cells Induce Infiltration and Activation of B Cells and CD4+ T Follicular Helper Cells to Sensitize Brain Metastases to Combination Immunotherapy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Brain metastasis is a poor prognostic factor in patients with cancer. Despite showing efficacy in many extracranial tumors, immunotherapy with anti–PD-1 mAb or anti–CTLA4 mAb seems to be less effective against intracranial tumors. Promisingly, recent clinical studies have reported that combination therapy with anti–PD-1 and anti–CTLA4 mAbs has a potent antitumor effect on brain metastasis, highlighting the need to elucidate the detailed mechanisms controlling the intracranial tumor microenvironment (TME) to develop effective immunotherapeutic strategies. In this study, we analyzed the tumor-infiltrating lymphocytes in murine models of brain metastasis that responded to anti–CTLA4 and anti–PD-1 mAbs. Activated CD4+ T follicular helper (TFH) cells with high CTLA4 expression characteristically infiltrated the intracranial TME, which were activated by combination anti–CTLA4 and anti–PD-1 treatment. The loss of TFH cells suppressed the additive effect of CTLA4 blockade on anti–PD-1 mAb. B-cell–activating factor belonging to the TNF family (BAFF) and a proliferation-inducing ligand (APRIL) produced by abundant myeloid cells, particularly CD80hiCD206lo proinflammatory M1-like macrophages, in the intracranial TME induced B-cell and TFH-cell infiltration and activation. Furthermore, the intracranial TME of patients with non–small cell lung cancer featured TFH- and B-cell infiltration as tertiary lymphoid structures. Together, these findings provide insights into the immune cell cross-talk in the intracranial TME that facilitates an additive antitumor effect of CTLA4 blockade with anti–PD-1 treatment, supporting the potential of a combination immunotherapeutic strategy for brain metastases.<br>
Significance: B-cell and CD4+ T follicular helper cell activation via BAFF/APRIL from abundant myeloid cells in the intracranial tumor microenvironment enables a combinatorial effect of CTLA4 and PD-1 blockade in brain metastases.
en-copyright=
kn-copyright=

en-aut-name=NinomiyaToshifumi
en-aut-sei=Ninomiya
en-aut-mei=Toshifumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KemmotsuNaoya
en-aut-sei=Kemmotsu
en-aut-mei=Naoya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MukoharaFumiaki
en-aut-sei=Mukohara
en-aut-mei=Fumiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MagariMasaki
en-aut-sei=Magari
en-aut-mei=Masaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MiyamotoAi
en-aut-sei=Miyamoto
en-aut-mei=Ai
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=UedaYouki
en-aut-sei=Ueda
en-aut-mei=Youki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=IshinoTakamasa
en-aut-sei=Ishino
en-aut-mei=Takamasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NagasakiJoji
en-aut-sei=Nagasaki
en-aut-mei=Joji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=FujiwaraTomohiro
en-aut-sei=Fujiwara
en-aut-mei=Tomohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=YamamotoHidetaka
en-aut-sei=Yamamoto
en-aut-mei=Hidetaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=HayashiHidetoshi
en-aut-sei=Hayashi
en-aut-mei=Hidetoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=TachibanaKota
en-aut-sei=Tachibana
en-aut-mei=Kota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=IshidaJoji
en-aut-sei=Ishida
en-aut-mei=Joji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=OtaniYoshihiro
en-aut-sei=Otani
en-aut-mei=Yoshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=TanakaShota
en-aut-sei=Tanaka
en-aut-mei=Shota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=ToyookaShinichi
en-aut-sei=Toyooka
en-aut-mei=Shinichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=OkamotoIsamu
en-aut-sei=Okamoto
en-aut-mei=Isamu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=TogashiYosuke
en-aut-sei=Togashi
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

affil-num=1
en-affil=Department of Tumor Microenvironment, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Tumor Microenvironment, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Tumor Microenvironment, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Applied Cell Biology, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=5
en-affil=Medical Protein Engineering, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Tumor Microenvironment, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Tumor Microenvironment, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Tumor Microenvironment, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Orthopaedic Surgery, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=10
en-affil=Department of Pathology and Oncology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=11
en-affil=Department of Medical Oncology, Kindai University Faculty of Medicine
kn-affil=

affil-num=12
en-affil=Department of Dermatology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=13
en-affil=Department of Neurological Surgery, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=14
en-affil=Department of Neurological Surgery, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=15
en-affil=Department of Neurological Surgery, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=16
en-affil=Department of General Thoracic Surgery, Breast and Endocrinological Surgery, Faculty of Medicine, Dentistry and Pharmaceutical Science, Okayama University
kn-affil=

affil-num=17
en-affil=Department of Respiratory Medicine, Graduate School of Medical Sciences, Kyushu University
kn-affil=

affil-num=18
en-affil=Department of Tumor Microenvironment, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=16
cd-vols=
no-issue=1
article-no=
start-page=1757
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250224
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Keratinocyte-driven dermal collagen formation in the axolotl skin
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Type I collagen is a major component of the dermis and is formed by dermal fibroblasts. The development of dermal collagen structures has not been fully elucidated despite the major presence and importance of the dermis. This lack of understanding is due in part to the opacity of mammalian skin and it has been an obstacle to cosmetic and medical developments. We reveal the process of dermal collagen formation using the highly transparent skin of the axolotl and fluorescent collagen probes. We clarify that epidermal cells, not dermal fibroblasts, contribute to dermal collagen formation. Mesenchymal cells (fibroblasts) play a role in modifying the collagen fibers already built by keratinocytes. We confirm that collagen production by keratinocytes is a widely conserved mechanism in other model organisms. Our findings warrant a change in the current consensus about dermal collagen formation and could lead to innovations in cosmetology and skin medication.
en-copyright=
kn-copyright=

en-aut-name=OhashiAyaka
en-aut-sei=Ohashi
en-aut-mei=Ayaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SakamotoHirotaka
en-aut-sei=Sakamoto
en-aut-mei=Hirotaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KurodaJunpei
en-aut-sei=Kuroda
en-aut-mei=Junpei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KondoYohei
en-aut-sei=Kondo
en-aut-mei=Yohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KameiYasuhiro
en-aut-sei=Kamei
en-aut-mei=Yasuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NonakaShigenori
en-aut-sei=Nonaka
en-aut-mei=Shigenori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=FurukawaSaya
en-aut-sei=Furukawa
en-aut-mei=Saya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YamamotoSakiya
en-aut-sei=Yamamoto
en-aut-mei=Sakiya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=SatohAkira
en-aut-sei=Satoh
en-aut-mei=Akira
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Graduate School of Environment, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Environment, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Frontier Biosciences, Osaka University
kn-affil=

affil-num=4
en-affil=Center for One Medicine Innovative Translational Research (COMIT), Nagoya University
kn-affil=

affil-num=5
en-affil=Laboratory for Biothermology, National Institute for Basic Biology
kn-affil=

affil-num=6
en-affil=The Graduate University for Advanced Studies (SOKENDAI)
kn-affil=

affil-num=7
en-affil=Graduate School of Environment, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=8
en-affil=Graduate School of Environment, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=9
en-affil=Graduate School of Environment, Life, Natural Science and Technology, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=752
cd-vols=
no-issue=
article-no=
start-page=151481
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250308
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Discovery of myeloid zinc finger (MZF) 1 nuclear bodies
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Myeloid zinc finger 1 (MZF1) is a multifaceted transcription factor that can act either as a transcriptional activator or a gene repressor. We examined its production of nuclear bodies (NBs) and subcellular localization. Proteomic and protein–protein interaction analysis were used to identify its cofactors and interactions. These revealed the presence of MZF1-NBs (intranuclear oligomers containing MZF1). MZF-NBs are similar to some other nuclear bodies, notably promyelocytic leukemia (PML) -NBs in terms of size and morphology. However the two structures appear to be different. MZF-NBs and PML-NBs were found to associate in the nucleus. Both MZF1 and PML are SUMO1-SUMOylated in PC-3 cells. Sumoylated MZF1 can interact with proteins containing SUMO-interaction motifs (SIM) through SUMO-SIM interaction. Interactome analysis revealed that its NBs participate in the stress response (TPR and UBAP2L), protein folding (CALR and ANKRD40), transcription, post-translational modification (TRIM33, ACOT7, CAMK2D, and CAMK2G), and RNA binding (ALURBP and CPSF5).

en-copyright=
kn-copyright=

en-aut-name=EguchiTakanori
en-aut-sei=Eguchi
en-aut-mei=Takanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=CalderwoodStuart K.
en-aut-sei=Calderwood
en-aut-mei=Stuart K.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

affil-num=1
en-affil=Department of Dental Pharmacology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Division of Molecular and Cellular Biology, Department of Radiation Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School
kn-affil=
en-keyword=Myeloid zinc finger 1
kn-keyword=Myeloid zinc finger 1
en-keyword=MZF1
kn-keyword=MZF1
en-keyword=Nuclear body
kn-keyword=Nuclear body
en-keyword=PML
kn-keyword=PML
en-keyword=Sumoylation
kn-keyword=Sumoylation
en-keyword=SCAN domain protein
kn-keyword=SCAN domain protein
END

start-ver=1.4
cd-journal=joma
no-vol=2
cd-vols=
no-issue=9
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2016
dt-pub=20160908
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=S-nitrosylation of laforin inhibits its phosphatase activity and is implicated in Lafora disease
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Recently, the relation between S-nitrosylation by nitric oxide (NO), which is over�produced under pathological conditions and neurodegenerative diseases, includingAlzheimer’s and Parkinson’s diseases, has become a focus of attention. Although mostcases of Parkinson’s disease are known to be caused by mutations in the Parkin gene, arecent finding has indicated that S-nitrosylation of Parkin affects its enzymatic activityand leads to the Parkinsonian phenotype. Therefore, it is important to understand thefunction of S-nitrosylated proteins in the pathogenesis of neurodegenerative diseases.Lafora disease (LD, OMIM 254780) is a neurodegenerative disease characterized by theaccumulation of insoluble glucans called Lafora bodies (LBs). LD is caused by mutationsin genes that encode the glucan phosphatase, Laforin, or the E3 ubiquitin ligase, Malin.In this study, we hypothesized that LD may be caused by S-nitrosylation of Laforin,which is similar to the finding that Parkinson’s disease is caused by S-nitrosylation ofParkin. To test this hypothesis, we first determined whether Laforin was S-nitrosylatedusing a biotin switch assay, and compared the three main functions of unmodified andS-nitrosylated Laforin, namely glucan- and Malin-binding activity and phosphataseactivity. Furthermore, we examined whether the numbers of LBs were changed byNO in the cells expressing wild-type Laforin. Here, we report for the first time thatS-nitrosylation of Laforin inhibited its phosphatase activity and that LB formation wasincreased by an NO donor. Our results suggest a possible hypothesis for LD pathogenesis; that is, the decrease in phosphatase activity of Laforin by S-nitrosylation leads toincreased LB formation. Therefore, LD may be caused not only by mutations in theLaforin or Malin genes, but also by the S-nitrosylation of Laforin.

en-copyright=
kn-copyright=

en-aut-name=ToyotaRikako
en-aut-sei=Toyota
en-aut-mei=Rikako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HonjoYasuko
en-aut-sei=Honjo
en-aut-mei=Yasuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ImajoRisa
en-aut-sei=Imajo
en-aut-mei=Risa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SatohAyano
en-aut-sei=Satoh
en-aut-mei=Ayano
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=
kn-affil=

affil-num=2
en-affil=Graduate School of Natural Science and Technology, Okayama University; Research Institute for Radiation Biology and Medicine, Hiroshima University
kn-affil=

affil-num=3
en-affil=Graduate School of Natural Science and Technology, Okayama University; Research Institute for Radiation Biology and Medicine, Hiroshima University
kn-affil=

affil-num=4
en-affil=Graduate School of Natural Science and Technology, Okayama University; Research Institute for Radiation Biology and Medicine, Hiroshima University
kn-affil=
en-keyword=S-Nitrosylation Of Laforin
kn-keyword=S-Nitrosylation Of Laforin
en-keyword=Post-Translational Modification 
kn-keyword=Post-Translational Modification 
en-keyword=Nitrosylation
kn-keyword=Nitrosylation
en-keyword=Phosphatase
kn-keyword=Phosphatase
en-keyword=Glucan-Binding
kn-keyword=Glucan-Binding
END

start-ver=1.4
cd-journal=joma
no-vol=34
cd-vols=
no-issue=1
article-no=
start-page=35
end-page=40
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=2025
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Evaluation of CT Findings in Squamous and Non-Squamous Cell Carcinomas of the Maxillary Sinus
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The aim of the present study was to compare CT images between squamous cell carcinoma (SCC) and non-SCC found in the maxillary sinus, and to identify features that could be used to differentiate between SCC and non-SCC. Patients who visited the Faculty of Dentistry, Okayama University Hospital, between April 2007 and March 2023, underwent head and neck CT, and had tumors extending into the maxillary sinus that were diagnosed histopathologically as malignancy, were enrolled. The main seat of the mass, bony changes in the maxillary sinus wall, and extension into the surrounding area were assessed. These imaging features were evaluated according to SCC or non-SCC, and the characteristics of the two classes were assessed. Comparisons between the two groups were made using the Fisher exact probability test. There were 11 cases each of SCC and non-SCC. In 11 SCC and 7 non-SCC cases, the main seat of the mass occupied the entire maxillary sinus. The frequency of mass occupying the whole sinus was significantly higher in SCC than in non-SCC (p<0.05). Bone-thickening type disease was found only in squamous cell carcinoma 4/11 (36.4%), with there being a significant difference between SCC and non-SCC (p<0.05). Occupancy of the entire maxillary sinus by the mass and bone thickening on CT images were useful for differentiating between SCC and non-SCC arising in the maxillary sinus.
en-copyright=
kn-copyright=

en-aut-name=AsaumiYuka
en-aut-sei=Asaumi
en-aut-mei=Yuka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=FujikuraMamiko
en-aut-sei=Fujikura
en-aut-mei=Mamiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HisatomiMiki
en-aut-sei=Hisatomi
en-aut-mei=Miki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=E. Al-HammadWlla
en-aut-sei=E. Al-Hammad
en-aut-mei=Wlla
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TakeshitaYohei
en-aut-sei=Takeshita
en-aut-mei=Yohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OkadaShunsuke
en-aut-sei=Okada
en-aut-mei=Shunsuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KawazuToshiyuki
en-aut-sei=Kawazu
en-aut-mei=Toshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YanagiYoshinobu
en-aut-sei=Yanagi
en-aut-mei=Yoshinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=AsaumiJunichi
en-aut-sei=Asaumi
en-aut-mei=Junichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Oral and Maxillofacial Radiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Oral and Maxillofacial Radiology, Okayama University Hospital
kn-affil=

affil-num=3
en-affil=Department of Oral and Maxillofacial Radiology, Okayama University Hospital
kn-affil=

affil-num=4
en-affil=Department of Oral and Maxillofacial Radiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Oral and Maxillofacial Radiology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Oral and Maxillofacial Radiology, Okayama University Hospital
kn-affil=

affil-num=7
en-affil=Department of Oral and Maxillofacial Radiology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Dental Informatics, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Oral and Maxillofacial Radiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Maxillary sinus
kn-keyword=Maxillary sinus
en-keyword=Squamous cell carcinoma
kn-keyword=Squamous cell carcinoma
en-keyword=Non-squamous cell carcinoma
kn-keyword=Non-squamous cell carcinoma
en-keyword=CT
kn-keyword=CT
END

start-ver=1.4
cd-journal=joma
no-vol=79
cd-vols=
no-issue=1
article-no=
start-page=1
end-page=7
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202502
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Endothelial Cell Polarity in Health and Disease
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Endothelial cell polarity is fundamental to the organization and function of blood vessels, influencing processes such as angiogenesis, vascular stability, and response to shear stress. This review elaborates on the molecular mechanisms that regulate endothelial cell polarity, focusing on key players like the PAR polarity complex and Rho family GTPases. These pathways coordinate the front–rear, apical–basal and planar polarity of endothelial cells, which are essential for the proper formation and maintenance of vascular structures. In health, endothelial polarity ensures not only the orderly development of blood vessels, with tip cells adopting distinct polarities during angiogenesis, but also ensures proper vascular integrity and function. In disease states, however, disruptions in polarity contribute to pathologies such as coronary artery disease, where altered planar polarity exacerbates atherosclerosis, and cancer, where disrupted polarity in tumor vasculature leads to abnormal vessel growth and function. Understanding cell polarity and its disruption is fundamental not only to comprehending how cells interact with their microenvironment and organize themselves into complex, organ-specific tissues but also to developing novel, targeted, and therapeutic strategies for a range of diseases, from cardiovascular disorders to malignancies, ultimately improving patient outcomes.
en-copyright=
kn-copyright=

en-aut-name=ThihaMoe
en-aut-sei=Thiha
en-aut-mei=Moe
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HikitaTakao
en-aut-sei=Hikita
en-aut-mei=Takao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NakayamaMasanori
en-aut-sei=Nakayama
en-aut-mei=Masanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Department of Pathophysiology and Drug Discovery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Pathophysiology and Drug Discovery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Pathophysiology and Drug Discovery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=blood vessel
kn-keyword=blood vessel
en-keyword=endothelial cell
kn-keyword=endothelial cell
en-keyword=cell polarity
kn-keyword=cell polarity
en-keyword=atherosclerosis
kn-keyword=atherosclerosis
en-keyword=cancer
kn-keyword=cancer
END

start-ver=1.4
cd-journal=joma
no-vol=121
cd-vols=
no-issue=35
article-no=
start-page=e2320189121
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240821
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Somatic mutations in tumor-infiltrating lymphocytes impact on antitumor immunity
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Immune checkpoint inhibitors (ICIs) exert clinical efficacy against various types of cancers by reinvigorating exhausted CD8+ T cells that can expand and directly attack cancer cells (cancer-specific T cells) among tumor-infiltrating lymphocytes (TILs). Although some reports have identified somatic mutations in TILs, their effect on antitumor immunity remains unclear. In this study, we successfully established 18 cancer-specific T cell clones, which have an exhaustion phenotype, from the TILs of four patients with melanoma. We conducted whole-genome sequencing for these T cell clones and identified various somatic mutations in them with high clonality. Among the somatic mutations, an SH2D2A loss-of-function frameshift mutation and TNFAIP3 deletion could activate T cell effector functions in vitro. Furthermore, we generated CD8+ T cell–specific Tnfaip3 knockout mice and showed that Tnfaip3 function loss in CD8+ T cell increased antitumor immunity, leading to remarkable response to PD-1 blockade in vivo. In addition, we analyzed bulk CD3+ T cells from TILs in additional 12 patients and identified an SH2D2A mutation in one patient through amplicon sequencing. These findings suggest that somatic mutations in TILs can affect antitumor immunity and suggest unique biomarkers and therapeutic targets.
en-copyright=
kn-copyright=

en-aut-name=MukoharaFumiaki
en-aut-sei=Mukohara
en-aut-mei=Fumiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=IwataKazuma
en-aut-sei=Iwata
en-aut-mei=Kazuma
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=IshinoTakamasa
en-aut-sei=Ishino
en-aut-mei=Takamasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=InozumeTakashi
en-aut-sei=Inozume
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NagasakiJoji
en-aut-sei=Nagasaki
en-aut-mei=Joji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=UedaYouki
en-aut-sei=Ueda
en-aut-mei=Youki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SuzawaKen
en-aut-sei=Suzawa
en-aut-mei=Ken
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=UenoToshihide
en-aut-sei=Ueno
en-aut-mei=Toshihide
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=IkedaHideki
en-aut-sei=Ikeda
en-aut-mei=Hideki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=KawaseKatsushige
en-aut-sei=Kawase
en-aut-mei=Katsushige
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=SaekiYuka
en-aut-sei=Saeki
en-aut-mei=Yuka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=KawashimaShusuke
en-aut-sei=Kawashima
en-aut-mei=Shusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=YamashitaKazuo
en-aut-sei=Yamashita
en-aut-mei=Kazuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=KawaharaYu
en-aut-sei=Kawahara
en-aut-mei=Yu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=NakamuraYasuhiro
en-aut-sei=Nakamura
en-aut-mei=Yasuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=Honobe-TabuchiAkiko
en-aut-sei=Honobe-Tabuchi
en-aut-mei=Akiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=WatanabeHiroko
en-aut-sei=Watanabe
en-aut-mei=Hiroko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=DansakoHiromichi
en-aut-sei=Dansako
en-aut-mei=Hiromichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=KawamuraTatsuyoshi
en-aut-sei=Kawamura
en-aut-mei=Tatsuyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=SuzukiYutaka
en-aut-sei=Suzuki
en-aut-mei=Yutaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

en-aut-name=HondaHiroaki
en-aut-sei=Honda
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=21
ORCID=

en-aut-name=ManoHiroyuki
en-aut-sei=Mano
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=22
ORCID=

en-aut-name=ToyookaShinichi
en-aut-sei=Toyooka
en-aut-mei=Shinichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=23
ORCID=

en-aut-name=KawazuMasahito
en-aut-sei=Kawazu
en-aut-mei=Masahito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=24
ORCID=

en-aut-name=TogashiYosuke
en-aut-sei=Togashi
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=25
ORCID=

affil-num=1
en-affil=Department of Tumor Microenvironment, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Tumor Microenvironment, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Tumor Microenvironment, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Dermatology, Chiba University Graduate School of Medicine
kn-affil=

affil-num=5
en-affil=Department of Tumor Microenvironment, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Tumor Microenvironment, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine, Okayama University
kn-affil=

affil-num=8
en-affil=Division of Cellular Signaling, National Cancer Center Research Institute
kn-affil=

affil-num=9
en-affil=Division of Cell Therapy, Chiba Cancer Research Institute
kn-affil=

affil-num=10
en-affil=Division of Cell Therapy, Chiba Cancer Research Institute
kn-affil=

affil-num=11
en-affil=Department of Dermatology, Chiba University Graduate School of Medicine
kn-affil=

affil-num=12
en-affil=Department of Dermatology, Chiba University Graduate School of Medicine
kn-affil=

affil-num=13
en-affil=KOTAI Biotechnologies, Inc.
kn-affil=

affil-num=14
en-affil=Department of Dermatology, Chiba University Graduate School of Medicine
kn-affil=

affil-num=15
en-affil=Department of Skin Oncology/Dermatology, Saitama Medical University International Medical Center
kn-affil=

affil-num=16
en-affil=Department of Dermatology, University of Yamanashi
kn-affil=

affil-num=17
en-affil=Department of Tumor Microenvironment, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=18
en-affil=Department of Tumor Microenvironment, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=19
en-affil=Department of Dermatology, University of Yamanashi
kn-affil=

affil-num=20
en-affil=Department of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo, Kashiwa
kn-affil=

affil-num=21
en-affil=Department of Pathology, Tokyo Women's Medical University
kn-affil=

affil-num=22
en-affil=Division of Cellular Signaling, National Cancer Center Research Institute
kn-affil=

affil-num=23
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine, Okayama University
kn-affil=

affil-num=24
en-affil=Division of Cell Therapy, Chiba Cancer Research Institute
kn-affil=

affil-num=25
en-affil=Department of Tumor Microenvironment, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=cancer immunology
kn-keyword=cancer immunology
en-keyword=somatic mutation
kn-keyword=somatic mutation
en-keyword=T cell
kn-keyword=T cell
en-keyword=tumor-infiltrating lymphocytes
kn-keyword=tumor-infiltrating lymphocytes
END

start-ver=1.4
cd-journal=joma
no-vol=361
cd-vols=
no-issue=
article-no=
start-page=114657
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202501
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Crosstalk between prolactin, insulin-like growth factors, and thyroid hormones in feather growth regulation in neonatal chick wings
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The elongation of primary feathers in neonatal chicks is delayed by the late-feathering K gene located on the Z chromosome. We recently found that the K gene slows feather growth by reducing the number of functional prolactin (PRL) receptor (PRLR) dimers. In this study, we investigated the molecular mechanisms by which PRL promotes feather elongation. RT-qPCR and immunohistochemistry analyses revealed that PRLRs are predominantly localized in the pulp rather than in the epidermal layer of the feather follicle. Treatment of primary cultured feather pulp cells with PRL increased the expression of mRNAs for insulin-like growth factors (IGFs; IGF-1 and IGF-2) and type 2 deiodinase (DIO2). Furthermore, treatments with IGF-1 and triiodothyronine (T3) reciprocally enhanced the expression of mRNAs for DIO2 and IGFs. Additionally, BrdU staining in neonatal chicks showed that T3 promoted cell proliferation in both the epidermal layer and pulp cells, while this effect was suppressed by an IGF-1 receptor (IGF1R) inhibitor. These findings suggest a novel model in which PRL upregulates IGFs and DIO2 in feather pulp cells, creating a positive feedback loop between IGFs and T3, ultimately leading to the promotion of cell proliferation in both the epidermal layer and the pulp cells by IGFs. This is the first report proposing crosstalk between PRL, thyroid hormone (TH), and IGFs in feather follicles.
en-copyright=
kn-copyright=

en-aut-name=NozawaYuri
en-aut-sei=Nozawa
en-aut-mei=Yuri
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OkamuraAyako
en-aut-sei=Okamura
en-aut-mei=Ayako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=FukuchiHibiki
en-aut-sei=Fukuchi
en-aut-mei=Hibiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ShinoharaMasamichi
en-aut-sei=Shinohara
en-aut-mei=Masamichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=AizawaSayaka
en-aut-sei=Aizawa
en-aut-mei=Sayaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TakeuchiSakae
en-aut-sei=Takeuchi
en-aut-mei=Sakae
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=4
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=5
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=6
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=
en-keyword=Prolactin
kn-keyword=Prolactin
en-keyword=Thyroid hormone
kn-keyword=Thyroid hormone
en-keyword=IGF
kn-keyword=IGF
en-keyword=Iodothyronine deiodinase
kn-keyword=Iodothyronine deiodinase
en-keyword=Feather growth
kn-keyword=Feather growth
END

start-ver=1.4
cd-journal=joma
no-vol=941
cd-vols=
no-issue=
article-no=
start-page=149244
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250315
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Identification of pennaceous barbule cell factor (PBCF), a novel gene with spatiotemporal expression in barbule cells during feather development
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Bird contour feathers exhibit a complex hierarchical structure composed of a rachis, barbs, and barbules, with barbules playing a crucial role in maintaining feather structure and function. Understanding the molecular mechanisms underlying barbule formation is essential for advancing our knowledge of avian biology and evolution. In this study, we identified a novel gene, pennaceous barbule cell factor (PBCF), using microarray analysis, RT-PCR, and in situ hybridization. PBCF is expressed in barbule cells adjacent to the ramus during pennaceous barbule formation, where these cells fuse with the ramus to establish the feather’s branching structure. PBCF expression occurs transiently after melanin pigmentation of the barbule plates but before the expression of barbule-specific keratin 1 (BlSK1). Orthologues of PBCF, predicted to be secreted proteins, are conserved across avian species, with potential homologues detected in reptiles, suggesting an evolutionary lineage-specific adaptation. Additionally, PBCF is expressed in non-vacuolated notochord cells and the extra-embryonic ectoderm of the yolk sac, hinting at its broader developmental significance. The PBCF gene produces two mRNA isoforms via alternative splicing, encoding a secreted protein and a glycophosphatidylinositol (GPI)-anchored membrane-bound protein, indicating functional versatility. These findings suggest that PBCF may be involved as an avian-specific extracellular matrix component in cell adhesion and/or communication, potentially contributing to both feather development and embryogenesis. Further investigation of PBCF’s role in feather evolution and its potential functions in other vertebrates could provide new insights into the interplay between development and evolution.
en-copyright=
kn-copyright=

en-aut-name=NakaokaMinori
en-aut-sei=Nakaoka
en-aut-mei=Minori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=FukuchiHibiki
en-aut-sei=Fukuchi
en-aut-mei=Hibiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OgoshiMaho
en-aut-sei=Ogoshi
en-aut-mei=Maho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=AizawaSayaka
en-aut-sei=Aizawa
en-aut-mei=Sayaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TakeuchiSakae
en-aut-sei=Takeuchi
en-aut-mei=Sakae
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=4
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=5
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=
en-keyword=Feather
kn-keyword=Feather
en-keyword=Barbule
kn-keyword=Barbule
en-keyword=Branching
kn-keyword=Branching
en-keyword=Chicken
kn-keyword=Chicken
en-keyword=Yolk sac membrane
kn-keyword=Yolk sac membrane
en-keyword=Notochord
kn-keyword=Notochord
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=1
article-no=
start-page=2577
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250120
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Plasma S100A8/A9 level predicts response to immune checkpoint inhibitors in patients with advanced non-small cell lung cancer
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Blood-based predictive markers for the efficacy of immune checkpoint inhibitors (ICIs) have not yet been established. We investigated the association of the plasma level of S100A8/A9 with the efficacy of immunotherapy. We evaluated patients with unresectable stage III/IV or recurrent non-small cell lung cancer (NSCLC) who were treated with ICIs at Okayama University Hospital. The pre-treatment plasma levels of S100A8/A9 were analyzed. Eighty-one eligible patients were included (median age, 69 years). Sixty-two patients were men, 54 had adenocarcinoma, 74 had performance status (PS) 0–1, and 47 received ICIs as first-line treatment. The median time to treatment failure (TTF) for ICIs was 5.7 months, and the median overall survival (OS) was 19.6 months. The TTF and OS were worse in patients with high plasma S100A8/A9 levels (≥ 2.475 µg/mL) (median TTF: 4.3 vs. 8.5 months, p = 0.009; median OS: 15.4 vs. 38.0 months, p = 0.001). Multivariate analysis revealed that PS ≥ 2, liver metastasis, and high plasma S100A8/A9 levels were significantly associated with short TTF and OS. In conclusion, plasma S100A8/A9 level may have a limited effect on ICI therapy for NSCLC.
en-copyright=
kn-copyright=

en-aut-name=KuribayashiTadahiro
en-aut-sei=Kuribayashi
en-aut-mei=Tadahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KinoshitaRie
en-aut-sei=Kinoshita
en-aut-mei=Rie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NinomiyaKiichiro
en-aut-sei=Ninomiya
en-aut-mei=Kiichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MakimotoGo
en-aut-sei=Makimoto
en-aut-mei=Go
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KuboToshio
en-aut-sei=Kubo
en-aut-mei=Toshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=RaiKammei
en-aut-sei=Rai
en-aut-mei=Kammei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=IchiharaEiki
en-aut-sei=Ichihara
en-aut-mei=Eiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=HottaKatsuyuki
en-aut-sei=Hotta
en-aut-mei=Katsuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TabataMasahiro
en-aut-sei=Tabata
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=MaedaYoshinobu
en-aut-sei=Maeda
en-aut-mei=Yoshinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=KiuraKatsuyuki
en-aut-sei=Kiura
en-aut-mei=Katsuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=ToyookaShinichi
en-aut-sei=Toyooka
en-aut-mei=Shinichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=SakaguchiMasakiyo
en-aut-sei=Sakaguchi
en-aut-mei=Masakiyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=OhashiKadoaki
en-aut-sei=Ohashi
en-aut-mei=Kadoaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

affil-num=1
en-affil=Department of Hematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital
kn-affil=

affil-num=4
en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital
kn-affil=

affil-num=5
en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital
kn-affil=

affil-num=6
en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital
kn-affil=

affil-num=7
en-affil=Center for Clinical Oncology, Okayama University Hospital
kn-affil=

affil-num=8
en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital
kn-affil=

affil-num=9
en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital
kn-affil=

affil-num=10
en-affil=Department of Hematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital
kn-affil=

affil-num=12
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=13
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=14
en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital
kn-affil=
en-keyword=S100A8/A9
kn-keyword=S100A8/A9
en-keyword=Lung cancer
kn-keyword=Lung cancer
en-keyword=Immune checkpoint inhibitors
kn-keyword=Immune checkpoint inhibitors
END

start-ver=1.4
cd-journal=joma
no-vol=33
cd-vols=
no-issue=4
article-no=
start-page=213
end-page=218
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=2024
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=β-catenin Binds to Gsk-3β in Liquid-Liquid Phase Separation Compartment in HEK293 Cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Liquid-liquid phase separation (LLPS) has emerged as a significant mechanism for cellular organization, impacting various biological processes, including Wnt/β-catenin signaling. This study investigates the role of LLPS in the regulation of β-catenin in HEK293 cells, particularly in response to Wnt3a signaling. Our findings demonstrate that β-catenin is regulated by LLPS, forming spherical droplets indicative of this phenomenon. Fluorescence recovery after photobleaching (FRAP) assays revealed that these droplets exhibit reversible dynamics, further confirming their phase-separated nature. Importantly, treatment with Wnt3a led to an increase in β-catenin levels, while simultaneously reducing the recovery of fluorescence intensity in FRAP experiments, suggesting that enhanced Wnt signaling may stimulate the release of β-catenin from LLPS. Immunoprecipitation studies indicated that β-catenin binds to glycogen synthase kinase 3β (Gsk-3β) within the LLPS state, highlighting a potential regulatory mechanism whereby LLPS facilitates the phosphorylation and subsequent degradation of β-catenin. The addition of 1,6-hexanediol disrupted the β-catenin/Gsk-3β interaction, reinforcing the idea that LLPS plays a critical role in modulating these biochemical interactions. The findings presented in this study suggest that LLPS is not only crucial for the spatial organization of β-catenin but also serves as a regulatory mechanism for its signaling functions in the Wnt pathway. Given the association of aberrant Wnt signaling with various diseases, including cancer and neurodegenerative disorders, understanding the role of LLPS in this context may provide new insights into therapeutic strategies targeting these pathological conditions.
en-copyright=
kn-copyright=

en-aut-name=KatoMari
en-aut-sei=Kato
en-aut-mei=Mari
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TanaiAiri
en-aut-sei=Tanai
en-aut-mei=Airi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=FukuharaYoko
en-aut-sei=Fukuhara
en-aut-mei=Yoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ZhengXinyu
en-aut-sei=Zheng
en-aut-mei=Xinyu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SitosariHeriati
en-aut-sei=Sitosari
en-aut-mei=Heriati
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YamamotoTadashi
en-aut-sei=Yamamoto
en-aut-mei=Tadashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=IkegameMika
en-aut-sei=Ikegame
en-aut-mei=Mika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=OkamuraHirohiko
en-aut-sei=Okamura
en-aut-mei=Hirohiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Oral Morphology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Oral Morphology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Oral Morphology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Oral Morphology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Oral Morphology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=The Center for Graduate Medical Education (Dental Division), Okayama University Hospital
kn-affil=

affil-num=7
en-affil=Department of Oral Morphology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Oral Morphology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=β-catenin
kn-keyword=β-catenin
en-keyword=Gsk-3β
kn-keyword=Gsk-3β
en-keyword=LLPS
kn-keyword=LLPS
en-keyword=Wnt
kn-keyword=Wnt
END

start-ver=1.4
cd-journal=joma
no-vol=78
cd-vols=
no-issue=6
article-no=
start-page=469
end-page=474
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202412
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Treatment of Tenosynovial Giant Cell Tumor of the Cervical Spine with Postoperative Anti-RANKL Antibody (Denosumab) Administration
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Tenosynovial giant cell tumor (TGCT) is a fibrous histiocytic tumor originating in the synovial membrane. While cervical TGCT may not be considered a common diagnosis preoperatively because it is relatively rare, it has a high recurrence rate and should be considered. Total resection is preferable, but it can be challenging due to the risk of damaging the vertebral artery. Denosumab has shown effectiveness as a postoperative treatment for osteolytic bone lesion. Denosumab administration coupled with close follow-up might offer an effective postoperative treatment option for unresectable TGCT with bone invasion.
en-copyright=
kn-copyright=

en-aut-name=HirataYuichi
en-aut-sei=Hirata
en-aut-mei=Yuichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NagaseTakayuki
en-aut-sei=Nagase
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SasadaSusumu
en-aut-sei=Sasada
en-aut-mei=Susumu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=AyadaYoshiyuki
en-aut-sei=Ayada
en-aut-mei=Yoshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MiyakeHayato
en-aut-sei=Miyake
en-aut-mei=Hayato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SugaharaChiaki
en-aut-sei=Sugahara
en-aut-mei=Chiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YamamotoHidetaka
en-aut-sei=Yamamoto
en-aut-mei=Hidetaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=OdaYoshinao
en-aut-sei=Oda
en-aut-mei=Yoshinao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=YasuharaTakao
en-aut-sei=Yasuhara
en-aut-mei=Takao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=TanakaShota
en-aut-sei=Tanaka
en-aut-mei=Shota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Pathology and Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Pathology and Oncology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Anatomic Pathology, Graduate School of Medical Sciences, Kyushu University
kn-affil=

affil-num=9
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=tenosynovial giant cell tumor
kn-keyword=tenosynovial giant cell tumor
en-keyword=bone tumor
kn-keyword=bone tumor
en-keyword=spine
kn-keyword=spine
END

start-ver=1.4
cd-journal=joma
no-vol=14
cd-vols=
no-issue=11
article-no=
start-page=e70476
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241121
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Genomic Introgression in the Hybrid zones at the Margins of the Species' Range Between Ecologically Distinct Rubus Species
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Populations in extreme environments at the margins of a species' range are often the most vulnerable to climate change, but they may also experience novel evolutionary processes, such as secondary contact and hybridization with their relatives. The range overlap resulting from secondary contact with related species that have adapted to different climatic zones may act as corridors for adaptive introgression. To test this hypothesis, we examined the hybrid zones along the altitude of two closely related Rubus species, one temperate and the other subtropical species, at their southern and northern limits on Yakushima Island, Japan. Genomic cline analysis revealed non-neutral introgression throughout the genome in both directions in the two species. Some of these genomic regions involve gene ontology terms related to the regulation of several biological processes. Our niche modeling suggests that, assuming niche conservatism, the temperate species are likely to lose their suitable habitat, and the backcrossed hybrids with the subtropical species are already expanding upslope on the island. Adaptive introgression through the hybrid zone may contribute to the persistence and expansion of the species in the southernmost and northernmost populations.
en-copyright=
kn-copyright=

en-aut-name=MimuraMakiko
en-aut-sei=Mimura
en-aut-mei=Makiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TangZhenxing
en-aut-sei=Tang
en-aut-mei=Zhenxing
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ShigenobuShuji
en-aut-sei=Shigenobu
en-aut-mei=Shuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YamaguchiKatsushi
en-aut-sei=Yamaguchi
en-aut-mei=Katsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YaharaTetsukazu
en-aut-sei=Yahara
en-aut-mei=Tetsukazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Department of Biology, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Biology, Okayama University
kn-affil=

affil-num=3
en-affil=Trans-Omics Facility, National Institute of Basic Biology
kn-affil=

affil-num=4
en-affil=Trans-Omics Facility, National Institute of Basic Biology
kn-affil=

affil-num=5
en-affil=Kyushu Open University
kn-affil=
en-keyword=adaptive introgression
kn-keyword=adaptive introgression
en-keyword=climate change
kn-keyword=climate change
en-keyword=hybrid zone
kn-keyword=hybrid zone
en-keyword=secondary contact
kn-keyword=secondary contact
END

start-ver=1.4
cd-journal=joma
no-vol=9
cd-vols=
no-issue=50
article-no=
start-page=50041
end-page=50048
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241205
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Conformational Flexibility of D1-Glu189: A Crucial Determinant in Substrate Water Selection, Positioning, and Stabilization within the Oxygen-Evolving Complex of Photosystem II
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Photosynthetic water oxidation is a vital process responsible for producing dioxygen and supplying the energy necessary to sustain life on Earth. This fundamental reaction is catalyzed by the oxygen-evolving complex (OEC) of photosystem II, which houses the Mn4CaO5 cluster as its catalytic core. In this study, we specifically focus on the D1-Glu189 amino acid residue, which serves as a direct ligand to the Mn4CaO5 cluster. Our primary goal is to explore, using density functional theory (DFT), how the conformational flexibility of the D1-Glu189 side chain influences crucial catalytic processes, particularly the selection, positioning, and stabilization of a substrate water molecule within the OEC. Our investigation is based on a hypothesis put forth by Li et al. (Nature, 2024, 626, 670), which suggests that during the transition from the S2 to S3 state, a specific water molecule temporarily coordinating with the Ca ion, referred to as O6*, may exist as a hydroxide ion (OH-). Our results demonstrate a key mechanism by which the detachment of the D1-Glu189 carboxylate group from its coordination with the Ca ion allows the creation of a specialized microenvironment within the OEC that enables the selective attraction of O6* in its deprotonated form (OH-) and stabilizes it at the catalytic metal (MnD) site. Our findings indicate that D1-Glu189 is not only a structural ligand for the Ca ion but may also play an active and dynamic role in the catalytic process, positioning O6* optimally for its subsequent participation in the oxidation sequence during the water-splitting cycle.
en-copyright=
kn-copyright=

en-aut-name=IsobeHiroshi
en-aut-sei=Isobe
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SuzukiTakayoshi
en-aut-sei=Suzuki
en-aut-mei=Takayoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SugaMichihiro
en-aut-sei=Suga
en-aut-mei=Michihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ShenJian-Ren
en-aut-sei=Shen
en-aut-mei=Jian-Ren
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YamaguchiKizashi
en-aut-sei=Yamaguchi
en-aut-mei=Kizashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Research Institute for Interdisciplinary Science, Okayama University
kn-affil=

affil-num=2
en-affil=Research Institute for Interdisciplinary Science, Okayama University
kn-affil=

affil-num=3
en-affil=Research Institute for Interdisciplinary Science, Okayama University
kn-affil=

affil-num=4
en-affil=Research Institute for Interdisciplinary Science, Okayama University
kn-affil=

affil-num=5
en-affil=Center for Quantum Information and Quantum Biology, Osaka University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=193
cd-vols=
no-issue=3
article-no=
start-page=2122
end-page=2140
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230720
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Calredoxin regulates the chloroplast NADPH-dependent thioredoxin reductase in Chlamydomonas reinhardtii
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Calredoxin (CRX) is a calcium (Ca2+)-dependent thioredoxin (TRX) in the chloroplast of Chlamydomonas (Chlamydomonas reinhardtii) with a largely unclear physiological role. We elucidated the CRX functionality by performing in-depth quantitative proteomics of wild-type cells compared with a crx insertional mutant (IMcrx), two CRISPR/Cas9 KO mutants, and CRX rescues. These analyses revealed that the chloroplast NADPH-dependent TRX reductase (NTRC) is co-regulated with CRX. Electron transfer measurements revealed that CRX inhibits NADPH-dependent reduction of oxidized chloroplast 2-Cys peroxiredoxin (PRX1) via NTRC and that the function of the NADPH-NTRC complex is under strict control of CRX. Via non-reducing SDS-PAGE assays and mass spectrometry, our data also demonstrated that PRX1 is more oxidized under high light (HL) conditions in the absence of CRX. The redox tuning of PRX1 and control of the NADPH-NTRC complex via CRX interconnect redox control with active photosynthetic electron transport and metabolism, as well as Ca2+ signaling. In this way, an economic use of NADPH for PRX1 reduction is ensured. The finding that the absence of CRX under HL conditions severely inhibited light-driven CO2 fixation underpins the importance of CRX for redox tuning, as well as for efficient photosynthesis.
en-copyright=
kn-copyright=

en-aut-name=ZinziusKaren
en-aut-sei=Zinzius
en-aut-mei=Karen
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MarchettiGiulia Maria
en-aut-sei=Marchetti
en-aut-mei=Giulia Maria
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=FischerRonja
en-aut-sei=Fischer
en-aut-mei=Ronja
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MilradYuval
en-aut-sei=Milrad
en-aut-mei=Yuval
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=OltmannsAnne
en-aut-sei=Oltmanns
en-aut-mei=Anne
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KelterbornSimon
en-aut-sei=Kelterborn
en-aut-mei=Simon
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YacobyIftach
en-aut-sei=Yacoby
en-aut-mei=Iftach
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=HegemannPeter
en-aut-sei=Hegemann
en-aut-mei=Peter
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=ScholzMartin
en-aut-sei=Scholz
en-aut-mei=Martin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=HipplerMichael
en-aut-sei=Hippler
en-aut-mei=Michael
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Institute of Plant Biology and Biotechnology, University of Münster
kn-affil=

affil-num=2
en-affil=Institute of Plant Biology and Biotechnology, University of Münster
kn-affil=

affil-num=3
en-affil=Institute of Plant Biology and Biotechnology, University of Münster
kn-affil=

affil-num=4
en-affil=School of Plant Sciences and Food Security, The George S. Wise Faculty of Life Sciences, Tel Aviv University
kn-affil=

affil-num=5
en-affil=Institute of Plant Biology and Biotechnology, University of Münster
kn-affil=

affil-num=6
en-affil=Institute of Biology, Experimental Biophysics, Humboldt University of Berlin
kn-affil=

affil-num=7
en-affil=School of Plant Sciences and Food Security, The George S. Wise Faculty of Life Sciences, Tel Aviv University
kn-affil=

affil-num=8
en-affil=Institute of Biology, Experimental Biophysics, Humboldt University of Berlin
kn-affil=

affil-num=9
en-affil=Institute of Plant Biology and Biotechnology, University of Münster
kn-affil=

affil-num=10
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=78
cd-vols=
no-issue=5
article-no=
start-page=387
end-page=399
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202410
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Effect of Radon Inhalation on Murine Brain Proteins: Investigation Using Proteomic and Multivariate Analyses
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Radon is a known risk factor for lung cancer; however, it can be used beneficially, such as in radon therapy. We have previously reported the enhancement of antioxidant effects associated with trace amounts of oxidative stress as one of the positive biological effects of radon inhalation. However, the biological effects of radon inhalation are incompletely understood, and more detailed and comprehensive studies are required. Although several studies have used proteomics to investigate the effects of radon inhalation on body proteins, none has focused on brain proteins. In this study, we evaluated the expression status of proteins in murine brains using proteomic and multivariate analyses to identify those whose expressions changed following two days of radon inhalation at a concentration of 1,500 Bq/m3. We found associations of radon inhalation with the expressions of seven proteins related to neurotransmission and heat shock. These proteins may be proposed as biomarkers indicative of radon inhalation. Although further studies are required to obtain the detailed biological significance of these protein alterations, this study contributes to the elucidation of the biological effects of radon
inhalation as a low-dose radiation.
en-copyright=
kn-copyright=

en-aut-name=NaoeShota
en-aut-sei=Naoe
en-aut-mei=Shota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TanakaAyumi
en-aut-sei=Tanaka
en-aut-mei=Ayumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KanzakiNorie
en-aut-sei=Kanzaki
en-aut-mei=Norie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TakenakaReiju
en-aut-sei=Takenaka
en-aut-mei=Reiju
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SakodaAkihiro
en-aut-sei=Sakoda
en-aut-mei=Akihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MiyajiTakaaki
en-aut-sei=Miyaji
en-aut-mei=Takaaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YamaokaKiyonori
en-aut-sei=Yamaoka
en-aut-mei=Kiyonori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KataokaTakahiro
en-aut-sei=Kataoka
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Ningyo-toge Environmental Engineering Center, Japan Atomic Energy Agency
kn-affil=

affil-num=4
en-affil=Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Ningyo-toge Environmental Engineering Center, Japan Atomic Energy Agency
kn-affil=

affil-num=6
en-affil=Advanced Science Research Center, Okayama University
kn-affil=

affil-num=7
en-affil=Faculty of Health Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Faculty of Health Sciences, Okayama University
kn-affil=
en-keyword=radon inhalation
kn-keyword=radon inhalation
en-keyword=proteomics
kn-keyword=proteomics
en-keyword=multivariate analysis
kn-keyword=multivariate analysis
en-keyword=brain
kn-keyword=brain
en-keyword=oxidative stress
kn-keyword=oxidative stress
END

start-ver=1.4
cd-journal=joma
no-vol=7
cd-vols=
no-issue=1
article-no=
start-page=1141
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240914
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Contribution of collagen-binding protein Cnm of Streptococcus mutans to induced IgA nephropathy-like nephritis in rats
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=IgA nephropathy (IgAN), the most common primary glomerulonephritis, is considered an intractable disease with unknown pathogenic factors. In our previous study, Streptococcus mutans, the major causative bacteria of dental caries, which expresses Cnm, was related to the induction of IgAN-like nephritis. In the present study, the Cnm-positive S. mutans parental strain, a Cnm-defective isogenic mutant strain, its complementation strain, and recombinant Cnm (rCnm) protein were administered intravenously to Sprague Dawley rats, and the condition of their kidneys was evaluated focusing on the pathogenicity of Cnm. Rats treated with parental and complement bacterial strains and rCnm protein developed IgAN-like nephritis with mesangial proliferation and IgA and C3 mesangial deposition. Scanning immunoelectron microscopy revealed that rCnm was present in the electron-dense deposition area of the mesangial region in the rCnm protein group. These results demonstrated that the Cnm protein itself is an important factor in the induction of IgAN in rats.
en-copyright=
kn-copyright=

en-aut-name=NakaShuhei
en-aut-sei=Naka
en-aut-mei=Shuhei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MatsuokaDaiki
en-aut-sei=Matsuoka
en-aut-mei=Daiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MisakiTaro
en-aut-sei=Misaki
en-aut-mei=Taro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NagasawaYasuyuki
en-aut-sei=Nagasawa
en-aut-mei=Yasuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ItoSeigo
en-aut-sei=Ito
en-aut-mei=Seigo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NomuraRyota
en-aut-sei=Nomura
en-aut-mei=Ryota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NakanoKazuhiko
en-aut-sei=Nakano
en-aut-mei=Kazuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=Matsumoto-NakanoMichiyo
en-aut-sei=Matsumoto-Nakano
en-aut-mei=Michiyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Pediatric Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Pediatric Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Division of Nephrology, Seirei Hamamatsu General Hospital
kn-affil=

affil-num=4
en-affil=Department of General Internal Medicine, Hyogo College of Medicine
kn-affil=

affil-num=5
en-affil=Department of Internal Medicine, Japan Self-Defense Force Iruma Hospital
kn-affil=

affil-num=6
en-affil=Department of Pediatric Dentistry, Graduate School of Biomedical and Health Sciences, Hiroshima University
kn-affil=

affil-num=7
en-affil=Department of Pediatric Dentistry, Graduate School of Dentistry, The University of Osaka
kn-affil=

affil-num=8
en-affil=Department of Pediatric Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=12
cd-vols=
no-issue=8
article-no=
start-page=1835
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240812
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Surface Pre-Reacted Glass-Ionomer Eluate Suppresses Osteoclastogenesis through Downregulation of the MAPK Signaling Pathway
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Surface pre-reacted glass-ionomer (S-PRG) is a new bioactive filler utilized for the restoration of decayed teeth by its ability to release six bioactive ions that prevent the adhesion of dental plaque to the tooth surface. Since ionic liquids are reported to facilitate transepithelial penetration, we reasoned that S-PRG applied to root caries could impact the osteoclasts (OCs) in the proximal alveolar bone. Therefore, this study aimed to investigate the effect of S-PRG eluate solution on RANKL-induced OC-genesis and mineral dissolution in vitro. Using RAW264.7 cells as OC precursor cells (OPCs), TRAP staining and pit formation assays were conducted to monitor OC-genesis and mineral dissolution, respectively, while OC-genesis-associated gene expression was measured using quantitative real-time PCR (qPCR). Expression of NFATc1, a master regulator of OC differentiation, and the phosphorylation of MAPK signaling molecules were measured using Western blotting. S-PRG eluate dilutions at 1/200 and 1/400 showed no cytotoxicity to RAW264.7 cells but did significantly suppress both OC-genesis and mineral dissolution. The same concentrations of S-PRG eluate downregulated the RANKL-mediated induction of OCSTAMP and CATK mRNAs, as well as the expression of NFATc1 protein and the phosphorylation of ERK, JNK, and p38. These results demonstrate that S-PRG eluate can downregulate RANKL-induced OC-genesis and mineral dissolution, suggesting that its application to root caries might prevent alveolar bone resorption.
en-copyright=
kn-copyright=

en-aut-name=ChandraJanaki
en-aut-sei=Chandra
en-aut-mei=Janaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakamuraShin
en-aut-sei=Nakamura
en-aut-mei=Shin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ShindoSatoru
en-aut-sei=Shindo
en-aut-mei=Satoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=LeonElizabeth
en-aut-sei=Leon
en-aut-mei=Elizabeth
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=CastellonMaria
en-aut-sei=Castellon
en-aut-mei=Maria
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=PastoreMaria Rita
en-aut-sei=Pastore
en-aut-mei=Maria Rita
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=HeidariAlireza
en-aut-sei=Heidari
en-aut-mei=Alireza
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=WitekLukasz
en-aut-sei=Witek
en-aut-mei=Lukasz
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=CoelhoPaulo G.
en-aut-sei=Coelho
en-aut-mei=Paulo G.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=NakatsukaToshiyuki
en-aut-sei=Nakatsuka
en-aut-mei=Toshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=KawaiToshihisa
en-aut-sei=Kawai
en-aut-mei=Toshihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

affil-num=1
en-affil=Department of Oral Science and Translational Research, College of Dental Medicine, Nova Southeastern University
kn-affil=

affil-num=2
en-affil=Department of Pathophysiology-Periodontal Science, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Oral Science and Translational Research, College of Dental Medicine, Nova Southeastern University
kn-affil=

affil-num=4
en-affil=Department of Oral Science and Translational Research, College of Dental Medicine, Nova Southeastern University
kn-affil=

affil-num=5
en-affil=Department of Oral Science and Translational Research, College of Dental Medicine, Nova Southeastern University
kn-affil=

affil-num=6
en-affil=Department of Oral Science and Translational Research, College of Dental Medicine, Nova Southeastern University
kn-affil=

affil-num=7
en-affil=Department of Oral Science and Translational Research, College of Dental Medicine, Nova Southeastern University
kn-affil=

affil-num=8
en-affil=Biomaterials Division, NYU Dentistry
kn-affil=

affil-num=9
en-affil=Department of Biochemistry and Molecular Biology, Miller School of Medicine, University of Miami
kn-affil=

affil-num=10
en-affil=R&D Department, Shofu Inc.
kn-affil=

affil-num=11
en-affil=Department of Oral Science and Translational Research, College of Dental Medicine, Nova Southeastern University
kn-affil=
en-keyword=S-PRG
kn-keyword=S-PRG
en-keyword=osteoclast
kn-keyword=osteoclast
en-keyword=hydroxyapatite
kn-keyword=hydroxyapatite
en-keyword=TRAP staining
kn-keyword=TRAP staining
en-keyword=bioactive filler
kn-keyword=bioactive filler
END

start-ver=1.4
cd-journal=joma
no-vol=357
cd-vols=
no-issue=
article-no=
start-page=114601
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241001
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Revisiting the hormonal control of sexual dimorphism in chicken feathers
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Sexual dimorphism in plumage is widespread among avian species. In chickens, adult females exhibit countershading, characterized by dull-colored round feathers lacking fringe on the saddle, while adult males display vibrant plumage with deeply fringed bright feathers. This dimorphism is estrogen-dependent, and administering estrogen to males transforms their showy plumage into cryptic female-like plumage. Extensive studies have shown that estrogen’s role in female plumage formation requires thyroid hormone; however, the precise mechanisms of their interaction remain unclear. In this study, we investigated the roles of estrogen and thyroid hormone in creating sexual dimorphism in the structure and coloration of saddle feathers by administering each hormone to adult males and observing the resulting changes in regenerated feathers induced by plucking. RT-PCR analysis revealed that the expression of type 3 deiodinase (DIO3), responsible for thyroid hormone inactivation, correlates with fringing. Estrogen suppressed DIO3 and agouti signaling protein (ASIP) expression while stimulating BlSK1, a marker of barbule cells, resulting in female-like feathers with mottled patterns and lacking fringes. Administration of thyroxine (T4) stimulated BlSK1 and proopiomelanocortin (POMC) expression, with no effect on ASIP, leading to the formation of solid black feathers lacking fringes. Triiodothyronine (T3) significantly increased POMC expression in pulp cells in culture. Taken together, these findings suggest that estrogen promotes the formation of solid vanes by suppressing DIO3 expression, while also inducing the formation of mottled patterns through inhibition of ASIP expression and indirect stimulation of melanocortin expression via changes in local T3 concentration. This is the first report describing molecular mechanism underlying hormonal crosstalk in creating sexual dimorphism in feathers.
en-copyright=
kn-copyright=

en-aut-name=YouLi
en-aut-sei=You
en-aut-mei=Li
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NishioKaori
en-aut-sei=Nishio
en-aut-mei=Kaori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KowataKinue
en-aut-sei=Kowata
en-aut-mei=Kinue
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HorikawaMinaru
en-aut-sei=Horikawa
en-aut-mei=Minaru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=FukuchiHibiki
en-aut-sei=Fukuchi
en-aut-mei=Hibiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OgoshiMaho
en-aut-sei=Ogoshi
en-aut-mei=Maho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=AizawaSayaka
en-aut-sei=Aizawa
en-aut-mei=Sayaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TakeuchiSakae
en-aut-sei=Takeuchi
en-aut-mei=Sakae
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Biology, Faculty of Science, Okayama University
kn-affil=

affil-num=5
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=6
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=7
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=8
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=
en-keyword=Melanocortin
kn-keyword=Melanocortin
en-keyword=Thyroid hormone
kn-keyword=Thyroid hormone
en-keyword=ASIP
kn-keyword=ASIP
en-keyword=Estrogen
kn-keyword=Estrogen
en-keyword=Deiodinase
kn-keyword=Deiodinase
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=
article-no=
start-page=1403922
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240820
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Lentil adaptation to drought stress: response, tolerance, and breeding approaches
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Lentil (Lens culinaris Medik.) is a cool season legume crop that plays vital roles in food and nutritional security, mostly in the least developed countries. Lentil is often cultivated in dry and semi-dry regions, where the primary abiotic factor is drought, which negatively impacts lentil growth and development, resulting in a reduction of yield. To withstand drought-induced multiple negative effects, lentil plants evolved a variety of adaptation strategies that can be classified within three broad categories of drought tolerance mechanisms (i.e., escape, avoidance, and tolerance). Lentil adapts to drought by the modulation of various traits in the root system, leaf architecture, canopy structure, branching, anatomical features, and flowering process. Furthermore, the activation of certain defensive biochemical pathways as well as the regulation of gene functions contributes to lentil drought tolerance. Plant breeders typically employ conventional and mutational breeding approaches to develop lentil varieties that can withstand drought effects; however, little progress has been made in developing drought-tolerant lentil varieties using genomics-assisted technologies. This review highlights the current understanding of morpho-physiological, biochemical, and molecular mechanisms of lentil adaptation to drought stress. We also discuss the potential application of omics-assisted breeding approaches to develop lentil varieties with superior drought tolerance traits.
en-copyright=
kn-copyright=

en-aut-name=NoorMd. Mahmud Al
en-aut-sei=Noor
en-aut-mei=Md. Mahmud Al
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=Tahjib-Ul-ArifMd.
en-aut-sei=Tahjib-Ul-Arif
en-aut-mei=Md.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=AlimS. M. Abdul
en-aut-sei=Alim
en-aut-mei=S. M. Abdul
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=IslamMd. Mohimenul
en-aut-sei=Islam
en-aut-mei=Md. Mohimenul
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HasanMd. Toufiq
en-aut-sei=Hasan
en-aut-mei=Md. Toufiq
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=BabarMd. Ali
en-aut-sei=Babar
en-aut-mei=Md. Ali
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=HossainMohammad Anwar
en-aut-sei=Hossain
en-aut-mei=Mohammad Anwar
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=JewelZilhas Ahmed
en-aut-sei=Jewel
en-aut-mei=Zilhas Ahmed
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MurataYoshiyuki
en-aut-sei=Murata
en-aut-mei=Yoshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=MostofaMohammad Golam
en-aut-sei=Mostofa
en-aut-mei=Mohammad Golam
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Plant Breeding Division, Bangladesh Institute of Nuclear Agriculture
kn-affil=

affil-num=2
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=3
en-affil=Plant Breeding Division, Bangladesh Institute of Nuclear Agriculture
kn-affil=

affil-num=4
en-affil=Horticulture Division, Bangladesh Institute of Nuclear Agriculture
kn-affil=

affil-num=5
en-affil=Department of Biotechnology, Bangladesh Agricultural University
kn-affil=

affil-num=6
en-affil=Agronomy Departments, University of Florida
kn-affil=

affil-num=7
en-affil=Department of Genetics and Plant Breeding, Bangladesh Agricultural University
kn-affil=

affil-num=8
en-affil=Faculty of Agriculture, Bangabandhu Sheikh Mujibur Rahman Science and Technology University
kn-affil=

affil-num=9
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=10
en-affil=Department of Biochemistry and Molecular Biology, Michigan State University
kn-affil=
en-keyword=abiotic stress
kn-keyword=abiotic stress
en-keyword=morphology
kn-keyword=morphology
en-keyword=pulse crop
kn-keyword=pulse crop
en-keyword=plant growth
kn-keyword=plant growth
en-keyword=omics
kn-keyword=omics
en-keyword=water-deficit
kn-keyword=water-deficit
END

start-ver=1.4
cd-journal=joma
no-vol=88
cd-vols=
no-issue=10
article-no=
start-page=1164
end-page=1171
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240716
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Cytosolic acidification and oxidation are the toxic mechanisms of SO2 in Arabidopsis guard cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=SO2/H2SO3 can damage plants. However, its toxic mechanism has still been controversial. Two models have been proposed, cytosolic acidification model and cellular oxidation model. Here, we assessed the toxic mechanism of H2SO3 in three cell types of Arabidopsis thaliana, mesophyll cells, guard cells (GCs), and petal cells. The sensitivity of GCs of Chloride channel a (CLCa)-knockout mutants to H2SO3 was significantly lower than those of wildtype plants. Expression of other CLC genes in mesophyll cells and petal cells were different from GCs. Treatment with antioxidant, disodium 4,5-dihydroxy-1,3-benzenedisulfonate (tiron), increased the median lethal concentration (LC50) of H2SO3 in GCs indicating the involvement of cellular oxidation, while the effect was negligible in mesophyll cells and petal cells. These results indicate that there are two toxic mechanisms of SO2 to Arabidopsis cells: cytosolic acidification and cellular oxidation, and the toxic mechanism may vary among cell types.
en-copyright=
kn-copyright=

en-aut-name=MozhganiMahdi
en-aut-sei=Mozhgani
en-aut-mei=Mahdi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OoiLia
en-aut-sei=Ooi
en-aut-mei=Lia
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=EspagneChristelle
en-aut-sei=Espagne
en-aut-mei=Christelle
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=FilleurSophie
en-aut-sei=Filleur
en-aut-mei=Sophie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MoriIzumi C
en-aut-sei=Mori
en-aut-mei=Izumi C
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=2
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=3
en-affil=Université Paris-Saclay, CEA, CNRS, Institute for Integrative Biology of the Cell (I2BC)
kn-affil=

affil-num=4
en-affil=Université Paris-Saclay, CEA, CNRS, Institute for Integrative Biology of the Cell (I2BC)
kn-affil=

affil-num=5
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=
en-keyword=cytosolic acidification
kn-keyword=cytosolic acidification
en-keyword=Arabidopsis
kn-keyword=Arabidopsis
en-keyword=cellular oxidation
kn-keyword=cellular oxidation
en-keyword=chloride channel a
kn-keyword=chloride channel a
en-keyword=sulfur dioxide
kn-keyword=sulfur dioxide
END

start-ver=1.4
cd-journal=joma
no-vol=5
cd-vols=
no-issue=9
article-no=
start-page=884
end-page=890
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240731
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Novel strategy for activating gene expression through triplex DNA formation targeting epigenetically suppressed genes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Triplex DNA formation is a useful genomic targeting tool that is expected to have a wide range of applications, including the antigene method; however, there are fundamental limitations in its forming sequence. We recently extended the triplex DNA-forming sequence to methylated DNA sequences containing 5mCG base pairs by developing guanidino-dN, which is capable of recognizing a 5mCG base pair with high affinity. We herein investigated the effect of triplex DNA formation using TFOs with guanidino-dN on methylated DNA sequences at the promoter of the RASSF1A gene, whose expression is epigenetically suppressed by DNA methylation in MCF-7 cells, on gene expression. Interestingly, triplex DNA formation increased the expression of the RASSF1A gene at the transcript and protein levels. Furthermore, RASSF1A-activated MCF-7 cells exhibited cell growth suppressing activity. Changes in the expression of various genes associated with the promotion of apoptosis and breast cancer survival accompanied the activation of RASSF1A in cells exhibited antiproliferative activity. These results suggest the potential of increases in gene expression through triplex DNA formation as a new genomic targeting tool.
en-copyright=
kn-copyright=

en-aut-name=NotomiRyotaro
en-aut-sei=Notomi
en-aut-mei=Ryotaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SasakiShigeki
en-aut-sei=Sasaki
en-aut-mei=Shigeki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TaniguchiYosuke
en-aut-sei=Taniguchi
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Graduate School of Pharmaceutical Sciences, Kyushu University
kn-affil=

affil-num=2
en-affil= Graduate School of Pharmaceutical Sciences, Nagasaki International University
kn-affil=

affil-num=3
en-affil=Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=9
cd-vols=
no-issue=8
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240729
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=New lineages of RNA viruses from clinical isolates of Rhizopus microsporus revealed by fragmented and primer-ligated dsRNA sequencing (FLDS) analysis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Rhizopus microsporus is a species in the order Mucorales that is known to cause mucormycosis, but it is poorly understood as a host of viruses. Here, we examined 25 clinical strains of R. microsporus for viral infection with a conventional double-stranded RNA (dsRNA) assay using agarose gel electrophoresis (AGE) and the recently established fragmented and primer-ligated dsRNA sequencing (FLDS) protocol. By AGE, five virus-infected strains were detected. Then, full-length genomic sequences of 12 novel RNA viruses were revealed by FLDS, which were related to the families Mitoviridae, Narnaviridae, and Endornaviridae, ill-defined groups of single-stranded RNA (ssRNA) viruses with similarity to the established families Virgaviridae and Phasmaviridae, and the proposed family "Ambiguiviridae." All the characterized viruses, except a potential phasmavirid with a negative-sense RNA genome, had positive-sense RNA genomes. One virus belonged to a previously established species within the family Mitoviridae, whereas the other 11 viruses represented new species or even new genera. These results show that the fungal pathogen R. microsporus harbors diverse RNA viruses and extend our understanding of the diversity of RNA viruses in the fungal order Mucorales, division Mucoromycota. Identifying RNA viruses from clinical isolates of R. microsporus may expand the repertoire of natural therapeutic agents for mucormycosis in the future.
en-copyright=
kn-copyright=

en-aut-name=Sa'diyahWasiatus
en-aut-sei=Sa'diyah
en-aut-mei=Wasiatus
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ZhaoYan-Jie
en-aut-sei=Zhao
en-aut-mei=Yan-Jie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ChibaYuto
en-aut-sei=Chiba
en-aut-mei=Yuto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KondoHideki
en-aut-sei=Kondo
en-aut-mei=Hideki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SuzukiNobuhiro
en-aut-sei=Suzuki
en-aut-mei=Nobuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=BanSayaka
en-aut-sei=Ban
en-aut-mei=Sayaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YaguchiTakashi
en-aut-sei=Yaguchi
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=UrayamaSyun-Ichi
en-aut-sei=Urayama
en-aut-mei=Syun-Ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=HagiwaraDaisuke
en-aut-sei=Hagiwara
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Life and Environmental Sciences, Laboratory of Fungal Interaction and Molecular Biology (Donated by IFO), University of Tsukuba
kn-affil=

affil-num=3
en-affil=Department of Life and Environmental Sciences, Laboratory of Fungal Interaction and Molecular Biology (Donated by IFO), University of Tsukuba
kn-affil=

affil-num=4
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=5
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=6
en-affil=Medical Mycology Research Center, Chiba University
kn-affil=

affil-num=7
en-affil=Medical Mycology Research Center, Chiba University
kn-affil=

affil-num=8
en-affil=Department of Life and Environmental Sciences, Laboratory of Fungal Interaction and Molecular Biology (Donated by IFO), University of Tsukuba
kn-affil=

affil-num=9
en-affil=Department of Life and Environmental Sciences, Laboratory of Fungal Interaction and Molecular Biology (Donated by IFO), University of Tsukuba
kn-affil=
en-keyword=Rhizopus microsporus
kn-keyword=Rhizopus microsporus
en-keyword=RNA virus
kn-keyword=RNA virus
en-keyword=diversity
kn-keyword=diversity
en-keyword=new lineage
kn-keyword=new lineage
en-keyword=FLDS
kn-keyword=FLDS
END

start-ver=1.4
cd-journal=joma
no-vol=8
cd-vols=
no-issue=8
article-no=
start-page=ziae085
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240704
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Macrophages modulate mesenchymal stem cell function via tumor necrosis factor alpha in tooth extraction model
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Mesenchymal stem cells (MSCs) and macrophages collaboratively contribute to bone regeneration after injury. However, detailed mechanisms underlying the interaction between MSCs and inflammatory macrophages (M1) remain unclear. A macrophage-depleted tooth extraction model was generated in 5-wk-old female C57BL/6J mice using clodronate liposome (12.5 mg/kg/mouse, intraperitoneally) or saline injection (control) before maxillary first molar extraction. Mice were sacrificed on days 1, 3, 5, 7, and 10 after tooth extraction (n = 4). Regenerated bone volume evaluation of tooth extraction socket (TES) and histochemical analysis of CD80+M1, CD206+M2 (anti-inflammatory macrophages), PDGFRα+MSC, and TNF-α+ cells were performed. In vitro, isolated MSCs with or without TNF-α stimulation (10 ng/mL, 24 h, n = 3) were bulk RNA-sequenced (RNA-Seq) to identify TNF-α stimulation-specific MSC transcriptomes. Day 7 micro-CT and HE staining revealed significantly lower mean bone volume (clodronate vs control: 0.01 mm3 vs 0.02 mm3, p<.0001) and mean percentage of regenerated bone area per total TES in clodronate group (41.97% vs 54.03%, p<.0001). Clodronate group showed significant reduction in mean number of CD80+, TNF-α+, PDGFRα+, and CD80+TNF-α+ cells on day 5 (306.5 vs 558.8, p<.0001; 280.5 vs 543.8, p<.0001; 365.0 vs 633.0, p<.0001, 29.0 vs 42.5, p<.0001), while these cells recovered significantly on day 7 (493.3 vs 396.0, p=.0004; 479.3 vs 384.5, p=.0008; 593.0 vs 473.0, p=.0010, 41.0 vs 32.5, p=.0003). RNA-Seq analysis showed that 15 genes (|log2FC| > 5.0, log2TPM > 5) after TNF-α stimulation were candidates for regulating MSC’s immunomodulatory capacity. In vivo, Clec4e and Gbp6 are involved in inflammation and bone formation. Clec4e, Gbp6, and Cxcl10 knockdown increased osteogenic differentiation of MSCs in vitro. Temporal reduction followed by apparent recovery of TNF-α-producing M1 macrophages and MSCs after temporal macrophage depletion suggests that TNF-α activated MSCs during TES healing. In vitro mimicking the effect of TNF-α on MSCs indicated that there are 15 candidate MSC genes for regulation of immunomodulatory capacity.
en-copyright=
kn-copyright=

en-aut-name=MunAung Ye
en-aut-sei=Mun
en-aut-mei=Aung Ye
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=AkiyamaKentaro
en-aut-sei=Akiyama
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=WangZiyi
en-aut-sei=Wang
en-aut-mei=Ziyi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ZhangJiewen
en-aut-sei=Zhang
en-aut-mei=Jiewen
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KitagawaWakana
en-aut-sei=Kitagawa
en-aut-mei=Wakana
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KohnoTeisaku
en-aut-sei=Kohno
en-aut-mei=Teisaku
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TagashiraRyuji
en-aut-sei=Tagashira
en-aut-mei=Ryuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=IshibashiKei
en-aut-sei=Ishibashi
en-aut-mei=Kei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MatsunagaNaoya
en-aut-sei=Matsunaga
en-aut-mei=Naoya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=ZouTingling
en-aut-sei=Zou
en-aut-mei=Tingling
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=OnoMitsuaki
en-aut-sei=Ono
en-aut-mei=Mitsuaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=KubokiTakuo
en-aut-sei=Kuboki
en-aut-mei=Takuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

affil-num=1
en-affil=Department of Oral Rehabilitation and Regenerative Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Oral Rehabilitation and Regenerative Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Molecular Biology and Biochemistry, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Oral Rehabilitation and Regenerative Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Oral Rehabilitation and Regenerative Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Oral Rehabilitation and Regenerative Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Oral Rehabilitation and Regenerative Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Oral Rehabilitation and Regenerative Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Oral Rehabilitation and Regenerative Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=10
en-affil=Department of Oral Rehabilitation and Regenerative Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=11
en-affil=Department of Molecular Biology and Biochemistry, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=12
en-affil=Department of Oral Rehabilitation and Regenerative Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=cytokines
kn-keyword=cytokines
en-keyword=dental biology
kn-keyword=dental biology
en-keyword=injury healing
kn-keyword=injury healing
en-keyword=osteoimmunology
kn-keyword=osteoimmunology
en-keyword=stem cells
kn-keyword=stem cells
END

start-ver=1.4
cd-journal=joma
no-vol=10
cd-vols=
no-issue=13
article-no=
start-page=e34206
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240715
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Resolvin D2-induced reparative dentin and pulp stem cells after pulpotomy in a rat model
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Introduction: Vital pulp therapy (VPT) is performed to preserve dental pulp. However, the biocompatibility of the existing materials is of concern. Therefore, novel materials that can induce pulp healing without adverse effects need to be developed. Resolvin D2 (RvD2), one of specialized pro-resolving mediators, can resolve inflammation and promote the healing of periapical lesions. Therefore, RvD2 may be suitable for use in VPT. In the present study, we evaluated the efficacy of RvD2 against VPT using in vivo and in vitro models.<br>
Methods: First molars of eight-week-old male Sprague–Dawley rats were used for pulpotomy. They were then divided into three treatment groups: RvD2, phosphate-buffered saline, and calcium hydroxide groups. Treatment results were assessed using radiological, histological, and immunohistochemical (GPR18, TNF-α, Ki67, VEGF, TGF-β, CD44, CD90, and TRPA1) analyses. Dental pulp-derived cells were treated with RvD2 in vitro and analyzed using cell-proliferation and cell-migration assays, real-time PCR (Gpr18, Tnf-α, Il-1β, Tgf-β, Vegf, Nanog, and Trpa1), ELISA (VEGF and TGF-β), immunocytochemistry (TRPA1), and flow cytometry (dental pulp stem cells: DPSCs).<br>
Results: The formation of calcified tissue in the pulp was observed in the RvD2 and calcium hydroxide groups. RvD2 inhibited inflammation in dental pulp cells. RvD2 promoted cell proliferation and migration and the expression of TGF-β and VEGF in vitro and in vivo. RvD2 increased the number of DPSCs. In addition, RvD2 suppressed TRPA1 expression as a pain receptor.<br>
Conclusion: RvD2 induced the formation of reparative dentin, anti-inflammatory effects, and decreased pain, along with the proliferation of DPSCs via the expression of VEGF and TGF-β, on the pulp surface in pulpotomy models.
en-copyright=
kn-copyright=

en-aut-name=YonedaMitsuhiro
en-aut-sei=Yoneda
en-aut-mei=Mitsuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=IdeguchiHidetaka
en-aut-sei=Ideguchi
en-aut-mei=Hidetaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NakamuraShin
en-aut-sei=Nakamura
en-aut-mei=Shin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=AriasZulema
en-aut-sei=Arias
en-aut-mei=Zulema
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=OnoMitsuaki
en-aut-sei=Ono
en-aut-mei=Mitsuaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OmoriKazuhiro
en-aut-sei=Omori
en-aut-mei=Kazuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YamamotoTadashi
en-aut-sei=Yamamoto
en-aut-mei=Tadashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TakashibaShogo
en-aut-sei=Takashiba
en-aut-mei=Shogo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Periodontics and Endodontics, Division of Dentistry, Okayama University Hospital
kn-affil=

affil-num=2
en-affil=Department of Pathophysiology-Periodontal Science, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Oral Science and Translational Research, College of Dental Medicine, Nova Southeastern University
kn-affil=

affil-num=4
en-affil=Department of Pathophysiology-Periodontal Science, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Molecular Biology and Biochemistry, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Pathophysiology-Periodontal Science, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=The Center for Graduate Medical Education (Dental Division), Okayama University Hospital
kn-affil=

affil-num=8
en-affil=Department of Pathophysiology-Periodontal Science, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Dental pulp
kn-keyword=Dental pulp
en-keyword=Regeneration
kn-keyword=Regeneration
en-keyword=Pulp-capping agents
kn-keyword=Pulp-capping agents
en-keyword=Specialized pro-resolving mediators
kn-keyword=Specialized pro-resolving mediators
en-keyword=Resolvin D2
kn-keyword=Resolvin D2
en-keyword=Calcification
kn-keyword=Calcification
en-keyword=Cytokine
kn-keyword=Cytokine
en-keyword=TRPA1
kn-keyword=TRPA1
en-keyword=Animal model
kn-keyword=Animal model
END

start-ver=1.4
cd-journal=joma
no-vol=60
cd-vols=
no-issue=10
article-no=
start-page=1138
end-page=1149
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240606
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=S100A11 is involved in the progression of colorectal cancer through the desmosome-catenin-TCF signaling pathway
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Compiling evidence has indicated that S100A11 expression at high levels is closely associated with various cancer species. Consistent with the results reported elsewhere, we have also revealed that S100A11 is highly expressed in squamous cell carcinoma, mesothelioma, and pancreatic cancers and plays a crucial role in cancer progression when secreted into extracellular fluid. Those studies are all focused on the extracellular role of S100A11. However, most of S100A11 is still present within cancer cells, although the intracellular role of S100A11 in cancer cells has not been fully elucidated. Thus, we aimed to investigate S100A11 functions within cancer cells, primarily focusing on colorectal cancer cells, whose S100A11 is abundantly present in cells and still poorly studied cancer for the protein. Our efforts revealed that overexpression of S100A11 promotes proliferation and migration, and downregulation inversely dampens those cancer behaviors. To clarify how intracellular S100A11 aids cancer cell activation, we tried to identify S100A11 binding proteins, resulting in novel binding partners in the inner membrane, many of which are desmosome proteins. Our molecular approach defined that S100A11 regulates the expression level of DSG1, a component protein of desmosome, by which S100A11 activates the TCF pathway via promoting nuclear translocation of γ-catenin from the desmosome. The identified new pathway greatly helps to comprehend S100A11’s nature in colorectal cancers and others.
en-copyright=
kn-copyright=

en-aut-name=ZhouJin
en-aut-sei=Zhou
en-aut-mei=Jin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MurataHitoshi
en-aut-sei=Murata
en-aut-mei=Hitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TomonobuNahoko
en-aut-sei=Tomonobu
en-aut-mei=Nahoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MizutaNaoko
en-aut-sei=Mizuta
en-aut-mei=Naoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YamakawaAtsuko
en-aut-sei=Yamakawa
en-aut-mei=Atsuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YamamotoKen-ichi
en-aut-sei=Yamamoto
en-aut-mei=Ken-ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KinoshitaRie
en-aut-sei=Kinoshita
en-aut-mei=Rie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=SakaguchiMasakiyo
en-aut-sei=Sakaguchi
en-aut-mei=Masakiyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=S100A11
kn-keyword=S100A11
en-keyword=Desmosome
kn-keyword=Desmosome
en-keyword=TCF signaling
kn-keyword=TCF signaling
en-keyword=Colorectal cancer
kn-keyword=Colorectal cancer
END

start-ver=1.4
cd-journal=joma
no-vol=12
cd-vols=
no-issue=2
article-no=
start-page=16
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240603
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Harderian Gland Development and Degeneration in the Fgf10-Deficient Heterozygous Mouse
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The mouse Harderian gland (HG) is a secretory gland that covers the posterior portion of the eyeball, opening at the base of the nictitating membrane. The HG serves to protect the eye surface from infection with its secretions. Mice open their eyelids at about 2 weeks of age, and the development of the HG primordium mechanically opens the eye by pushing the eyeball from its rear. Therefore, when HG formation is disturbed, the eye exhibits enophthalmos (the slit-eye phenotype), and a line of Fgf10(+/-) heterozygous loss-of-function mice exhibits slit-eye due to the HG atrophy. However, it has not been clarified how and when HGs degenerate and atrophy in Fgf10(+/-) mice. In this study, we observed the HGs in embryonic (E13.5 to E19), postnatal (P0.5 to P18) and 74-week-old Fgf10(+/-) mice. We found that more than half of the Fgf10(+/-) mice had markedly degenerated HGs, often unilaterally. The degenerated HG tissue had a melanized appearance and was replaced by connective tissue, which was observed by P10. The development of HGs was delayed or disrupted in the similar proportion of Fgf10(+/-) embryos, as revealed via histology and the loss of HG-marker expression. In situ hybridization showed Fgf10 expression was observed in the Harderian mesenchyme in wild-type as well as in the HG-lacking heterozygote at E19. These results show that the Fgf10 haploinsufficiency causes delayed or defective HG development, often unilaterally from the unexpectedly early neonatal period.
en-copyright=
kn-copyright=

en-aut-name=IkedaShiori
en-aut-sei=Ikeda
en-aut-mei=Shiori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SatoKeita
en-aut-sei=Sato
en-aut-mei=Keita
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=FujitaHirofumi
en-aut-sei=Fujita
en-aut-mei=Hirofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=Ono-MinagiHitomi
en-aut-sei=Ono-Minagi
en-aut-mei=Hitomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MiyaishiSatoru
en-aut-sei=Miyaishi
en-aut-mei=Satoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NohnoTsutomu
en-aut-sei=Nohno
en-aut-mei=Tsutomu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=OhuchiHideyo
en-aut-sei=Ohuchi
en-aut-mei=Hideyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Department of Cytology and Histology, Medical School, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Cytology and Histology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Cytology and Histology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Cytology and Histology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Legal Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Cytology and Histology, Medical School, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Cytology and Histology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Harderian gland
kn-keyword=Harderian gland
en-keyword=Fgf10
kn-keyword=Fgf10
en-keyword=haploinsufficiency
kn-keyword=haploinsufficiency
en-keyword=mouse
kn-keyword=mouse
END

start-ver=1.4
cd-journal=joma
no-vol=32
cd-vols=
no-issue=11
article-no=
start-page=1419
end-page=1432
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202411
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Inverse genetics tracing the differentiation pathway of human chondrocytes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Objective: Mammalian somatic cells can be reprogrammed into induced pluripotent stem cells (iPSCs) via the forced expression of Yamanaka reprogramming factors. However, only a limited population of the cells that pass through a particular pathway can metamorphose into iPSCs, while the others do not. This study aimed to clarify the pathways that chondrocytes follow during the reprogramming process.<br>
Design: The fate of human articular chondrocytes under reprogramming was investigated through a time-coursed single-cell transcriptomic analysis, which we termed an inverse genetic approach. The iPS interference technique was also employed to verify that chondrocytes inversely return to pluripotency following the proper differentiation pathway.<br>
Results: We confirmed that human chondrocytes could be converted into cells with an iPSC phenotype. Moreover, it was clarified that a limited population that underwent the silencing of SOX9, a master gene for chondrogenesis, at a specific point during the proper transcriptome transition pathway, could eventually become iPSCs. Interestingly, the other cells, which failed to be reprogrammed, followed a distinct pathway toward cells with a surface zone chondrocyte phenotype. The critical involvement of cellular communication network factors (CCNs) in this process was indicated. The idea that chondrocytes, when reprogrammed into iPSCs, follow the differentiation pathway backward was supported by the successful iPS interference using SOX9.<br>
Conclusions: This inverse genetic strategy may be useful for seeking candidates for the master genes for the differentiation of various somatic cells. The utility of CCNs in articular cartilage regeneration is also supported.
en-copyright=
kn-copyright=

en-aut-name=DoH.T.
en-aut-sei=Do
en-aut-mei=H.T.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OnoM.
en-aut-sei=Ono
en-aut-mei=M.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=WangZ.
en-aut-sei=Wang
en-aut-mei=Z.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KitagawaW.
en-aut-sei=Kitagawa
en-aut-mei=W.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=DangA.T.
en-aut-sei=Dang
en-aut-mei=A.T.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YonezawaT.
en-aut-sei=Yonezawa
en-aut-mei=T.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KubokiT.
en-aut-sei=Kuboki
en-aut-mei=T.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=OohashiT.
en-aut-sei=Oohashi
en-aut-mei=T.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KubotaS.
en-aut-sei=Kubota
en-aut-mei=S.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Oral Rehabilitation and Regenerative Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Biochemistry and Molecular Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Cartilage
kn-keyword=Cartilage
en-keyword=Chondrocyte
kn-keyword=Chondrocyte
en-keyword=Differentiation
kn-keyword=Differentiation
en-keyword=Reprogramming
kn-keyword=Reprogramming
en-keyword=CCN family
kn-keyword=CCN family
END

start-ver=1.4
cd-journal=joma
no-vol=25
cd-vols=
no-issue=12
article-no=
start-page=6648
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240617
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Local E-rhBMP-2/β-TCP Application Rescues Osteocyte Dendritic Integrity and Reduces Microstructural Damage in Alveolar Bone Post-Extraction in MRONJ-like Mouse Model
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The pathology of medication-related osteonecrosis of the jaw (MRONJ), often associated with antiresorptive therapy, is still not fully understood. Osteocyte networks are known to play a critical role in maintaining bone homeostasis and repair, but the exact condition of these networks in MRONJ is unknown. On the other hand, the local application of E-coli-derived Recombinant Human Bone Morphogenetic Protein 2/beta-Tricalcium phosphate (E-rhBMP-2/beta-TCP) has been shown to promote bone regeneration and mitigate osteonecrosis in MRONJ-like mouse models, indicating its potential therapeutic application for the treatment of MRONJ. However, the detailed effect of BMP-2 treatment on restoring bone integrity, including its osteocyte network, in an MRONJ condition remains unclear. Therefore, in the present study, by applying a scanning electron microscope (SEM) analysis and a 3D osteocyte network reconstruction workflow on the alveolar bone surrounding the tooth extraction socket of an MRONJ-like mouse model, we examined the effectiveness of BMP-2/beta-TCP therapy on the alleviation of MRONJ-related bone necrosis with a particular focus on the osteocyte network and alveolar bone microstructure (microcrack accumulation). The 3D osteocyte dendritic analysis showed a significant decrease in osteocyte dendritic parameters along with a delay in bone remodeling in the MRONJ group compared to the healthy counterpart. The SEM analysis also revealed a notable increase in the number of microcracks in the alveolar bone surface in the MRONJ group compared to the healthy group. In contrast, all of those parameters were restored in the E-rhBMP-2/beta-TCP-treated group to levels that were almost similar to those in the healthy group. In summary, our study reveals that MRONJ induces osteocyte network degradation and microcrack accumulation, while application of E-rhBMP-2/beta-TCP can restore a compromised osteocyte network and abrogate microcrack accumulation in MRONJ.
en-copyright=
kn-copyright=

en-aut-name=DangAnh Tuan
en-aut-sei=Dang
en-aut-mei=Anh Tuan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OnoMitsuaki
en-aut-sei=Ono
en-aut-mei=Mitsuaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=WangZiyi
en-aut-sei=Wang
en-aut-mei=Ziyi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TosaIkue
en-aut-sei=Tosa
en-aut-mei=Ikue
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HaraEmilio Satoshi
en-aut-sei=Hara
en-aut-mei=Emilio Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MikaiAkihiro
en-aut-sei=Mikai
en-aut-mei=Akihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KitagawaWakana
en-aut-sei=Kitagawa
en-aut-mei=Wakana
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YonezawaTomoko
en-aut-sei=Yonezawa
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KubokiTakuo
en-aut-sei=Kuboki
en-aut-mei=Takuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=OohashiToshitaka
en-aut-sei=Oohashi
en-aut-mei=Toshitaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Oral Rehabilitation and Regenerative Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Advanced Research Center for Oral and Craniofacial Sciences, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Oral Rehabilitation and Regenerative Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=medication-related osteonecrosis of the jaw
kn-keyword=medication-related osteonecrosis of the jaw
en-keyword=BMP-2
kn-keyword=BMP-2
en-keyword=osteocyte dendritic network
kn-keyword=osteocyte dendritic network
en-keyword=microcrack accumulation
kn-keyword=microcrack accumulation
en-keyword=bone remodeling
kn-keyword=bone remodeling
END

start-ver=1.4
cd-journal=joma
no-vol=25
cd-vols=
no-issue=13
article-no=
start-page=6986
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240626
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Genome-Wide Association Study with Three Control Cohorts of Japanese Patients with Esotropia and Exotropia of Comitant Strabismus and Idiopathic Superior Oblique Muscle Palsy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Esotropia and exotropia in the entity of comitant strabismus are multifactorial diseases with both genetic and environmental backgrounds. Idiopathic superior oblique muscle palsy, as the predominant entity of non-comitant (paralytic) strabismus, also has a genetic background, as evidenced by varying degrees of muscle hypoplasia. A genome-wide association study (GWAS) was conducted of 711 Japanese patients with esotropia (n= 253), exotropia (n = 356), and idiopathic superior oblique muscle palsy (n = 102). The genotypes of single nucleotide polymorphisms (SNPs) were determined by Infinium Asian Screening Array. Three control cohorts from the Japanese population were used: two cohorts from BioBank Japan (BBJ) and the Nagahama Cohort. BBJ (180K) was genotyped by a different array, Illumina Infinium OmniExpressExome or HumanOmniExpress, while BBJ (ASA) and the Nagahama Cohort were genotyped by the same Asian array. After quality control of SNPs and individuals, common SNPs between the case cohort and the control cohort were chosen in the condition of genotyping by different arrays, while all SNPs genotyped by the same array were used for SNP imputation. The SNPs imputed with R-square values ≥ 0.3 were used to compare the case cohort of each entity or the combined entity with the control cohort. In comparison with BBJ (180K), the esotropia group and the exotropia group showed CDCA7 and HLA-F, respectively, as candidate genes at a significant level of p < 5 × 10−8, while the idiopathic superior oblique muscle palsy group showed DAB1 as a candidate gene which is involved in neuronal migration. DAB1 was also detected as a candidate in comparison with BBJ (ASA) and the Nagahama Cohort at a weak level of significance of p < 1 × 10−6. In comparison with BBJ (180K), RARB (retinoic acid receptor-β) was detected as a candidate at a significant level of p < 5 × 10−8 in the combined group of esotropia, exotropia, and idiopathic superior oblique muscle palsy. In conclusion, a series of GWASs with three different control cohorts would be an effective method with which to search for candidate genes for multifactorial diseases such as strabismus.
en-copyright=
kn-copyright=

en-aut-name=MatsuoToshihiko
en-aut-sei=Matsuo
en-aut-mei=Toshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HamasakiIchiro
en-aut-sei=Hamasaki
en-aut-mei=Ichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KamataniYoichiro
en-aut-sei=Kamatani
en-aut-mei=Yoichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KawaguchiTakahisa
en-aut-sei=Kawaguchi
en-aut-mei=Takahisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YamaguchiIzumi
en-aut-sei=Yamaguchi
en-aut-mei=Izumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MatsudaFumihiko
en-aut-sei=Matsuda
en-aut-mei=Fumihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SaitoAkira
en-aut-sei=Saito
en-aut-mei=Akira
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NakazonoKazuyuki
en-aut-sei=Nakazono
en-aut-mei=Kazuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KamitsujiShigeo
en-aut-sei=Kamitsuji
en-aut-mei=Shigeo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Ophthalmology, Okayama University Hospital
kn-affil=

affil-num=3
en-affil=Department of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo
kn-affil=

affil-num=4
en-affil=Center for Genomic Medicine, Graduate School of Medicine, Kyoto University
kn-affil=

affil-num=5
en-affil=Center for Genomic Medicine, Graduate School of Medicine, Kyoto University
kn-affil=

affil-num=6
en-affil=Center for Genomic Medicine, Graduate School of Medicine, Kyoto University
kn-affil=

affil-num=7
en-affil=StaGen Co., Ltd.
kn-affil=

affil-num=8
en-affil=StaGen Co., Ltd.
kn-affil=

affil-num=9
en-affil=StaGen Co., Ltd.
kn-affil=
en-keyword=esotropia
kn-keyword=esotropia
en-keyword=exotropia
kn-keyword=exotropia
en-keyword=superior oblique muscle palsy
kn-keyword=superior oblique muscle palsy
en-keyword=genome-wide association study
kn-keyword=genome-wide association study
en-keyword=comitant strabismus
kn-keyword=comitant strabismus
en-keyword=non-comitant strabismus
kn-keyword=non-comitant strabismus
en-keyword=Japanese population
kn-keyword=Japanese population
en-keyword=BioBank Japan
kn-keyword=BioBank Japan
en-keyword=Nagahama Cohort
kn-keyword=Nagahama Cohort
en-keyword=Asian array
kn-keyword=Asian array
END

start-ver=1.4
cd-journal=joma
no-vol=14
cd-vols=
no-issue=1
article-no=
start-page=5938
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240311
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Palaeoproteomic investigation of an ancient human skeleton with abnormal deposition of dental calculus
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Detailed investigation of extremely severe pathological conditions in ancient human skeletons is important as it could shed light on the breadth of potential interactions between humans and disease etiologies in the past. Here, we applied palaeoproteomics to investigate an ancient human skeletal individual with severe oral pathology, focusing our research on bacterial pathogenic factors and host defense response. This female skeleton, from the Okhotsk period (i.e., fifth to thirteenth century) of Northern Japan, poses relevant amounts of abnormal dental calculus deposition and exhibits oral dysfunction due to severe periodontal disease. A shotgun mass-spectrometry analysis identified 81 human proteins and 15 bacterial proteins from the calculus of the subject. We identified two pathogenic or bioinvasive proteins originating from two of the three "red complex" bacteria, the core species associated with severe periodontal disease in modern humans, as well as two additional bioinvasive proteins of periodontal-associated bacteria. Moreover, we discovered defense response system-associated human proteins, although their proportion was mostly similar to those reported in ancient and modern human individuals with lower calculus deposition. These results suggest that the bacterial etiology was similar and the host defense response was not necessarily more intense in ancient individuals with significant amounts of abnormal dental calculus deposition.
en-copyright=
kn-copyright=

en-aut-name=Uchida-FukuharaYoko
en-aut-sei=Uchida-Fukuhara
en-aut-mei=Yoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ShimamuraShigeru
en-aut-sei=Shimamura
en-aut-mei=Shigeru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SawafujiRikai
en-aut-sei=Sawafuji
en-aut-mei=Rikai
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NishiuchiTakumi
en-aut-sei=Nishiuchi
en-aut-mei=Takumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YonedaMinoru
en-aut-sei=Yoneda
en-aut-mei=Minoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=IshidaHajime
en-aut-sei=Ishida
en-aut-mei=Hajime
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MatsumuraHirofumi
en-aut-sei=Matsumura
en-aut-mei=Hirofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TsutayaTakumi
en-aut-sei=Tsutaya
en-aut-mei=Takumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Oral Morphology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama  University
kn-affil=

affil-num=2
en-affil=Institute for Extra-Cutting-Edge  Science and Technology Avant-Garde Research (X-STAR), Japan Agency for Marine-Earth Science and  Technology (JAMSTEC)
kn-affil=

affil-num=3
en-affil=Research Center for Integrative Evolutionary Science, The Graduate  University for Advanced Studies (SOKENDAI)
kn-affil=

affil-num=4
en-affil=Research Center for Experimental  Modeling of Human Disease, Kanazawa University
kn-affil=

affil-num=5
en-affil=The University Museum, The  University of Tokyo
kn-affil=

affil-num=6
en-affil=Department of Human Biology and Anatomy, Graduate  School of Medicine, University of the Ryukyus
kn-affil=

affil-num=7
en-affil=School of Health  Sciences, Sapporo Medical University
kn-affil=

affil-num=8
en-affil=Research Center for Integrative Evolutionary Science, The Graduate  University for Advanced Studies (SOKENDAI)
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=14
cd-vols=
no-issue=
article-no=
start-page=1371307
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240528
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Dissection of the signal transduction machinery responsible for the lysyl oxidase-like 4-mediated increase in invasive motility in triple-negative breast cancer cells: mechanistic insight into the integrin-β1-NF-κB-MMP9 axis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background Triple-negative breast cancer (TNBC) cells are a highly formidable cancer to treat. Nonetheless, by continued investigation into the molecular biology underlying the complex regulation of TNBC cell activity, vulnerabilities can be exposed as potential therapeutic targets at the molecular level. We previously revealed that lysyl oxidase-like 4 (LOXL4) promotes the invasiveness of TNBC cells via cell surface annexin A2 as a novel binding substrate of LOXL4, which promotes the abundant localization of integrin-beta 1 at the cancer plasma membrane. However, it has yet to be uncovered how the LOXL4-mediated abundance of integrin-beta 1 hastens the invasive outgrowth of TNBC cells at the molecular level.<br>
Methods LOXL4-overexpressing stable clones were established from MDA-MB-231 cells and subjected to molecular analyses, real-time qPCR and zymography to clarify their invasiveness, signal transduction, and matrix metalloprotease (MMP) activity, respectively.<br>
Results Our results show that LOXL4 potently promotes the induction of matrix metalloprotease 9 (MMP9) via activation of nuclear factor-kappa B (NF-kappa B). Our molecular analysis revealed that TNF receptor-associated factor 4 (TRAF4) and TGF-beta activated kinase 1 (TAK1) were required for the activation of NF-kappa B through I kappa beta kinase kinase (IKK alpha/beta) phosphorylation.<br>
Conclusion Our results demonstrate that the newly identified LOXL4-mediated axis, integrin-beta 1-TRAF4-TAK1-IKK alpha/beta-I kappa beta alpha-NF-kappa B-MMP9, is crucial for TNBC cell invasiveness.
en-copyright=
kn-copyright=

en-aut-name=JiangFan
en-aut-sei=Jiang
en-aut-mei=Fan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ChenYouyi
en-aut-sei=Chen
en-aut-mei=Youyi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TomonobuNahoko
en-aut-sei=Tomonobu
en-aut-mei=Nahoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KinoshitaRie
en-aut-sei=Kinoshita
en-aut-mei=Rie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KomalasariNi Luh Gede Yoni
en-aut-sei=Komalasari
en-aut-mei=Ni Luh Gede Yoni
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=Kasano-CamonesCarlos Ichiro
en-aut-sei=Kasano-Camones
en-aut-mei=Carlos Ichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NinomiyaKazumi
en-aut-sei=Ninomiya
en-aut-mei=Kazumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MurataHitoshi
en-aut-sei=Murata
en-aut-mei=Hitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=YamamotoKen-Ichi
en-aut-sei=Yamamoto
en-aut-mei=Ken-Ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=GoharaYuma
en-aut-sei=Gohara
en-aut-mei=Yuma
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=OchiToshiki
en-aut-sei=Ochi
en-aut-mei=Toshiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=RumaI. Made Winarsa
en-aut-sei=Ruma
en-aut-mei=I. Made Winarsa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=SumardikaI. Wayan
en-aut-sei=Sumardika
en-aut-mei=I. Wayan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=ZhouJin
en-aut-sei=Zhou
en-aut-mei=Jin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=HonjoTomoko
en-aut-sei=Honjo
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=SakaguchiYoshihiko
en-aut-sei=Sakaguchi
en-aut-mei=Yoshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=YamauchiAkira
en-aut-sei=Yamauchi
en-aut-mei=Akira
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=KuribayashiFutoshi
en-aut-sei=Kuribayashi
en-aut-mei=Futoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=FutamiJunichiro
en-aut-sei=Futami
en-aut-mei=Junichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=KondoEisaku
en-aut-sei=Kondo
en-aut-mei=Eisaku
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

en-aut-name=InoueYusuke
en-aut-sei=Inoue
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=21
ORCID=

en-aut-name=ToyookaShinichi
en-aut-sei=Toyooka
en-aut-mei=Shinichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=22
ORCID=

en-aut-name=SakaguchiMasakiyo
en-aut-sei=Sakaguchi
en-aut-mei=Masakiyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=23
ORCID=

affil-num=1
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Breast Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine
kn-affil=

affil-num=3
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Faculty of Medicine, Udayana University
kn-affil=

affil-num=6
en-affil=Faculty of Science and Technology, Division of Molecular Science, Gunma University
kn-affil=

affil-num=7
en-affil=Faculty of Science and Technology, Division of Molecular Science, Gunma University
kn-affil=

affil-num=8
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=12
en-affil=Faculty of Medicine, Udayana University
kn-affil=

affil-num=13
en-affil=Faculty of Medicine, Udayana University
kn-affil=

affil-num=14
en-affil=Medical Oncology Department of Gastrointestinal Tumors, Liaoning Cancer Hospital & Institute, Cancer Hospital of the Dalian University of Technology
kn-affil=

affil-num=15
en-affil=Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=16
en-affil=Department of Microbiology, Tokushima Bunri University
kn-affil=

affil-num=17
en-affil=Department of Biochemistry, Kawasaki Medical School
kn-affil=

affil-num=18
en-affil=Department of Biochemistry, Kawasaki Medical School
kn-affil=

affil-num=19
en-affil=Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=20
en-affil=Division of Tumor Pathology, Near InfraRed Photo-Immuno-Therapy Research Institute, Kansai Medical University
kn-affil=

affil-num=21
en-affil=Faculty of Science and Technology, Division of Molecular Science, Gunma University
kn-affil=

affil-num=22
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=23
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=breast cancer
kn-keyword=breast cancer
en-keyword=invasion
kn-keyword=invasion
en-keyword=lysyl oxidase
kn-keyword=lysyl oxidase
en-keyword=NF-κB
kn-keyword=NF-κB
en-keyword=MMP9
kn-keyword=MMP9
END

start-ver=1.4
cd-journal=joma
no-vol=25
cd-vols=
no-issue=11
article-no=
start-page=6269
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240606
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=SPRED2 Is a Novel Regulator of Autophagy in Hepatocellular Carcinoma Cells and Normal Hepatocytes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Sprouty-related enabled/vasodilator-stimulated phosphoprotein homology 1 domain containing 2 (SPRED2) is an inhibitor of the mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) pathway and has been shown to promote autophagy in several cancers. Here, we aimed to determine whether SPRED2 plays a role in autophagy in hepatocellular carcinoma (HCC) cells. The Cancer Genome Atlas (TCGA) Liver Cancer Database showed a negative association between the level of SPRED2 and p62, a ubiquitin-binding scaffold protein that accumulates when autophagy is inhibited. Immunohistochemically, accumulation of p62 was detected in human HCC tissues with low SPRED2 expression. Overexpression of SPRED2 in HCC cells increased the number of autophagosomes and autophagic vacuoles containing damaged mitochondria, decreased p62 levels, and increased levels of light-chain-3 (LC3)-II, an autophagy marker. In contrast, SPRED2 deficiency increased p62 levels and decreased LC3-II levels. SPRED2 expression levels were negatively correlated with translocase of outer mitochondrial membrane 20 (TOM20) expression levels, suggesting its role in mitophagy. Mechanistically, SPRED2 overexpression reduced ERK activation followed by the mechanistic or mammalian target of rapamycin complex 1 (mTORC1)-mediated signaling pathway, and SPRED2 deficiency showed the opposite pattern. Finally, hepatic autophagy was impaired in the liver of SPRED2-deficient mice with hepatic lipid droplet accumulation in response to starvation. These results indicate that SPRED2 is a critical regulator of autophagy not only in HCC cells, but also in hepatocytes, and thus the manipulation of this process may provide new insights into liver pathology.
en-copyright=
kn-copyright=

en-aut-name=WangTianyi
en-aut-sei=Wang
en-aut-mei=Tianyi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=GaoTong
en-aut-sei=Gao
en-aut-mei=Tong
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=FujisawaMasayoshi
en-aut-sei=Fujisawa
en-aut-mei=Masayoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OharaToshiaki
en-aut-sei=Ohara
en-aut-mei=Toshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SakaguchiMasakiyo
en-aut-sei=Sakaguchi
en-aut-mei=Masakiyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YoshimuraTeizo
en-aut-sei=Yoshimura
en-aut-mei=Teizo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MatsukawaAkihiro
en-aut-sei=Matsukawa
en-aut-mei=Akihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Department of Pathology and Experimental Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Pathology and Experimental Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Pathology and Experimental Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Pathology and Experimental Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Cell Biology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Pathology and Experimental Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Pathology and Experimental Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=autophagy
kn-keyword=autophagy
en-keyword=mitophagy
kn-keyword=mitophagy
en-keyword=SPRED proteins
kn-keyword=SPRED proteins
en-keyword=MAPK/ERK
kn-keyword=MAPK/ERK
en-keyword=mTOR
kn-keyword=mTOR
en-keyword=hepatocellular carcinoma
kn-keyword=hepatocellular carcinoma
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=1
article-no=
start-page=4610
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240530
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=An NLR paralog Pit2 generated from tandem duplication of Pit1 fine-tunes Pit1 localization and function
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=NLR family proteins act as intracellular receptors. Gene duplication amplifies the number of NLR genes, and subsequent mutations occasionally provide modifications to the second gene that benefits immunity. However, evolutionary processes after gene duplication and functional relationships between duplicated NLRs remain largely unclear. Here, we report that the rice NLR protein Pit1 is associated with its paralogue Pit2. The two are required for the resistance to rice blast fungus but have different functions: Pit1 induces cell death, while Pit2 competitively suppresses Pit1-mediated cell death. During evolution, the suppression of Pit1 by Pit2 was probably generated through positive selection on two fate-determining residues in the NB-ARC domain of Pit2, which account for functional differences between Pit1 and Pit2. Consequently, Pit2 lost its plasma membrane localization but acquired a new function to interfere with Pit1 in the cytosol. These findings illuminate the evolutionary trajectory of tandemly duplicated NLR genes after gene duplication.
en-copyright=
kn-copyright=

en-aut-name=LiYuying
en-aut-sei=Li
en-aut-mei=Yuying
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=WangQiong
en-aut-sei=Wang
en-aut-mei=Qiong
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=JiaHuimin
en-aut-sei=Jia
en-aut-mei=Huimin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=IshikawaKazuya
en-aut-sei=Ishikawa
en-aut-mei=Kazuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KosamiKen-Ichi
en-aut-sei=Kosami
en-aut-mei=Ken-Ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=UebaTakahiro
en-aut-sei=Ueba
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TsujimotoAtsumi
en-aut-sei=Tsujimoto
en-aut-mei=Atsumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YamanakaMiki
en-aut-sei=Yamanaka
en-aut-mei=Miki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=YabumotoYasuyuki
en-aut-sei=Yabumoto
en-aut-mei=Yasuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=MikiDaisuke
en-aut-sei=Miki
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=SasakiEriko
en-aut-sei=Sasaki
en-aut-mei=Eriko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=FukaoYoichiro
en-aut-sei=Fukao
en-aut-mei=Yoichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=FujiwaraMasayuki
en-aut-sei=Fujiwara
en-aut-mei=Masayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=Kaneko-KawanoTakako
en-aut-sei=Kaneko-Kawano
en-aut-mei=Takako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=TanLi
en-aut-sei=Tan
en-aut-mei=Li
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=KojimaChojiro
en-aut-sei=Kojima
en-aut-mei=Chojiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=WingRod A.
en-aut-sei=Wing
en-aut-mei=Rod A.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=SebastianAlfino
en-aut-sei=Sebastian
en-aut-mei=Alfino
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=NishimuraHideki
en-aut-sei=Nishimura
en-aut-mei=Hideki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=FukadaFumi
en-aut-sei=Fukada
en-aut-mei=Fumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

en-aut-name=NiuQingfeng
en-aut-sei=Niu
en-aut-mei=Qingfeng
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=21
ORCID=

en-aut-name=ShimizuMotoki
en-aut-sei=Shimizu
en-aut-mei=Motoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=22
ORCID=

en-aut-name=YoshidaKentaro
en-aut-sei=Yoshida
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=23
ORCID=

en-aut-name=TerauchiRyohei
en-aut-sei=Terauchi
en-aut-mei=Ryohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=24
ORCID=

en-aut-name=ShimamotoKo
en-aut-sei=Shimamoto
en-aut-mei=Ko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=25
ORCID=

en-aut-name=KawanoYoji
en-aut-sei=Kawano
en-aut-mei=Yoji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=26
ORCID=

affil-num=1
en-affil=Shenzhen Branch, Guangdong Laboratory of Lingnan Modern Agriculture, Key Laboratory of Synthetic Biology, Ministry of Agriculture and Rural Affairs, Agricultural Genomics Institute at Shenzhen, Chinese Academy of Agricultural Sciences
kn-affil=

affil-num=2
en-affil=Shanghai Center for Plant Stress Biology, CAS Center for Excellence in Molecular Plant Sciences, Chinese Academy of Sciences
kn-affil=

affil-num=3
en-affil=College of Agronomy, Jiangxi Agricultural University
kn-affil=

affil-num=4
en-affil=Shanghai Center for Plant Stress Biology, CAS Center for Excellence in Molecular Plant Sciences, Chinese Academy of Sciences
kn-affil=

affil-num=5
en-affil=Shanghai Center for Plant Stress Biology, CAS Center for Excellence in Molecular Plant Sciences, Chinese Academy of Sciences
kn-affil=

affil-num=6
en-affil=Laboratory of Plant Molecular Genetics, Nara Institute of Science and Technology
kn-affil=

affil-num=7
en-affil=Laboratory of Plant Molecular Genetics, Nara Institute of Science and Technology
kn-affil=

affil-num=8
en-affil=Laboratory of Plant Molecular Genetics, Nara Institute of Science and Technology
kn-affil=

affil-num=9
en-affil=Laboratory of Plant Molecular Genetics, Nara Institute of Science and Technology
kn-affil=

affil-num=10
en-affil=Shanghai Center for Plant Stress Biology, CAS Center for Excellence in Molecular Plant Sciences, Chinese Academy of Sciences
kn-affil=

affil-num=11
en-affil=Faculty of Science, Kyushu University
kn-affil=

affil-num=12
en-affil=Department of Bioinformatics, Ritsumeikan University
kn-affil=

affil-num=13
en-affil=YANMAR HOLDINGS Co., Ltd.
kn-affil=

affil-num=14
en-affil=College of Pharmaceutical Sciences, Ritsumeikan University
kn-affil=

affil-num=15
en-affil=Shanghai Center for Plant Stress Biology, CAS Center for Excellence in Molecular Plant Sciences, Chinese Academy of Sciences
kn-affil=

affil-num=16
en-affil=Graduate School of Engineering Science, Yokohama National University
kn-affil=

affil-num=17
en-affil=Arizona Genomics Institute, School of Plant Sciences, University of Arizona
kn-affil=

affil-num=18
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=19
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=20
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=

affil-num=21
en-affil=Advanced Academy, Anhui Agricultural University, Research Centre for Biological Breeding Technology
kn-affil=

affil-num=22
en-affil=Iwate Biotechnology Research Center
kn-affil=

affil-num=23
en-affil=Graduate School of Agriculture, Kyoto University 
kn-affil=

affil-num=24
en-affil=Iwate Biotechnology Research Center
kn-affil=

affil-num=25
en-affil=Laboratory of Plant Molecular Genetics, Nara Institute of Science and Technology
kn-affil=

affil-num=26
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=13
cd-vols=
no-issue=10
article-no=
start-page=807
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240509
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Exploring the Regulators of Keratinization: Role of BMP-2 in Oral Mucosa
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The oral mucosa functions as a physico-chemical and immune barrier to external stimuli, and an adequate width of the keratinized mucosa around the teeth or implants is crucial to maintaining them in a healthy and stable condition. In this study, for the first time, bulk RNA-seq analysis was performed to explore the gene expression of laser microdissected epithelium and lamina propria from mice, aiming to investigate the differences between keratinized and non-keratinized oral mucosa. Based on the differentially expressed genes (DEGs) and Gene Ontology (GO) Enrichment Analysis, bone morphogenetic protein 2 (BMP-2) was identified to be a potential regulator of oral mucosal keratinization. Monoculture and epithelial-mesenchymal cell co-culture models in the air-liquid interface (ALI) indicated that BMP-2 has direct and positive effects on epithelial keratinization and proliferation. We further performed bulk RNA-seq of the ALI monoculture stimulated with BMP-2 in an attempt to identify the downstream factors promoting epithelial keratinization and proliferation. Analysis of the DEGs identified, among others, IGF2, ID1, LTBP1, LOX, SERPINE1, IL24, and MMP1 as key factors. In summary, these results revealed the involvement of a well-known growth factor responsible for bone development, BMP-2, in the mechanism of oral mucosal keratinization and proliferation, and pointed out the possible downstream genes involved in this mechanism.
en-copyright=
kn-copyright=

en-aut-name=MuXindi
en-aut-sei=Mu
en-aut-mei=Xindi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OnoMitsuaki
en-aut-sei=Ono
en-aut-mei=Mitsuaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NguyenHa Thi Thu
en-aut-sei=Nguyen
en-aut-mei=Ha Thi Thu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=WangZiyi
en-aut-sei=Wang
en-aut-mei=Ziyi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ZhaoKun
en-aut-sei=Zhao
en-aut-mei=Kun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KomoriTaishi
en-aut-sei=Komori
en-aut-mei=Taishi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YonezawaTomoko
en-aut-sei=Yonezawa
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KubokiTakuo
en-aut-sei=Kuboki
en-aut-mei=Takuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=OohashiToshitaka
en-aut-sei=Oohashi
en-aut-mei=Toshitaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=
kn-affil=Department of Oral Rehabilitation and Regenerative Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

affil-num=7
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Oral Rehabilitation and Implantology, Okayama University Hospital
kn-affil=

affil-num=9
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=cell differentiation
kn-keyword=cell differentiation
en-keyword=epithelia
kn-keyword=epithelia
en-keyword=growth factor(s)
kn-keyword=growth factor(s)
en-keyword=bioinformatics
kn-keyword=bioinformatics
en-keyword=extracellular matrix (ECM)
kn-keyword=extracellular matrix (ECM)
en-keyword=mucocutaneous disorders
kn-keyword=mucocutaneous disorders
END

start-ver=1.4
cd-journal=joma
no-vol=165
cd-vols=
no-issue=
article-no=
start-page=106013
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202409
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Salivary buffering capacity is correlated with umami but not sour taste sensitivity in healthy adult Japanese subjects
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Objective: Saliva serves multiple important functions crucial for maintaining a healthy oral and systemic environment. Among them, the pH buffering effect, which is primarily mediated by bicarbonate ions, helps maintain oral homeostasis by neutralizing acidity from ingested foods. Therefore, higher buffering capacity, reflecting the ability to neutralize oral acidity, may influence taste sensitivity, especially for sour taste since it involves sensing H+ ions. This study aims to explore the relationship between salivary buffering capacity and taste sensitivities to the five basic tastes in healthy adult humans.<br>
Design: Eighty seven healthy adult students participated in this study. Resting saliva volume was measured using the spitting method. The liquid colorimetric test was used to assess salivary buffering capacity. The whole-mouth taste testing method was employed to determine the recognition threshold for each tastant (NaCl, sucrose, citric acid, quinine-HCl, monosodium glutamate).<br>
Results: Taste recognition thresholds for sour taste as well as sweet, salty, and bitter tastes showed no correlation with salivary buffering capacity. Interestingly, a negative relationship was observed between recognition threshold for umami taste and salivary buffering capacity. Furthermore, a positive correlation between salivary buffering capacity and resting saliva volume was observed.<br>
Conclusions: Salivary buffering capacity primarily influences sensitivity to umami taste, but not sour and other tastes.
en-copyright=
kn-copyright=

en-aut-name=HyodoAiko
en-aut-sei=Hyodo
en-aut-mei=Aiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MikamiAyaka
en-aut-sei=Mikami
en-aut-mei=Ayaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HorieKengo
en-aut-sei=Horie
en-aut-mei=Kengo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MitohYoshihiro
en-aut-sei=Mitoh
en-aut-mei=Yoshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NinomiyaYuzo
en-aut-sei=Ninomiya
en-aut-mei=Yuzo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=IidaSeiji
en-aut-sei=Iida
en-aut-mei=Seiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YoshidaRyusuke
en-aut-sei=Yoshida
en-aut-mei=Ryusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Oral and Maxillofacial Reconstructive Surgery, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=taste recognition threshold
kn-keyword=taste recognition threshold
en-keyword=resting saliva
kn-keyword=resting saliva
en-keyword=bicarbonate
kn-keyword=bicarbonate
en-keyword=xerostomia
kn-keyword=xerostomia
en-keyword=TAS1R
kn-keyword=TAS1R
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=外来種アメリカザリガニの生態に関する研究：繁殖生物学および在来水生動物への影響
kn-title=Study on ecology of the invasive crayfish Procambarus clarkii in Japan: reproductive biology and the negative effects on native aquatic animal species
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=LUONG QUANG TUONG
en-aut-sei=LUONG QUANG TUONG
en-aut-mei=
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=岡山大学大学院環境生命科学研究科
END

start-ver=1.4
cd-journal=joma
no-vol=57
cd-vols=
no-issue=2
article-no=
start-page=85
end-page=88
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240425
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Membrane-Targeted palGFP Predominantly Localizes to the Plasma Membrane but not to Neurosecretory Vesicle Membranes in Rat Oxytocin Neurons
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Recent advances in viral vector technology, specifically using adeno-associated virus (AAV) vectors, have significantly expanded possibilities in neuronal tracing. We have utilized the Cre/loxP system in combination with AAV techniques in rats to explore the subcellular localization of palmitoylation signal-tagged GFP (palGFP) in oxytocin-producing neurosecretory neurons. A distinctive branching pattern of single axons was observed at the level of the terminals in the posterior pituitary. Despite challenges in detecting palGFP signals by fluorescent microscopy, immunoelectron microscopy demonstrated predominant localization on the plasma membrane, with a minor presence on the neurosecretory vesicle membrane. These findings suggest that membrane-anchored palGFP may undergo exocytosis, translocating from the plasma membrane to the neurosecretory vesicle membrane. In this study, we observed characteristic axon terminal structures in the posterior pituitary of oxytocin neurons. This study indicates the importance of understanding the plasma membrane-specific sorting system in neuronal membrane migration and encourages future studies on the underlying mechanisms.
en-copyright=
kn-copyright=

en-aut-name=SakamotoHirotaka
en-aut-sei=Sakamoto
en-aut-mei=Hirotaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=InutsukaAyumu
en-aut-sei=Inutsuka
en-aut-mei=Ayumu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

affil-num=1
en-affil=Department of Biology, Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Division of Brain and Neurophysiology, Department of Physiology, Jichi Medical University
kn-affil=
en-keyword=GFP with a palmitoylation signal (palGFP)
kn-keyword=GFP with a palmitoylation signal (palGFP)
en-keyword=plasmalemma localization
kn-keyword=plasmalemma localization
en-keyword=neurosecretory vesicle
kn-keyword=neurosecretory vesicle
en-keyword=immunoelectron microscopy
kn-keyword=immunoelectron microscopy
en-keyword=oxytocin
kn-keyword=oxytocin
END

start-ver=1.4
cd-journal=joma
no-vol=52
cd-vols=
no-issue=10
article-no=
start-page=5825
end-page=5840
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240425
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The ABCF proteins in Escherichia coli individually cope with 'hard-to-translate' nascent peptide sequences
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Organisms possess a wide variety of proteins with diverse amino acid sequences, and their synthesis relies on the ribosome. Empirical observations have led to the misconception that ribosomes are robust protein factories, but in reality, they have several weaknesses. For instance, ribosomes stall during the translation of the proline-rich sequences, but the elongation factor EF-P assists in synthesizing proteins containing the poly-proline sequences. Thus, living organisms have evolved to expand the translation capability of ribosomes through the acquisition of translation elongation factors. In this study, we have revealed that Escherichia coli ATP-Binding Cassette family-F (ABCF) proteins, YheS, YbiT, EttA and Uup, individually cope with various problematic nascent peptide sequences within the exit tunnel. The correspondence between noncanonical translations and ABCFs was YheS for the translational arrest by nascent SecM, YbiT for poly-basic sequence-dependent stalling and poly-acidic sequence-dependent intrinsic ribosome destabilization (IRD), EttA for IRD at the early stage of elongation, and Uup for poly-proline-dependent stalling. Our results suggest that ATP hydrolysis-coupled structural rearrangement and the interdomain linker sequence are pivotal for handling 'hard-to-translate' nascent peptides. Our study highlights a new aspect of ABCF proteins to reduce the potential risks that are encoded within the nascent peptide sequences. Graphical Abstract
en-copyright=
kn-copyright=

en-aut-name=ChadaniYuhei
en-aut-sei=Chadani
en-aut-mei=Yuhei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YamanouchiShun
en-aut-sei=Yamanouchi
en-aut-mei=Shun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=UemuraEri
en-aut-sei=Uemura
en-aut-mei=Eri
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YamasakiKohei
en-aut-sei=Yamasaki
en-aut-mei=Kohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NiwaTatsuya
en-aut-sei=Niwa
en-aut-mei=Tatsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=IkedaToma
en-aut-sei=Ikeda
en-aut-mei=Toma
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KuriharaMiku
en-aut-sei=Kurihara
en-aut-mei=Miku
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=IwasakiWataru
en-aut-sei=Iwasaki
en-aut-mei=Wataru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TaguchiHideki
en-aut-sei=Taguchi
en-aut-mei=Hideki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Biological Sciences, Graduate School of Science, the University of Tokyo
kn-affil=

affil-num=3
en-affil=Cell Biology Center, Institute of Innovative Research, Tokyo Institute of Technology
kn-affil=

affil-num=4
en-affil=Faculty of Science, Okayama University
kn-affil=

affil-num=5
en-affil=Cell Biology Center, Institute of Innovative Research, Tokyo Institute of Technology
kn-affil=

affil-num=6
en-affil=School of Life Science and Technology, Tokyo Institute of Technology
kn-affil=

affil-num=7
en-affil=School of Life Science and Technology, Tokyo Institute of Technology
kn-affil=

affil-num=8
en-affil=Department of Biological Sciences, Graduate School of Science, the University of Tokyo
kn-affil=

affil-num=9
en-affil=Cell Biology Center, Institute of Innovative Research, Tokyo Institute of Technology
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=202
cd-vols=
no-issue=3
article-no=
start-page=473
end-page=483
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230909
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Prognostic impact of adjuvant endocrine therapy for estrogen receptor-positive and HER2-negative T1a/bN0M0 breast cancer
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Purpose Mammography screening has increased the detection of subcentimeter breast cancers. The prognosis for estrogen receptor (ER)-positive and human epidermal growth factor receptor 2 (HER2)-negative T1a/bN0M0 breast cancers is excellent; however, the necessity of adjuvant endocrine therapy (ET) is uncertain.<br>
Methods We evaluated the effectiveness of adjuvant ET in patients with ER-positive and HER2-negative T1a/bN0M0 breast cancer who underwent surgery from 2008 to 2012. Standard ET was administrated after surgery. The primary endpoint was the cumulative incidence of distant metastasis. All statistical tests were 2-sided.<br>
Results Adjuvant ET was administered to 3991 (83%) of the 4758 eligible patients (1202 T1a [25.3%] and 3556 T1b [74.7%], diseases). The median follow-up period was 9.2 years. The 9-year cumulative incidence of distant metastasis was 1.5% with ET and 2.6% without ET (adjusted subdistribution hazard ratio [sHR], 0.54; 95% CI, 0.32–0.93). In multivariate analysis, the independent risk factors for distant metastasis were no history of ET, mastectomy, high-grade, and lymphatic invasion. The 9-year overall survival was 97.0% and 94.4% with and without ET, respectively (adjusted HR, 0.57; 95% CI, 0.39–0.83). In addition, adjuvant ET reduced the incidence of ipsilateral and contralateral breast cancer (9-year rates; 1.1% vs. 6.9%; sHR, 0.17, and 1.9% vs. 5.2%; sHR, 0.33).<br>
Conclusions The prognosis was favorable in patients with ER-positive and HER2-negative T1a/bN0M0 breast cancer. Furthermore, adjuvant ET reduced the incidence of distant metastasis with minimal absolute risk difference. These findings support considering the omission of adjuvant ET, especially for patients with low-grade and no lymphatic invasion disease.
en-copyright=
kn-copyright=

en-aut-name=SasadaShinsuke
en-aut-sei=Sasada
en-aut-mei=Shinsuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KondoNaoto
en-aut-sei=Kondo
en-aut-mei=Naoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HashimotoHiroya
en-aut-sei=Hashimoto
en-aut-mei=Hiroya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TakahashiYuko
en-aut-sei=Takahashi
en-aut-mei=Yuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TerataKaori
en-aut-sei=Terata
en-aut-mei=Kaori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KidaKumiko
en-aut-sei=Kida
en-aut-mei=Kumiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SagaraYasuaki
en-aut-sei=Sagara
en-aut-mei=Yasuaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=UenoTakayuki
en-aut-sei=Ueno
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=AnanKeisei
en-aut-sei=Anan
en-aut-mei=Keisei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=SutoAkihiko
en-aut-sei=Suto
en-aut-mei=Akihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=KanbayashiChizuko
en-aut-sei=Kanbayashi
en-aut-mei=Chizuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=TakahashiMina
en-aut-sei=Takahashi
en-aut-mei=Mina
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=NakamuraRikiya
en-aut-sei=Nakamura
en-aut-mei=Rikiya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=IshibaToshiyuki
en-aut-sei=Ishiba
en-aut-mei=Toshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=TsuneizumiMichiko
en-aut-sei=Tsuneizumi
en-aut-mei=Michiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=NishimuraSeiichiro
en-aut-sei=Nishimura
en-aut-mei=Seiichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=NaitoYoichi
en-aut-sei=Naito
en-aut-mei=Yoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=HaraFumikata
en-aut-sei=Hara
en-aut-mei=Fumikata
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=ShienTadahiko
en-aut-sei=Shien
en-aut-mei=Tadahiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=IwataHiroji
en-aut-sei=Iwata
en-aut-mei=Hiroji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

affil-num=1
en-affil=Department of Surgical Oncology, Research Institute for Radiation Biology and Medicine, Hiroshima University
kn-affil=

affil-num=2
en-affil=Department of Breast Surgery, Nagoya City University Graduate School of Medical Sciences
kn-affil=

affil-num=3
en-affil=Core Laboratory, Nagoya City University Graduate School of Medical Sciences
kn-affil=

affil-num=4
en-affil=Department of Breast and Endocrine Surgery, Okayama University Hospital
kn-affil=

affil-num=5
en-affil=Department of Breast and Endocrine Surgery, Akita University Hospital
kn-affil=

affil-num=6
en-affil=Department of Breast Surgical Oncology, St. Luke’s International Hospital
kn-affil=

affil-num=7
en-affil=Department of Breast and Thyroid Surgical Oncology, Social medical corporation Hakuaikai, Sagara Hospital
kn-affil=

affil-num=8
en-affil=Breast Oncology Center, The Cancer Institute Hospital of Japanese Foundation for Cancer Research
kn-affil=

affil-num=9
en-affil=Department of Surgery, Kitakyushu Municipal Medical Center
kn-affil=

affil-num=10
en-affil=Department of Breast Surgery, National Cancer Center Hospital
kn-affil=

affil-num=11
en-affil=Department of Breast Oncology, Niigata Cancer Center Hospital
kn-affil=

affil-num=12
en-affil=Department of Breast Oncology, National Hospital Organization Shikoku Cancer Center
kn-affil=

affil-num=13
en-affil=Department of Breast Surgery, Chiba Cancer Center
kn-affil=

affil-num=14
en-affil=Department of Breast Surgery, Tokyo Metropolitan Cancer and Infectious Diseases Center, Komagome Hospital
kn-affil=

affil-num=15
en-affil=Department of Breast Surgery, Shizuoka General Hospital
kn-affil=

affil-num=16
en-affil=Department of Breast Surgery, Shizuoka Cancer Center Hospital
kn-affil=

affil-num=17
en-affil=Department of General Internal Medicine, National Cancer Center Hospital East
kn-affil=

affil-num=18
en-affil=Breast Oncology Center, The Cancer Institute Hospital of Japanese Foundation for Cancer Research
kn-affil=

affil-num=19
en-affil=Department of Breast and Endocrine Surgery, Okayama University Hospital
kn-affil=

affil-num=20
en-affil=Department of Breast Oncology, Aichi Cancer Center Hospital
kn-affil=
en-keyword=Breast cancer
kn-keyword=Breast cancer
en-keyword=T1a/b
kn-keyword=T1a/b
en-keyword=Endocrine therapy
kn-keyword=Endocrine therapy
en-keyword=Estrogen receptor
kn-keyword=Estrogen receptor
en-keyword=Prognosis
kn-keyword=Prognosis
END

start-ver=1.4
cd-journal=joma
no-vol=101
cd-vols=
no-issue=4
article-no=
start-page=431
end-page=447
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230304
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Novel extracellular role of REIC/Dkk-3 protein in PD-L1 regulation in cancer cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The adenovirus-REIC/Dkk-3 expression vector (Ad-REIC) has been the focus of numerous clinical studies due to its potential for the quenching of cancers. The cancer-suppressing mechanisms of the REIC/DKK-3 gene depend on multiple pathways that exert both direct and indirect effects on cancers. The direct effect is triggered by REIC/Dkk-3-mediated ER stress that causes cancer-selective apoptosis, and the indirect effect can be classified in two ways: (i) induction, by Ad-REIC-mis-infected cancer-associated fibroblasts, of the production of IL-7, an important activator of T cells and NK cells, and (ii) promotion, by the secretory REIC/Dkk-3 protein, of dendritic cell polarization from monocytes. These unique features allow Ad-REIC to exert effective and selective cancer-preventative effects in the manner of an anticancer vaccine. However, the question of how the REIC/Dkk-3 protein leverages anticancer immunity has remained to be answered. We herein report a novel function of the extracellular REIC/Dkk-3—namely, regulation of an immune checkpoint via modulation of PD-L1 on the cancer-cell surface. First, we identified novel interactions of REIC/Dkk-3 with the membrane proteins C5aR, CXCR2, CXCR6, and CMTM6. These proteins all functioned to stabilize PD-L1 on the cell surface. Due to the dominant expression of CMTM6 among the proteins in cancer cells, we next focused on CMTM6 and observed that REIC/Dkk-3 competed with CMTM6 for PD-L1, thereby liberating PD-L1 from its complexation with CMTM6. The released PD-L1 immediately underwent endocytosis-mediated degradation. These results will enhance our understanding of not only the physiological nature of the extracellular REIC/Dkk-3 protein but also the Ad-REIC-mediated anticancer effects.
en-copyright=
kn-copyright=

en-aut-name=GoharaYuma
en-aut-sei=Gohara
en-aut-mei=Yuma
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TomonobuNahoko
en-aut-sei=Tomonobu
en-aut-mei=Nahoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KinoshitaRie
en-aut-sei=Kinoshita
en-aut-mei=Rie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=FutamiJunichiro
en-aut-sei=Futami
en-aut-mei=Junichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=AudebertLéna
en-aut-sei=Audebert
en-aut-mei=Léna
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ChenYouyi
en-aut-sei=Chen
en-aut-mei=Youyi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KomalasariNi Luh Gede Yoni
en-aut-sei=Komalasari
en-aut-mei=Ni Luh Gede Yoni
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=JiangFan
en-aut-sei=Jiang
en-aut-mei=Fan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=YoshizawaChikako
en-aut-sei=Yoshizawa
en-aut-mei=Chikako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=MurataHitoshi
en-aut-sei=Murata
en-aut-mei=Hitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=YamamotoKen-ichi
en-aut-sei=Yamamoto
en-aut-mei=Ken-ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=WatanabeMasami
en-aut-sei=Watanabe
en-aut-mei=Masami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=KumonHiromi
en-aut-sei=Kumon
en-aut-mei=Hiromi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=SakaguchiMasakiyo
en-aut-sei=Sakaguchi
en-aut-mei=Masakiyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

affil-num=1
en-affil=Department of Cell Biology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=2
en-affil=Department of Cell Biology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=3
en-affil=Department of Cell Biology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=4
en-affil=Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Cell Biology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=6
en-affil=Department of Cell Biology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=7
en-affil=Department of Cell Biology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=8
en-affil=Department of Cell Biology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=9
en-affil=Department of Cell Biology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=10
en-affil=Department of Cell Biology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=11
en-affil=Department of Cell Biology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=12
en-affil=Department of Urology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=13
en-affil=Innovation Center Okayama for Nanobio-Targeted Therapy, Okayama University
kn-affil=

affil-num=14
en-affil=Department of Cell Biology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=
en-keyword=Breast cancer
kn-keyword=Breast cancer
en-keyword=REIC/Dkk-3
kn-keyword=REIC/Dkk-3
en-keyword=PD-L1
kn-keyword=PD-L1
en-keyword=Immune checkpoint
kn-keyword=Immune checkpoint
en-keyword=Cancer therapy
kn-keyword=Cancer therapy
END

start-ver=1.4
cd-journal=joma
no-vol=174
cd-vols=
no-issue=6
article-no=
start-page=533
end-page=548
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230919
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Phosphorylated SARM1 is involved in the pathological process of rotenone-induced neurodegeneration
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Sterile alpha and Toll/interleukin receptor motif-containing protein 1 (SARM1) is a NAD+ hydrolase that plays a key role in axonal degeneration and neuronal cell death. We reported that c-Jun N-terminal kinase (JNK) activates SARM1 through phosphorylation at Ser-548. The importance of SARM1 phosphorylation in the pathological process of Parkinson’s disease (PD) has not been determined. We thus conducted the present study by using rotenone (an inducer of PD-like pathology) and neurons derived from induced pluripotent stem cells (iPSCs) from healthy donors and a patient with familial PD PARK2 (FPD2). The results showed that compared to the healthy neurons, FPD2 neurons were more vulnerable to rotenone-induced stress and had higher levels of SARM1 phosphorylation. Similar cellular events were obtained when we used PARK2-knockdown neurons derived from healthy donor iPSCs. These events in both types of PD-model neurons were suppressed in neurons treated with JNK inhibitors, Ca2+-signal inhibitors, or by a SARM1-knockdown procedure. The degenerative events were enhanced in neurons overexpressing wild-type SARM1 and conversely suppressed in neurons overexpressing the SARM1-S548A mutant. We also detected elevated SARM1 phosphorylation in the midbrain of PD-model mice. The results indicate that phosphorylated SARM1 plays an important role in the pathological process of rotenone-induced neurodegeneration.
en-copyright=
kn-copyright=

en-aut-name=MurataHitoshi
en-aut-sei=Murata
en-aut-mei=Hitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=PhooMay Tha Zin
en-aut-sei=Phoo
en-aut-mei=May Tha Zin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OchiToshiki
en-aut-sei=Ochi
en-aut-mei=Toshiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TomonobuNahoko
en-aut-sei=Tomonobu
en-aut-mei=Nahoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YamamotoKen-ichi
en-aut-sei=Yamamoto
en-aut-mei=Ken-ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KinoshitaRie
en-aut-sei=Kinoshita
en-aut-mei=Rie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MiyazakiIkuko
en-aut-sei=Miyazaki
en-aut-mei=Ikuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NishiboriMasahiro
en-aut-sei=Nishibori
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=AsanumaMasato
en-aut-sei=Asanuma
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=SakaguchiMasakiyo
en-aut-sei=Sakaguchi
en-aut-mei=Masakiyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Translational Research and Drug Development, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=JNK
kn-keyword=JNK
en-keyword=PARK2
kn-keyword=PARK2
en-keyword=Parkinson’sdisease
kn-keyword=Parkinson’sdisease
en-keyword=Phosphorylation
kn-keyword=Phosphorylation
en-keyword=SARM1
kn-keyword=SARM1
END

start-ver=1.4
cd-journal=joma
no-vol=290
cd-vols=
no-issue=2000
article-no=
start-page=20230549
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230614
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Diacamma ants adjust liquid foraging strategies in response to biophysical constraints
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Ant foragers provide food to the rest of the colony, often requiring transport over long distances. Foraging for liquid is challenging because it is difficult to transport and share. Many social insects store liquids inside the crop to transport them to the nest, and then regurgitate to distribute to nest-mates through a behaviour called trophallaxis. Some ants instead transport fluids with a riskier behaviour called pseudotrophallaxis—holding a drop of liquid between the mandibles through surface tension. Ants share this droplet with nest-mates without ingestion or regurgitation. We hypothesised that ants optimize their liquid-collection approach depending on viscosity. Using an ant that employs both trophallaxis and pseudotrophallaxis, we investigated the conditions where each liquid-collection behaviour is favoured by measuring biophysical properties, collection time and reaction to food quality for typical and viscosity-altered sucrose solutions. We found that ants collected more liquid per unit time by mandibular grabbing than by drinking. At high viscosities ants switched liquid collection method to mandibular grabbing in response to viscosity and not to sweetness. Our results demonstrate that ants change transport and sharing methods according to viscosity–a natural proxy for sugar concentration–thus increasing the mass of sugar returned to the nest per trip.
en-copyright=
kn-copyright=

en-aut-name=FujiokaHaruna
en-aut-sei=Fujioka
en-aut-mei=Haruna
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MarchandManon
en-aut-sei=Marchand
en-aut-mei=Manon
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=LeBoeufAdria C.
en-aut-sei=LeBoeuf
en-aut-mei=Adria C.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Faculty of Environmental and Life Science, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Physics, University of Fribourg
kn-affil=

affil-num=3
en-affil=Department of Biology, University of Fribourg
kn-affil=
en-keyword=mandibular pseudotrophallaxis
kn-keyword=mandibular pseudotrophallaxis
en-keyword=social bucket
kn-keyword=social bucket
en-keyword=liquid transportation
kn-keyword=liquid transportation
en-keyword=liquid collection
kn-keyword=liquid collection
en-keyword=optimal foraging theory
kn-keyword=optimal foraging theory
en-keyword=biophysics
kn-keyword=biophysics
END

start-ver=1.4
cd-journal=joma
no-vol=64
cd-vols=
no-issue=11
article-no=
start-page=1323
end-page=1330
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230524
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Transcriptomic Interpretation on Explainable AI-Guided Intuition Uncovers Premonitory Reactions of Disordering Fate in Persimmon Fruit
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Deep neural network (DNN) techniques, as an advanced machine learning framework, have allowed various image diagnoses in plants, which often achieve better prediction performance than human experts in each specific field. Notwithstanding, in plant biology, the application of DNNs is still mostly limited to rapid and effective phenotyping. The recent development of explainable CNN frameworks has allowed visualization of the features in the prediction by a convolutional neural network (CNN), which potentially contributes to the understanding of physiological mechanisms in objective phenotypes. In this study, we propose an integration of explainable CNN and transcriptomic approach to make a physiological interpretation of a fruit internal disorder in persimmon, rapid over-softening. We constructed CNN models to accurately predict the fate to be rapid softening in persimmon cv. Soshu, only with photo images. The explainable CNNs, such as Gradient-weighted Class Activation Mapping (Grad-Class Activation Mapping (CAM)) and guided Grad-CAM, visualized specific featured regions relevant to the prediction of rapid softening, which would correspond to the premonitory symptoms in a fruit. Transcriptomic analyses to compare the featured regions of the predicted rapid-softening and control fruits suggested that rapid softening is triggered by precocious ethylene signal–dependent cell wall modification, despite exhibiting no direct phenotypic changes. Further transcriptomic comparison between the featured and non-featured regions in the predicted rapid-softening fruit suggested that premonitory symptoms reflected hypoxia and the related stress signals finally to induce ethylene signals. These results would provide a good example for the collaboration of image analysis and omics approaches in plant physiology, which uncovered a novel aspect of fruit premonitory reactions in the rapid-softening fate.
en-copyright=
kn-copyright=

en-aut-name=MasudaKanae
en-aut-sei=Masuda
en-aut-mei=Kanae
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KuwadaEriko
en-aut-sei=Kuwada
en-aut-mei=Eriko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SuzukiMaria
en-aut-sei=Suzuki
en-aut-mei=Maria
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SuzukiTetsuya
en-aut-sei=Suzuki
en-aut-mei=Tetsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NiikawaTakeshi
en-aut-sei=Niikawa
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=UchidaSeiichi
en-aut-sei=Uchida
en-aut-mei=Seiichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=AkagiTakashi
en-aut-sei=Akagi
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=4
en-affil=Gifu Prefectural Agricultural Technology Center
kn-affil=

affil-num=5
en-affil=Gifu Prefectural Agricultural Technology Center
kn-affil=

affil-num=6
en-affil=Faculty of Information Science and Electrical Engineering, Kyusyu University
kn-affil=

affil-num=7
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
en-keyword=Artificial intelligence
kn-keyword=Artificial intelligence
en-keyword=Backpropagation
kn-keyword=Backpropagation
en-keyword=Convolutional neural network
kn-keyword=Convolutional neural network
en-keyword=Image diagnosis
kn-keyword=Image diagnosis
en-keyword=Physiological disorder
kn-keyword=Physiological disorder
END

start-ver=1.4
cd-journal=joma
no-vol=14
cd-vols=
no-issue=1
article-no=
start-page=6723
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240320
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Development of a novel AAK1 inhibitor via Kinobeads-based screening
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=A chemical proteomics approach using Ca2+/calmodulin-dependent protein kinase kinase (CaMKK) inhibitor-immobilized sepharose (TIM-063-Kinobeads) identified main targets such as CaMKK alpha/1 and beta/2, and potential off-target kinases, including AP2-associated protein kinase 1 (AAK1), as TIM-063 interactants. Because TIM-063 interacted with the AAK1 catalytic domain and inhibited its enzymatic activity moderately (IC50 = 8.51 mu M), we attempted to identify potential AAK1 inhibitors from TIM-063-derivatives and found a novel AAK1 inhibitor, TIM-098a (11-amino-2-hydroxy-7H-benzo[de]benzo[4,5]imidazo[2,1-a]isoquinolin-7-one) which is more potent (IC50 = 0.24 mu M) than TIM-063 without any inhibitory activity against CaMKK isoforms and a relative AAK1-selectivity among the Numb-associated kinases family. TIM-098a could inhibit AAK1 activity in transfected cultured cells (IC50 = 0.87 mu M), indicating cell-membrane permeability of the compound. Overexpression of AAK1 in HeLa cells significantly reduced the number of early endosomes, which was blocked by treatment with 10 mu M TIM-098a. These results indicate TIM-063-Kinobeads-based chemical proteomics is efficient for identifying off-target kinases and re-evaluating the kinase inhibitor (TIM-063), leading to the successful development of a novel inhibitory compound (TIM-098a) for AAK1, which could be a molecular probe for AAK1. TIM-098a may be a promising lead compound for a more potent, selective and therapeutically useful AAK1 inhibitor.
en-copyright=
kn-copyright=

en-aut-name=YoshidaAkari
en-aut-sei=Yoshida
en-aut-mei=Akari
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OhtsukaSatomi
en-aut-sei=Ohtsuka
en-aut-mei=Satomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MatsumotoFumiya
en-aut-sei=Matsumoto
en-aut-mei=Fumiya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MiyagawaTomoyuki
en-aut-sei=Miyagawa
en-aut-mei=Tomoyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=OkinoRei
en-aut-sei=Okino
en-aut-mei=Rei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=IkedaYumeya
en-aut-sei=Ikeda
en-aut-mei=Yumeya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
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en-aut-name=TadaNatsume
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en-aut-name=GotohAkira
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en-aut-name=HatanoNaoya
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en-aut-name=MorishitaRyo
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en-aut-name=SatohAyano
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en-aut-name=SunatsukiYukinari
en-aut-sei=Sunatsuki
en-aut-mei=Yukinari
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aut-affil-num=13
ORCID=

en-aut-name=NilssonUlf J.
en-aut-sei=Nilsson
en-aut-mei=Ulf J.
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kn-aut-sei=
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aut-affil-num=14
ORCID=

en-aut-name=IshikawaTeruhiko
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en-aut-name=TokumitsuHiroshi
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affil-num=1
en-affil=Applied Cell Biology, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=2
en-affil=Applied Cell Biology, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Science Education, Graduate School of Education, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Science Education, Graduate School of Education, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Science Education, Graduate School of Education, Okayama University
kn-affil=

affil-num=6
en-affil=Applied Cell Biology, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=7
en-affil=Applied Cell Biology, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=8
en-affil=Applied Cell Biology, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=9
en-affil=Applied Cell Biology, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=10
en-affil=Applied Cell Biology, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=11
en-affil=CellFree Sciences Co. Ltd
kn-affil=

affil-num=12
en-affil=Organelle Systems Biotechnology, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=13
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=14
en-affil=Department of Chemistry, Lund University
kn-affil=

affil-num=15
en-affil=Department of Science Education, Graduate School of Education, Okayama University
kn-affil=

affil-num=16
en-affil=Applied Cell Biology, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=14
cd-vols=
no-issue=
article-no=
start-page=1371342
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240326
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Lysyl oxidase-like 4 promotes the invasiveness of triple-negative breast cancer cells by orchestrating the invasive machinery formed by annexin A2 and S100A11 on the cell surface
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Our earlier research revealed that the secreted lysyl oxidase-like 4 (LOXL4) that is highly elevated in triple-negative breast cancer (TNBC) acts as a catalyst to lock annexin A2 on the cell membrane surface, which accelerates invasive outgrowth of the cancer through the binding of integrin-β1 on the cell surface. However, whether this machinery is subject to the LOXL4-mediated intrusive regulation remains uncertain.<br>
<br>
Methods: Cell invasion was assessed using a transwell-based assay, protein–protein interactions by an immunoprecipitation–Western blotting technique and immunocytochemistry, and plasmin activity in the cell membrane by gelatin zymography.<br>
<br>
Results: We revealed that cell surface annexin A2 acts as a receptor of plasminogen via interaction with S100A10, a key cell surface annexin A2-binding factor, and S100A11. We found that the cell surface annexin A2/S100A11 complex leads to mature active plasmin from bound plasminogen, which actively stimulates gelatin digestion, followed by increased invasion.<br>
<br>
Conclusion: We have refined our understanding of the role of LOXL4 in TNBC cell invasion: namely, LOXL4 mediates the upregulation of annexin A2 at the cell surface, the upregulated annexin 2 binds S100A11 and S100A10, and the resulting annexin A2/S100A11 complex acts as a receptor of plasminogen, readily converting it into active-form plasmin and thereby enhancing invasion.
en-copyright=
kn-copyright=

en-aut-name=TakahashiTetta
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ORCID=

en-aut-name=TomonobuNahoko
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en-aut-name=KinoshitaRie
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en-aut-name=YamamotoKen-Ichi
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ORCID=

en-aut-name=MurataHitoshi
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ORCID=

en-aut-name=KomalasariNi Luh Gede Yoni
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aut-affil-num=6
ORCID=

en-aut-name=ChenYouyi
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ORCID=

en-aut-name=JiangFan
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en-aut-name=OchiToshiki
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aut-affil-num=10
ORCID=

en-aut-name=RumaI. Made Winarsa
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en-aut-mei=I. Made Winarsa
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kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=SumardikaI. Wayan
en-aut-sei=Sumardika
en-aut-mei=I. Wayan
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kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=ZhouJin
en-aut-sei=Zhou
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ORCID=

en-aut-name=HonjoTomoko
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aut-affil-num=14
ORCID=

en-aut-name=SakaguchiYoshihiko
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aut-affil-num=15
ORCID=

en-aut-name=YamauchiAkira
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aut-affil-num=16
ORCID=

en-aut-name=KuribayashiFutoshi
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ORCID=

en-aut-name=KondoEisaku
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en-aut-name=InoueYusuke
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aut-affil-num=19
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en-aut-name=FutamiJunichiro
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en-aut-name=ZamamiYoshito
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ORCID=

en-aut-name=SakaguchiMasakiyo
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kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=23
ORCID=

affil-num=1
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Faculty of Medicine, Udayana University
kn-affil=

affil-num=7
en-affil=Department of Breast Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine
kn-affil=

affil-num=8
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Faculty of Medicine, Udayana University
kn-affil=

affil-num=12
en-affil=Faculty of Medicine, Udayana University
kn-affil=

affil-num=13
en-affil=Medical Oncology Department of Gastrointestinal Tumors, Liaoning Cancer Hospital & Institute, Cancer Hospital of the Dalian University of Technology
kn-affil=

affil-num=14
en-affil=Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=15
en-affil=Department of Microbiology, Tokushima Bunri University
kn-affil=

affil-num=16
en-affil=Department of Biochemistry, Kawasaki Medical School
kn-affil=

affil-num=17
en-affil=Department of Biochemistry, Kawasaki Medical School
kn-affil=

affil-num=18
en-affil=Division of Tumor Pathology, Near InfraRed Photo-Immuno-Therapy Research Institute, Kansai Medical University
kn-affil=

affil-num=19
en-affil=Faculty of Science and Technology, Division of Molecular Science, Gunma University
kn-affil=

affil-num=20
en-affil=Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=21
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=22
en-affil=Department of Pharmacy, Okayama University Hospital
kn-affil=

affil-num=23
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=breast cancer
kn-keyword=breast cancer
en-keyword=lysyl oxidase
kn-keyword=lysyl oxidase
en-keyword=annexin A2
kn-keyword=annexin A2
en-keyword=S100A11
kn-keyword=S100A11
en-keyword=plasmin
kn-keyword=plasmin
en-keyword=cancer microenvironment
kn-keyword=cancer microenvironment
END

start-ver=1.4
cd-journal=joma
no-vol=626
cd-vols=
no-issue=7999
article-no=
start-page=670
end-page=677
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240131
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Oxygen-evolving photosystem II structures during S1–S2–S3 transitions
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Photosystem II (PSII) catalyses the oxidation of water through a four-step cycle of Si states (i = 0–4) at the Mn4CaO5 cluster1,2,3, during which an extra oxygen (O6) is incorporated at the S3 state to form a possible dioxygen4,5,6,7. Structural changes of the metal cluster and its environment during the S-state transitions have been studied on the microsecond timescale. Here we use pump-probe serial femtosecond crystallography to reveal the structural dynamics of PSII from nanoseconds to milliseconds after illumination with one flash (1F) or two flashes (2F). YZ, a tyrosine residue that connects the reaction centre P680 and the Mn4CaO5 cluster, showed structural changes on a nanosecond timescale, as did its surrounding amino acid residues and water molecules, reflecting the fast transfer of electrons and protons after flash illumination. Notably, one water molecule emerged in the vicinity of Glu189 of the D1 subunit of PSII (D1-E189), and was bound to the Ca2+ ion on a sub-microsecond timescale after 2F illumination. This water molecule disappeared later with the concomitant increase of O6, suggesting that it is the origin of O6. We also observed concerted movements of water molecules in the O1, O4 and Cl-1 channels and their surrounding amino acid residues to complete the sequence of electron transfer, proton release and substrate water delivery. These results provide crucial insights into the structural dynamics of PSII during S-state transitions as well as O–O bond formation.
en-copyright=
kn-copyright=

en-aut-name=LiHongjie
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ORCID=

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ORCID=

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ORCID=

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ORCID=

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affil-num=1
en-affil=Research Institute for Interdisciplinary Science, Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Research Institute for Interdisciplinary Science, Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=3
en-affil=Institute of Multidisciplinary Research for Advanced Materials, Tohoku University
kn-affil=

affil-num=4
en-affil=Japan Synchrotron Radiation Research Institute
kn-affil=

affil-num=5
en-affil=Department of Picobiology, Graduate School of Life Science, University of Hyogo
kn-affil=

affil-num=6
en-affil=Research Institute for Interdisciplinary Science, Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=7
en-affil=Japan Synchrotron Radiation Research Institute
kn-affil=

affil-num=8
en-affil=RIKEN SPring-8 Center
kn-affil=

affil-num=9
en-affil=Research Institute for Interdisciplinary Science, Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=10
en-affil=Research Institute for Interdisciplinary Science, Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=11
en-affil=RIKEN SPring-8 Center
kn-affil=

affil-num=12
en-affil=Research Institute for Interdisciplinary Science, Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=13
en-affil=Research Institute for Interdisciplinary Science, Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=14
en-affil=Research Institute for Interdisciplinary Science, Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=15
en-affil=Research Institute for Interdisciplinary Science, Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=16
en-affil=Research Institute for Interdisciplinary Science, Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=17
en-affil=Japan Synchrotron Radiation Research Institute
kn-affil=

affil-num=18
en-affil=Institute for Protein Research, Osaka University
kn-affil=

affil-num=19
en-affil=Division of Food and Nutrition, Faculty of Agriculture, Ryukoku University
kn-affil=

affil-num=20
en-affil=Department of Chemistry, Graduate School of Science, Kobe University
kn-affil=

affil-num=21
en-affil=Research Institute for Interdisciplinary Science, Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=22
en-affil=Research Institute for Interdisciplinary Science, Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=23
en-affil=Research Institute for Interdisciplinary Science, Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=24
en-affil=RIKEN SPring-8 Center
kn-affil=

affil-num=25
en-affil=Japan Synchrotron Radiation Research Institute
kn-affil=

affil-num=26
en-affil=Japan Synchrotron Radiation Research Institute
kn-affil=

affil-num=27
en-affil=Japan Synchrotron Radiation Research Institute
kn-affil=

affil-num=28
en-affil=Japan Synchrotron Radiation Research Institute
kn-affil=

affil-num=29
en-affil=Department of Picobiology, Graduate School of Life Science, University of Hyogo
kn-affil=

affil-num=30
en-affil=RIKEN SPring-8 Center
kn-affil=

affil-num=31
en-affil=Research Institute for Interdisciplinary Science, Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=32
en-affil=Center for Quantum Information and Quantum Biology, Osaka University
kn-affil=

affil-num=33
en-affil=Research Institute for Interdisciplinary Science, Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=34
en-affil=Research Institute for Interdisciplinary Science, Graduate School of Natural Science and Technology, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=130
cd-vols=
no-issue=9
article-no=
start-page=1493
end-page=1504
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240306
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=PRRX1-TOP2A interaction is a malignancy-promoting factor in human malignant peripheral nerve sheath tumours
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Paired related-homeobox 1 (PRRX1) is a transcription factor in the regulation of developmental morphogenetic processes. There is growing evidence that PRRX1 is highly expressed in certain cancers and is critically involved in human survival prognosis. However, the molecular mechanism of PRRX1 in cancer malignancy remains to be elucidated.<br>
Methods: PRRX1 expression in human Malignant peripheral nerve sheath tumours (MPNSTs) samples was detected immunohistochemically to evaluate survival prognosis. MPNST models with PRRX1 gene knockdown or overexpression were constructed in vitro and the phenotype of MPNST cells was evaluated. Bioinformatics analysis combined with co-immunoprecipitation, mass spectrometry, RNA-seq and structural prediction were used to identify proteins interacting with PRRX1.<br>
Results: High expression of PRRX1 was associated with a poor prognosis for MPNST. PRRX1 knockdown suppressed the tumorigenic potential. PRRX1 overexpressed in MPNSTs directly interacts with topoisomerase 2 A (TOP2A) to cooperatively promote epithelial-mesenchymal transition and increase expression of tumour malignancy-related gene sets including mTORC1, KRAS and SRC signalling pathways. Etoposide, a TOP2A inhibitor used in the treatment of MPNST, may exhibit one of its anticancer effects by inhibiting the PRRX1–TOP2A interaction.<br>
Conclusion: Targeting the PRRX1–TOP2A interaction in malignant tumours with high PRRX1 expression might provide a novel tumour-selective therapeutic strategy.
en-copyright=
kn-copyright=

en-aut-name=TakihiraShota
en-aut-sei=Takihira
en-aut-mei=Shota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YamadaDaisuke
en-aut-sei=Yamada
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OsoneTatsunori
en-aut-sei=Osone
en-aut-mei=Tatsunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TakaoTomoka
en-aut-sei=Takao
en-aut-mei=Tomoka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SakaguchiMasakiyo
en-aut-sei=Sakaguchi
en-aut-mei=Masakiyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=HakozakiMichiyuki
en-aut-sei=Hakozaki
en-aut-mei=Michiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=ItanoTakuto
en-aut-sei=Itano
en-aut-mei=Takuto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NakataEiji
en-aut-sei=Nakata
en-aut-mei=Eiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=FujiwaraTomohiro
en-aut-sei=Fujiwara
en-aut-mei=Tomohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=KunisadaToshiyuki
en-aut-sei=Kunisada
en-aut-mei=Toshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=OzakiToshifumi
en-aut-sei=Ozaki
en-aut-mei=Toshifumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=TakaradaTakeshi
en-aut-sei=Takarada
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

affil-num=1
en-affil=Department of Regenerative Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Regenerative Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Regenerative Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Regenerative Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Orthopedic Surgery, Fukushima Medical University School of Medicine
kn-affil=

affil-num=7
en-affil=Department of Orthopedic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Orthopedic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Orthopedic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Orthopedic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Department of Orthopedic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=12
en-affil=Department of Regenerative Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=7
cd-vols=
no-issue=1
article-no=
start-page=273
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240312
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The eukaryotic-like characteristics of small GTPase, roadblock and TRAPPC3 proteins from Asgard archaea
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Membrane-enclosed organelles are defining features of eukaryotes in distinguishing these organisms from prokaryotes. Specification of distinct membranes is critical to assemble and maintain discrete compartments. Small GTPases and their regulators are the signaling molecules that drive membrane-modifying machineries to the desired location. These signaling molecules include Rab and Rag GTPases, roadblock and longin domain proteins, and TRAPPC3-like proteins. Here, we take a structural approach to assess the relatedness of these eukaryotic-like proteins in Asgard archaea, the closest known prokaryotic relatives to eukaryotes. We find that the Asgard archaea GTPase core domains closely resemble eukaryotic Rabs and Rags. Asgard archaea roadblock, longin and TRAPPC3 domain-containing proteins form dimers similar to those found in the eukaryotic TRAPP and Ragulator complexes. We conclude that the emergence of these protein architectures predated eukaryogenesis, however further adaptations occurred in proto-eukaryotes to allow these proteins to regulate distinct internal membranes.
en-copyright=
kn-copyright=

en-aut-name=TranLinh T.
en-aut-sei=Tran
en-aut-mei=Linh T.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=AkilCaner
en-aut-sei=Akil
en-aut-mei=Caner
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SenjuYosuke
en-aut-sei=Senju
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=RobinsonRobert C.
en-aut-sei=Robinson
en-aut-mei=Robert C.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=Research Institute for Interdisciplinary Science, Okayama University
kn-affil=

affil-num=2
en-affil=Research Institute for Interdisciplinary Science, Okayama University
kn-affil=

affil-num=3
en-affil=Research Institute for Interdisciplinary Science, Okayama University
kn-affil=

affil-num=4
en-affil=Research Institute for Interdisciplinary Science, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=299
cd-vols=
no-issue=7
article-no=
start-page=104839
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=202307
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Structural insights into the action mechanisms of artificial electron acceptors in photosystem II
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Photosystem II (PSII) utilizes light energy to split water, and the electrons extracted from water are transferred to QB, a plastoquinone molecule bound to the D1 subunit of PSII. Many artificial electron acceptors (AEAs) with molecular structures similar to that of plastoquinone can accept electrons from PSII. However, the molecular mechanism by which AEAs act on PSII is unclear. Here, we solved the crystal structure of PSII treated with three different AEAs, 2,5-dibromo-1,4-benzoquinone, 2,6dichloro-1,4-benzoquinone, and 2-phenyl-1,4-benzoquinone, at 1.95 to 2.10 angstrom resolution. Our results show that all AEAs substitute for QB and are bound to the QB-binding site (QB site) to receive electrons, but their binding strengths are different, resulting in differences in their efficiencies to accept electrons. The acceptor 2-phenyl-1,4-benzoquinone binds most weakly to the QB site and showed the highest oxygen-evolving activity, implying a reverse relationship between the binding strength and oxygen-evolving activity. In addition, a novel quinonebinding site, designated the QD site, was discovered, which is located in the vicinity of QB site and close to QC site, a binding site reported previously. This QD site is expected to play a role as a channel or a storage site for quinones to be transported to the QB site. These results provide the structural basis for elucidating the actions of AEAs and exchange mechanism of QB in PSII and also provide information for the design of more efficient electron acceptors.
en-copyright=
kn-copyright=

en-aut-name=KamadaShinji
en-aut-sei=Kamada
en-aut-mei=Shinji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakajimaYoshiki
en-aut-sei=Nakajima
en-aut-mei=Yoshiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ShenJian-Ren
en-aut-sei=Shen
en-aut-mei=Jian-Ren
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Faculty of Science, Okayama University
kn-affil=

affil-num=2
en-affil=Research Institute for Interdisciplinary Science and Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=3
en-affil=Research Institute for Interdisciplinary Science and Graduate School of Natural Science and Technology, Okayama University
kn-affil=
en-keyword=Photosystem II
kn-keyword=Photosystem II
en-keyword=photosynthesis
kn-keyword=photosynthesis
en-keyword=electron transfer
kn-keyword=electron transfer
en-keyword=structural biology
kn-keyword=structural biology
en-keyword=crystal structure
kn-keyword=crystal structure
en-keyword=electron acceptor
kn-keyword=electron acceptor
END

start-ver=1.4
cd-journal=joma
no-vol=43
cd-vols=
no-issue=2
article-no=
start-page=113797
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240227
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Stem-like progenitor and terminally differentiated TFH-like CD4+ T cell exhaustion in the tumor microenvironment
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Immune checkpoint inhibitors exert clinical efficacy against various types of cancer through reinvigoration of exhausted CD8+ T cells that attack cancer cells directly in the tumor microenvironment (TME). Using single-cell sequencing and mouse models, we show that CXCL13, highly expressed in tumor-infiltrating exhausted CD8+ T cells, induces CD4+ follicular helper T (TFH) cell infiltration, contributing to anti-tumor immunity. Furthermore, a part of the TFH cells in the TME exhibits cytotoxicity and directly attacks major histocompatibility complex-II-expressing tumors. TFH-like cytotoxic CD4+ T cells have high LAG-3/BLIMP1 and low TCF1 expression without self-renewal ability, whereas non-cytotoxic TFH cells express low LAG-3/BLIMP1 and high TCF1 with self-renewal ability, closely resembling the relationship between terminally differentiated and stem-like progenitor exhaustion in CD8+ T cells, respectively. Our findings provide deep insights into TFH-like CD4+ T cell exhaustion with helper progenitor and cytotoxic differentiated functions, mediating anti-tumor immunity orchestrally with CD8+ T cells.
en-copyright=
kn-copyright=

en-aut-name=ZhouWenhao
en-aut-sei=Zhou
en-aut-mei=Wenhao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KawashimaShusuke
en-aut-sei=Kawashima
en-aut-mei=Shusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=IshinoTakamasa
en-aut-sei=Ishino
en-aut-mei=Takamasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KawaseKatsushige
en-aut-sei=Kawase
en-aut-mei=Katsushige
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=UedaYouki
en-aut-sei=Ueda
en-aut-mei=Youki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YamashitaKazuo
en-aut-sei=Yamashita
en-aut-mei=Kazuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=WatanabeTomofumi
en-aut-sei=Watanabe
en-aut-mei=Tomofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KawazuMasahito
en-aut-sei=Kawazu
en-aut-mei=Masahito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=DansakoHiromichi
en-aut-sei=Dansako
en-aut-mei=Hiromichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=SuzukiYutaka
en-aut-sei=Suzuki
en-aut-mei=Yutaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=NishikawaHiroyoshi
en-aut-sei=Nishikawa
en-aut-mei=Hiroyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=InozumeTakashi
en-aut-sei=Inozume
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=NagasakiJoji
en-aut-sei=Nagasaki
en-aut-mei=Joji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=TogashiYosuke
en-aut-sei=Togashi
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

affil-num=1
en-affil=Department of Tumor Microenvironment, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Dermatology, Chiba University Graduate School of Medicine
kn-affil=

affil-num=3
en-affil=Department of Tumor Microenvironment, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Chiba Cancer Center, Research Institute
kn-affil=

affil-num=5
en-affil=Department of Tumor Microenvironment, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=KOTAI Biotechnologies, Inc. 
kn-affil=

affil-num=7
en-affil=Department of Tumor Microenvironment, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Chiba Cancer Center, Research Institute, Division of Cell Therapy
kn-affil=

affil-num=9
en-affil=Department of Tumor Microenvironment, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo
kn-affil=

affil-num=11
en-affil=Department of Immunology, Nagoya University Graduate School of Medicine
kn-affil=

affil-num=12
en-affil=Department of Dermatology, Chiba University Graduate School of Medicine
kn-affil=

affil-num=13
en-affil=Department of Tumor Microenvironment, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=14
en-affil=Department of Tumor Microenvironment, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=cancer immunology
kn-keyword=cancer immunology
en-keyword=follicular helper T cell
kn-keyword=follicular helper T cell
en-keyword=cytotoxic CD4+ T cell
kn-keyword=cytotoxic CD4+ T cell
en-keyword=CXCL13
kn-keyword=CXCL13
en-keyword=T cell exhaustion
kn-keyword=T cell exhaustion
en-keyword=stem-like progenitor exhaustion
kn-keyword=stem-like progenitor exhaustion
en-keyword=terminally differentiated exhaustion
kn-keyword=terminally differentiated exhaustion
en-keyword=PD-1
kn-keyword=PD-1
en-keyword=LAG-3
kn-keyword=LAG-3
en-keyword=TCF1
kn-keyword=TCF1
END

start-ver=1.4
cd-journal=joma
no-vol=49
cd-vols=
no-issue=2
article-no=
start-page=55
end-page=60
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=2024
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Methylmercury-induced brain neuronal death in CHOP-knockout mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Apoptosis is one of the hallmarks of MeHg-induced neuronal cell death; however, its molecular mechanism remains unclear. We previously reported that MeHg exposure induces neuron-specific ER stress in the mouse brain. Excessive ER stress contributes to apoptosis, and CHOP induction is considered to be one of the major mechanisms. CHOP is also increased by MeHg exposure in the mouse brain, suggesting that it correlates with increased apoptosis. In this study, to clarify whether CHOP mediates MeHg-induced apoptosis, we examined the effect of CHOP deletion on MeHg exposure in CHOP-knockout mice. Our data showed that CHOP deletion had no effect on MeHg exposure-induced weight loss or hindlimb impairment in mice, nor did it increase apoptosis or inhibit neuronal cell loss. Hence, CHOP plays little role in MeHg toxicity, and other apoptotic pathways coupled with ER stress may be involved in MeHg-induced cell death.
en-copyright=
kn-copyright=

en-aut-name=IijimaYuta
en-aut-sei=Iijima
en-aut-mei=Yuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MikiRyohei
en-aut-sei=Miki
en-aut-mei=Ryohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=FujimuraMasatake
en-aut-sei=Fujimura
en-aut-mei=Masatake
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OyadomariSeiichi
en-aut-sei=Oyadomari
en-aut-mei=Seiichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=UeharaTakashi
en-aut-sei=Uehara
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Basic Medical Science, National Institute for Minamata Disease
kn-affil=

affil-num=4
en-affil=Division of Molecular Biology, Institute of Advanced Medical Sciences, Tokushima University
kn-affil=

affil-num=5
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Methylmercury
kn-keyword=Methylmercury
en-keyword=Neuronal cell death
kn-keyword=Neuronal cell death
en-keyword=Apoptosis
kn-keyword=Apoptosis
en-keyword=CHOP
kn-keyword=CHOP
en-keyword=Knockout mouse
kn-keyword=Knockout mouse
END

start-ver=1.4
cd-journal=joma
no-vol=18
cd-vols=
no-issue=1
article-no=
start-page=1
end-page=12
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240118
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Rhizoviticin is an alphaproteobacterial tailocin that mediates biocontrol of grapevine crown gall disease
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Tailocins are headless phage tail structures that mediate interbacterial antagonism. Although the prototypical tailocins, R- and F-pyocins, in Pseudomonas aeruginosa, and other predominantly R-type tailocins have been studied, their presence in Alphaproteobacteria remains unexplored. Here, we report the first alphaproteobacterial F-type tailocin, named rhizoviticin, as a determinant of the biocontrol activity of Allorhizobium vitis VAR03-1 against crown gall. Rhizoviticin is encoded by a chimeric prophage genome, one providing transcriptional regulators and the other contributing to tail formation and cell lysis, but lacking head formation genes. The rhizoviticin genome retains a nearly intact early phage region containing an integrase remnant and replication-related genes critical for downstream gene transcription, suggesting an ongoing transition of this locus from a prophage to a tailocin-coding region. Rhizoviticin is responsible for the most antagonistic activity in VAR03-1 culture supernatant against pathogenic A. vitis strain, and rhizoviticin deficiency resulted in a significant reduction in the antitumorigenic activity in planta. We identified the rhizoviticin-coding locus in eight additional A. vitis strains from diverse geographical locations, highlighting a unique survival strategy of certain Rhizobiales bacteria in the rhizosphere. These findings advance our understanding of the evolutionary dynamics of tailocins and provide a scientific foundation for employing rhizoviticin-producing strains in plant disease control.
en-copyright=
kn-copyright=

en-aut-name=IshiiTomoya
en-aut-sei=Ishii
en-aut-mei=Tomoya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TsuchidaNatsuki
en-aut-sei=Tsuchida
en-aut-mei=Natsuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HemeldaNiarsi Merry
en-aut-sei=Hemelda
en-aut-mei=Niarsi Merry
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SaitoKirara
en-aut-sei=Saito
en-aut-mei=Kirara
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=BaoJiyuan
en-aut-sei=Bao
en-aut-mei=Jiyuan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=WatanabeMegumi
en-aut-sei=Watanabe
en-aut-mei=Megumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=ToyodaAtsushi
en-aut-sei=Toyoda
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MatsubaraTakehiro
en-aut-sei=Matsubara
en-aut-mei=Takehiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=SatoMayuko
en-aut-sei=Sato
en-aut-mei=Mayuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=ToyookaKiminori
en-aut-sei=Toyooka
en-aut-mei=Kiminori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=IshihamaNobuaki
en-aut-sei=Ishihama
en-aut-mei=Nobuaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=ShirasuKen
en-aut-sei=Shirasu
en-aut-mei=Ken
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=MatsuiHidenori
en-aut-sei=Matsui
en-aut-mei=Hidenori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=ToyodaKazuhiro
en-aut-sei=Toyoda
en-aut-mei=Kazuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=IchinoseYuki
en-aut-sei=Ichinose
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=HayashiTetsuya
en-aut-sei=Hayashi
en-aut-mei=Tetsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=KawaguchiAkira
en-aut-sei=Kawaguchi
en-aut-mei=Akira
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=NoutoshiYoshiteru
en-aut-sei=Noutoshi
en-aut-mei=Yoshiteru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

affil-num=1
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Faculty of Agriculture, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=4
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=5
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=6
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Genomics and Evolutionary Biology, National Institute of Genetics
kn-affil=

affil-num=8
en-affil=Okayama University Hospital Biobank, Okayama University Hospital
kn-affil=

affil-num=9
en-affil=Mass Spectrometry and Microscopy Unit, Technology Platform Division, RIKEN Center for Sustainable Resource Science
kn-affil=

affil-num=10
en-affil=Mass Spectrometry and Microscopy Unit, Technology Platform Division, RIKEN Center for Sustainable Resource Science
kn-affil=

affil-num=11
en-affil=Plant Immunity Research Group, RIKEN Center for Sustainable Resource Science
kn-affil=

affil-num=12
en-affil=Plant Immunity Research Group, RIKEN Center for Sustainable Resource Science
kn-affil=

affil-num=13
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=14
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=15
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=16
en-affil=Department of Bacteriology, Graduate School of Medical Sciences, Kyushu University
kn-affil=

affil-num=17
en-affil=Western Region Agricultural Research Center (WARC), National Agricultural and Food Research Organization (NARO)
kn-affil=

affil-num=18
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=
en-keyword=tailocin
kn-keyword=tailocin
en-keyword=phage tail-like bacteriocin
kn-keyword=phage tail-like bacteriocin
en-keyword=Allorhizobium vitris
kn-keyword=Allorhizobium vitris
en-keyword=Alphaproteobacteria
kn-keyword=Alphaproteobacteria
en-keyword=biocontrol
kn-keyword=biocontrol
en-keyword=crown gall disease
kn-keyword=crown gall disease
en-keyword=interbacterial antagonism
kn-keyword=interbacterial antagonism
en-keyword=grapevine
kn-keyword=grapevine
END

start-ver=1.4
cd-journal=joma
no-vol=115
cd-vols=
no-issue=4
article-no=
start-page=1317
end-page=1332
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240126
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Antitumor activity of α-pinene in T-cell tumors
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=T-cell acute leukemia and lymphoma have a poor prognosis. Although new therapeu-tic agents have been developed, their therapeutic effects are suboptimal. α- Pinene, a monoterpene compound, has an antitumor effect on solid tumors; however, few comprehensive investigations have been conducted on its impact on hematologic ma-lignancies. This report provides a comprehensive analysis of the potential benefits of using α- pinene as an antitumor agent for the treatment of T-cell tumors. We found that α- pinene inhibited the proliferation of hematologic malignancies, especially in T-  cell tumor cell lines EL-4 and Molt-4, induced mitochondrial dysfunction and re-active oxygen species accumulation, and inhibited NF-κB p65 translocation into the nucleus, leading to robust apoptosis in EL-4 cells. Collectively, these findings suggest that α- pinene has potential as a therapeutic agent for T-cell malignancies, and further investigation is warranted.
en-copyright=
kn-copyright=

en-aut-name=AbeMasaya
en-aut-sei=Abe
en-aut-mei=Masaya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=AsadaNoboru
en-aut-sei=Asada
en-aut-mei=Noboru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KimuraMaiko
en-aut-sei=Kimura
en-aut-mei=Maiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=FukuiChie
en-aut-sei=Fukui
en-aut-mei=Chie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YamadaDaisuke
en-aut-sei=Yamada
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=WangZiyi
en-aut-sei=Wang
en-aut-mei=Ziyi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MiyakeMasayuki
en-aut-sei=Miyake
en-aut-mei=Masayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TakaradaTakeshi
en-aut-sei=Takarada
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=OnoMitsuaki
en-aut-sei=Ono
en-aut-mei=Mitsuaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=AoeMichinori
en-aut-sei=Aoe
en-aut-mei=Michinori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=KitamuraWataru
en-aut-sei=Kitamura
en-aut-mei=Wataru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=MatsudaMasayuki
en-aut-sei=Matsuda
en-aut-mei=Masayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=MoriyamaTakashi
en-aut-sei=Moriyama
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=MatsumuraAkifumi
en-aut-sei=Matsumura
en-aut-mei=Akifumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=MaedaYoshinobu
en-aut-sei=Maeda
en-aut-mei=Yoshinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

affil-num=1
en-affil=Department of Hematology, Oncology  and Respiratory Medicine, Okayama  University Graduate School of Medicine,  Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Hematology and  Oncology, Okayama University Hospital
kn-affil=

affil-num=3
en-affil=Department of Hematology, Oncology  and Respiratory Medicine, Okayama  University Graduate School of Medicine,  Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Division of Hematology, Department of  Medicine, Kobe University Hospital
kn-affil=

affil-num=5
en-affil=Department of Regenerative Science,  Okayama University Graduate School of  Medicine, Dentistry and Pharmaceutical  Sciences
kn-affil=

affil-num=6
en-affil=Department of Molecular Biology and  Biochemistry, Okayama University  Graduate School of Medicine, Dentistry  and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Division of Medical Support, Okayama  University Hospital
kn-affil=

affil-num=8
en-affil=Department of Regenerative Science,  Okayama University Graduate School of  Medicine, Dentistry and Pharmaceutical  Sciences
kn-affil=

affil-num=9
en-affil=Department of Molecular Biology and  Biochemistry, Okayama University  Graduate School of Medicine, Dentistry  and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Division of Medical Support, Okayama  University Hospital
kn-affil=

affil-num=11
en-affil=Department of Hematology, Oncology  and Respiratory Medicine, Okayama  University Graduate School of Medicine,  Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=12
en-affil=Department of Hematology, Oncology  and Respiratory Medicine, Okayama  University Graduate School of Medicine,  Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=13
en-affil=Department of Hematology, Oncology  and Respiratory Medicine, Okayama  University Graduate School of Medicine,  Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=14
en-affil=Department of Hematology, Oncology  and Respiratory Medicine, Okayama  University Graduate School of Medicine,  Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=15
en-affil=Department of Hematology, Oncology  and Respiratory Medicine, Okayama  University Graduate School of Medicine,  Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=alpha-pinene
kn-keyword=alpha-pinene
en-keyword=apoptosis
kn-keyword=apoptosis
en-keyword=hematologic malignancies
kn-keyword=hematologic malignancies
en-keyword=lymphoblastic leukemia, acute, T-cell
kn-keyword=lymphoblastic leukemia, acute, T-cell
en-keyword=T-cell lymphoma
kn-keyword=T-cell lymphoma
END

start-ver=1.4
cd-journal=joma
no-vol=42
cd-vols=
no-issue=12
article-no=
start-page=113569
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20231226
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Mechanistic dissection of premature translation termination induced by acidic residues-enriched nascent peptide
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Ribosomes polymerize nascent peptides through repeated inter-subunit rearrangements between the classic and hybrid states. The peptidyl-tRNA, the intermediate species during translation elongation, stabi-lizes the translating ribosome to ensure robust continuity of elongation. However, the translation of acidic residue-rich sequences destabilizes the ribosome, leading to a stochastic premature translation cessation termed intrinsic ribosome destabilization (IRD), which is still ill-defined. Here, we dissect the molecular mechanisms underlying IRD in Escherichia coli. Reconstitution of the IRD event reveals that (1) the prolonged ribosome stalling enhances IRD-mediated translation discontinuation, (2) IRD depends on temperature, (3) the destabilized 70S ribosome complex is not necessarily split, and (4) the destabilized ribosome is subjected to peptidyl-tRNA hydrolase-mediated hydrolysis of the peptidyl-tRNA without subunit splitting or recycling factors-mediated subunit splitting. Collectively, our data indicate that the translation of acidic-rich sequences alters the conformation of the 70S ribosome to an aberrant state that allows the noncanonical pre-mature termination.
en-copyright=
kn-copyright=

en-aut-name=ChadaniYuhei
en-aut-sei=Chadani
en-aut-mei=Yuhei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KanamoriTakashi
en-aut-sei=Kanamori
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NiwaTatsuya
en-aut-sei=Niwa
en-aut-mei=Tatsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=IchiharaKazuya
en-aut-sei=Ichihara
en-aut-mei=Kazuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NakayamaKeiichi I.
en-aut-sei=Nakayama
en-aut-mei=Keiichi I.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MatsumotoAkinobu
en-aut-sei=Matsumoto
en-aut-mei=Akinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TaguchiHideki
en-aut-sei=Taguchi
en-aut-mei=Hideki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=GeneFrontier Corporation
kn-affil=

affil-num=3
en-affil=Cell Biology Center, Institute of Innovative Research, Tokyo Institute of Technology
kn-affil=

affil-num=4
en-affil=Division of Biological Science, Graduate School of Science, Nagoya University
kn-affil=

affil-num=5
en-affil=Anticancer Strategies Laboratory, TMDU Advanced Research Institute, Tokyo Medical and Dental University
kn-affil=

affil-num=6
en-affil=Division of Biological Science, Graduate School of Science, Nagoya University
kn-affil=

affil-num=7
en-affil=Cell Biology Center, Institute of Innovative Research, Tokyo Institute of Technology
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=12
cd-vols=
no-issue=
article-no=
start-page=RP88822
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20231121
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Characterization of tryptophan oxidation affecting D1 degradation by FtsH in the photosystem II quality control of chloroplasts
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Photosynthesis is one of the most important reactions for sustaining our environment. Photosystem II (PSII) is the initial site of photosynthetic electron transfer by water oxidation. Light in excess, however, causes the simultaneous production of reactive oxygen species (ROS), leading to photo-oxidative damage in PSII. To maintain photosynthetic activity, the PSII reaction center protein D1, which is the primary target of unavoidable photo-oxidative damage, is efficiently degraded by FtsH protease. In PSII subunits, photo-oxidative modifications of several amino acids such as Trp have been indeed documented, whereas the linkage between such modifications and D1 degradation remains elusive. Here, we show that an oxidative post-translational modification of Trp residue at the N-terminal tail of D1 is correlated with D1 degradation by FtsH during high-light stress. We revealed that Arabidopsis mutant lacking FtsH2 had increased levels of oxidative Trp residues in D1, among which an N-terminal Trp-14 was distinctively localized in the stromal side. Further characterization of Trp-14 using chloroplast transformation in Chlamydomonas indicated that substitution of D1 Trp-14 to Phe, mimicking Trp oxidation enhanced FtsH-mediated D1 degradation under high light, although the substitution did not affect protein stability and PSII activity. Molecular dynamics simulation of PSII implies that both Trp-14 oxidation and Phe substitution cause fluctuation of D1 N-terminal tail. Furthermore, Trp-14 to Phe modification appeared to have an additive effect in the interaction between FtsH and PSII core in vivo. Together, our results suggest that the Trp oxidation at its N-terminus of D1 may be one of the key oxidations in the PSII repair, leading to processive degradation by FtsH.
en-copyright=
kn-copyright=

en-aut-name=KatoYusuke
en-aut-sei=Kato
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KurodaHiroshi
en-aut-sei=Kuroda
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OzawaShin-Ichiro
en-aut-sei=Ozawa
en-aut-mei=Shin-Ichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SaitoKeisuke
en-aut-sei=Saito
en-aut-mei=Keisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=DograVivek
en-aut-sei=Dogra
en-aut-mei=Vivek
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ScholzMartin
en-aut-sei=Scholz
en-aut-mei=Martin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=ZhangGuoxian
en-aut-sei=Zhang
en-aut-mei=Guoxian
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=de VitryCatherine
en-aut-sei=de Vitry
en-aut-mei=Catherine
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=IshikitaHiroshi
en-aut-sei=Ishikita
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=KimChanhong
en-aut-sei=Kim
en-aut-mei=Chanhong
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=HipplerMichael
en-aut-sei=Hippler
en-aut-mei=Michael
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=TakahashiYuichiro
en-aut-sei=Takahashi
en-aut-mei=Yuichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=SakamotoWataru
en-aut-sei=Sakamoto
en-aut-mei=Wataru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

affil-num=1
en-affil=Institute of Plant Science and Resources (IPSR), Okayama University
kn-affil=

affil-num=2
en-affil=Research Institute  for Interdisciplinary Science, Okayama University
kn-affil=

affil-num=3
en-affil=Institute of Plant Science and Resources (IPSR), Okayama University
kn-affil=

affil-num=4
en-affil=Research Center  for Advanced Science and Technology, The University of Tokyo
kn-affil=

affil-num=5
en-affil=Shanghai Center for Plant Stress Biology, Center for Excellence in Molecular Plant  Sciences, Chinese Academy of Sciences
kn-affil=

affil-num=6
en-affil=Institute of  Plant Biology and Biotechnology, University of Münster
kn-affil=

affil-num=7
en-affil=Institute of Plant Science and Resources (IPSR), Okayama University
kn-affil=

affil-num=8
en-affil=Institut  de Biologie Physico-Chimique, Unité Mixte de Recherche 7141, Centre National de la  Recherche Scientifique and Sorbonne Université Pierre et Marie Curie
kn-affil=

affil-num=9
en-affil=Research Center  for Advanced Science and Technology, The University of Tokyo
kn-affil=

affil-num=10
en-affil=Shanghai Center for Plant Stress Biology, Center for Excellence in Molecular Plant  Sciences, Chinese Academy of Sciences
kn-affil=

affil-num=11
en-affil=Institute of Plant Science and Resources (IPSR), Okayama University
kn-affil=

affil-num=12
en-affil=Research Institute  for Interdisciplinary Science, Okayama University
kn-affil=

affil-num=13
en-affil=Institute of Plant Science and Resources (IPSR), Okayama University
kn-affil=
en-keyword=post-translational modification
kn-keyword=post-translational modification
en-keyword=Arabidopsis thaliana
kn-keyword=Arabidopsis thaliana
en-keyword=protein degradation
kn-keyword=protein degradation
en-keyword=photosystem II
kn-keyword=photosystem II
en-keyword=photo-oxidative damage
kn-keyword=photo-oxidative damage
en-keyword=tryptophan oxidation
kn-keyword=tryptophan oxidation
en-keyword=Chlamydomonas reinhardtii
kn-keyword=Chlamydomonas reinhardtii
END

start-ver=1.4
cd-journal=joma
no-vol=436
cd-vols=
no-issue=5
article-no=
start-page=168319
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240301
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Molecular Property, Manipulation, and Potential Use of Opn5 and Its Homologs
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Animal opsin is a G-protein coupled receptor (GPCR) and binds retinal as a chromophore to form a photopigment. The Opsin 5 (Opn5) group within the animal opsin family comprises a diverse array of related proteins, such as Opn5m, a protein conserved across all vertebrate lineages including mammals, and other members like Opn5L1 and Opn5L2 found in non-mammalian vertebrate genomes, and Opn6 found in non-therian vertebrate genomes, along with Opn5 homologs present in invertebrates. Although these proteins collectively constitute a single clade within the molecular phylogenetic tree of animal opsins, they exhibit markedly distinct molecular characteristics in areas such as retinal binding properties, photoreaction, and G-protein coupling specificity. Based on their molecular features, they are believed to play a significant role in physiological functions. However, our understanding of their precise physiological functions and molecular characteristics is still developing and only partially realized. Furthermore, their unique molecular characteristics of Opn5-related proteins suggest a high potential for their use as optogenetic tools through more specialized manipulations. This review intends to encapsulate our current understanding of Opn5, discuss potential manipulations of its molecular attributes, and delve into its prospective utility in the burgeoning field of animal opsin optogenetics.
en-copyright=
kn-copyright=

en-aut-name=SatoKeita
en-aut-sei=Sato
en-aut-mei=Keita
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OhuchiHideyo
en-aut-sei=Ohuchi
en-aut-mei=Hideyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

affil-num=1
en-affil=Department of Cytology and Histology, Faculty of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Cytology and Histology, Faculty of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Opn5
kn-keyword=Opn5
en-keyword=rhodopsin
kn-keyword=rhodopsin
en-keyword=optogenetics
kn-keyword=optogenetics
en-keyword=retinal protein
kn-keyword=retinal protein
en-keyword=non-image-forming opsin
kn-keyword=non-image-forming opsin
END

start-ver=1.4
cd-journal=joma
no-vol=186
cd-vols=
no-issue=
article-no=
start-page=4189
end-page=4203.e22
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230914
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Structure of the thrombopoietin-MPL receptor complex is a blueprint for biasing hematopoiesis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Thrombopoietin (THPO or TPO) is an essential cytokine for hematopoietic stem cell (HSC) maintenance and megakaryocyte differentiation. Here, we report the 3.4 Å resolution cryoelectron microscopy structure of the extracellular TPO-TPO receptor (TpoR or MPL) signaling complex, revealing the basis for homodimeric MPL activation and providing a structural rationalization for genetic loss-of-function thrombocytopenia mutations. The structure guided the engineering of TPO variants (TPOmod) with a spectrum of signaling activities, from neutral antagonists to partial- and super-agonists. Partial agonist TPOmod decoupled JAK/STAT from ERK/AKT/CREB activation, driving a bias for megakaryopoiesis and platelet production without causing significant HSC expansion in mice and showing superior maintenance of human HSCs in vitro. These data demonstrate the functional uncoupling of the two primary roles of TPO, highlighting the potential utility of TPOmod in hematology research and clinical HSC transplantation.
en-copyright=
kn-copyright=

en-aut-name=TsutsumiNaotaka
en-aut-sei=Tsutsumi
en-aut-mei=Naotaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MasoumiZahra
en-aut-sei=Masoumi
en-aut-mei=Zahra
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=JamesSophie C.
en-aut-sei=James
en-aut-mei=Sophie C.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TuckerJulie A.
en-aut-sei=Tucker
en-aut-mei=Julie A.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=WinkelmannHauke
en-aut-sei=Winkelmann
en-aut-mei=Hauke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=GreyWilliam
en-aut-sei=Grey
en-aut-mei=William
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=PictonLora K.
en-aut-sei=Picton
en-aut-mei=Lora K.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MossLucie
en-aut-sei=Moss
en-aut-mei=Lucie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=WilsonSteven C.
en-aut-sei=Wilson
en-aut-mei=Steven C.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=CaveneyNathanael A.
en-aut-sei=Caveney
en-aut-mei=Nathanael A.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=JudeKevin M.
en-aut-sei=Jude
en-aut-mei=Kevin M.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=GatiCornelius
en-aut-sei=Gati
en-aut-mei=Cornelius
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=PiehlerJacob
en-aut-sei=Piehler
en-aut-mei=Jacob
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=HitchcockIan S.
en-aut-sei=Hitchcock
en-aut-mei=Ian S.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=GarciaK. Christopher
en-aut-sei=Garcia
en-aut-mei=K. Christopher
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

affil-num=1
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=York Biomedical Research Institute, Department of Biology, University of York
kn-affil=

affil-num=3
en-affil=York Biomedical Research Institute, Department of Biology, University of York
kn-affil=

affil-num=4
en-affil=York Biomedical Research Institute, Department of Biology, University of York
kn-affil=

affil-num=5
en-affil=Department of Biology/Chemistry and Center of Cellular Nanoanalytics, Osnabrück University
kn-affil=

affil-num=6
en-affil=York Biomedical Research Institute, Department of Biology, University of York
kn-affil=

affil-num=7
en-affil=Department of Molecular and Cellular Physiology, Stanford University School of Medicine
kn-affil=

affil-num=8
en-affil=York Biomedical Research Institute, Department of Biology, University of York
kn-affil=

affil-num=9
en-affil=Department of Molecular and Cellular Physiology, Stanford University School of Medicine
kn-affil=

affil-num=10
en-affil=Department of Molecular and Cellular Physiology, Stanford University School of Medicine
kn-affil=

affil-num=11
en-affil=Department of Molecular and Cellular Physiology, Stanford University School of Medicine
kn-affil=

affil-num=12
en-affil=Department of Structural Biology, Stanford University School of Medicine
kn-affil=

affil-num=13
en-affil=Department of Biology/Chemistry and Center of Cellular Nanoanalytics, Osnabrück University
kn-affil=

affil-num=14
en-affil=York Biomedical Research Institute, Department of Biology, University of York
kn-affil=

affil-num=15
en-affil=Department of Molecular and Cellular Physiology, Stanford University School of Medicine
kn-affil=
en-keyword=thrombopoietin
kn-keyword=thrombopoietin
en-keyword=TpoR
kn-keyword=TpoR
en-keyword=c-MPL
kn-keyword=c-MPL
en-keyword=structure
kn-keyword=structure
en-keyword=cryo-EM
kn-keyword=cryo-EM
en-keyword=signaling
kn-keyword=signaling
en-keyword=JAK-STAT
kn-keyword=JAK-STAT
en-keyword=mTOR
kn-keyword=mTOR
en-keyword=hematopoiesis
kn-keyword=hematopoiesis
en-keyword=ligand engineering
kn-keyword=ligand engineering
END

start-ver=1.4
cd-journal=joma
no-vol=12
cd-vols=
no-issue=12
article-no=
start-page=1481
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20231201
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Random Mutational Analysis Targeting Residue K155 within the Transmembrane β-Hairpin of the Mosquitocidal Mpp46Ab Toxin
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Mpp46Ab is a mosquito-larvicidal pore-forming toxin derived from Bacillus thuringiensis TK-E6. Pore formation is believed to be a central mode of Mpp46Ab action, and the cation selectivity of the channel pores, in particular, is closely related to its mosquito-larvicidal activity. In the present study, we constructed a mutant library in which residue K155 within the transmembrane β-hairpin was randomly replaced with other amino acid residues. Upon mutagenesis and following primary screening using Culex pipiens mosquito larvae, we obtained 15 mutants in addition to the wild-type toxin. Bioassays using purified proteins revealed that two mutants, K155E and K155I, exhibited toxicity significantly higher than that of the wild-type toxin. Although increased cation selectivity was previously reported for K155E channel pores, we demonstrated in the present study that the cation selectivity of K155I channel pores was also significantly increased. Considering the characteristics of the amino acids, the charge of residue 155 may not directly affect the cation selectivity of Mpp46Ab channel pores. Replacement of K155 with glutamic acid or isoleucine may induce a similar conformational change in the region associated with the ion selectivity of the Mpp46Ab channel pores. Mutagenesis targeting the transmembrane β-hairpin may be an effective strategy for enhancing the ion permeability of the channel pores and the resulting mosquito-larvicidal activity of Mpp46Ab.
en-copyright=
kn-copyright=

en-aut-name=MiyazakiMidoka
en-aut-sei=Miyazaki
en-aut-mei=Midoka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=AsakuraMami
en-aut-sei=Asakura
en-aut-mei=Mami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=IdeToru
en-aut-sei=Ide
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HayakawaTohru
en-aut-sei=Hayakawa
en-aut-mei=Tohru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=4
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
en-keyword=mosquito-larvicidal toxin
kn-keyword=mosquito-larvicidal toxin
en-keyword=Bacillus thuringiensis TK-E6
kn-keyword=Bacillus thuringiensis TK-E6
en-keyword=Culex pipiens mosquito larvae
kn-keyword=Culex pipiens mosquito larvae
en-keyword=site-directed mutagenesis
kn-keyword=site-directed mutagenesis
en-keyword=electrophysiologic analysis
kn-keyword=electrophysiologic analysis
END

start-ver=1.4
cd-journal=joma
no-vol=135
cd-vols=
no-issue=3
article-no=
start-page=181
end-page=182
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20231201
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=The 95th Annual Meeting of the Japanese Tissue Culture Association
kn-title=日本組織培養学会第95回大会報告
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=SakaguchiMasakiyo
en-aut-sei=Sakaguchi
en-aut-mei=Masakiyo
kn-aut-name=阪口政清
kn-aut-sei=阪口
kn-aut-mei=政清
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Department of Cell Biology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=岡山大学学術研究院医歯薬学域　細胞生物学
END

start-ver=1.4
cd-journal=joma
no-vol=135
cd-vols=
no-issue=3
article-no=
start-page=174
end-page=174
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20231201
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=The 55th Annual Meeting of the Japanese Society for Matrix Biology and Medicine
kn-title=第55回日本結合組織学会学術大会開催報告
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=OohashiToshitaka
en-aut-sei=Oohashi
en-aut-mei=Toshitaka
kn-aut-name=大橋俊孝
kn-aut-sei=大橋
kn-aut-mei=俊孝
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Department of Molecular Biology and Biochemistry, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=岡山大学学術研究院医歯薬学域　分子医化学
END

start-ver=1.4
cd-journal=joma
no-vol=43
cd-vols=
no-issue=1
article-no=
start-page=BSR20220369
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230124
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Remodeling of algal photosystem I through phosphorylation
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Photosystem I (PSI) with its associated light-harvesting system is the most important generator of reducing power in photosynthesis. The PSI core complex is highly conserved, whereas peripheral subunits as well as light-harvesting proteins (LHCI) reveal a dynamic plasticity. Moreover, in green alga, PSI-LHCI complexes are found as monomers, dimers, and state transition complexes, where two LHCII trimers are associated. Herein, we show light-dependent phosphorylation of PSI subunits PsaG and PsaH as well as Lhca6. Potential consequences of the dynamic phosphorylation of PsaG and PsaH are structurally analyzed and discussed in regard to the formation of the monomeric, dimeric, and LHCII-associated PSI-LHCI complexes.
en-copyright=
kn-copyright=

en-aut-name=YounasMuhammad
en-aut-sei=Younas
en-aut-mei=Muhammad
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ScholzMartin
en-aut-sei=Scholz
en-aut-mei=Martin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MarchettiGiulia Maria
en-aut-sei=Marchetti
en-aut-mei=Giulia Maria
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HipplerMichael
en-aut-sei=Hippler
en-aut-mei=Michael
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=Institute of Plant Biology and Biotechnology, University of Munster
kn-affil=

affil-num=2
en-affil=Institute of Plant Biology and Biotechnology, University of Munster
kn-affil=

affil-num=3
en-affil=Institute of Plant Biology and Biotechnology, University of Munster
kn-affil=

affil-num=4
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=
en-keyword=green algae
kn-keyword=green algae
en-keyword=Light harvesting proteins
kn-keyword=Light harvesting proteins
en-keyword=phosphorylation/dephosphorylation
kn-keyword=phosphorylation/dephosphorylation
en-keyword=photosystems
kn-keyword=photosystems
END

start-ver=1.4
cd-journal=joma
no-vol=155
cd-vols=
no-issue=
article-no=
start-page=105797
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=202311
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Ruxolitinib altered IFN-β induced necroptosis of human dental pulp stem cells during osteoblast differentiation
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Objective: This study aimed to evaluate the role of ruxolitinib in the interferon beta (IFN-β) mediated osteoblast differentiation using human dental pulp stem cells (hDPSCs).<br>
Design: hDPSCs from five deciduous teeth of healthy patients were stimulated by adding human recombinant IFN-β protein (1 or 2 ng/ml) to the osteogenic differentiation induction medium. Substrate formation was determined using Alizarin Red staining, calcium concentration, and osteoblast marker expression levels. Ruxolitinib was used to inhibit the Janus kinase/signal transducers and activators of transcription (JAK-STAT) pathway. Apoptosis was detected using terminal deoxynucleotidyl nick-end labeling (TUNEL) staining, and necroptosis was detected using propidium iodide staining and phosphorylated mixed lineage kinase domain-like protein (pMLKL) expression.<br>
Results: In the IFN-β-treated group, substrate formation was inhibited by a reduction in alkaline phosphatase (ALP) expression in a concentration-dependent manner. Although the proliferation potency was unchanged between the IFN-β-treated and control groups, the cell number was significantly reduced in the experimental group. TUNEL-positive cell number was not significantly different; however, the protein level of necroptosis markers, interleukin-6 (IL-6) and pMLKL were significantly increased in the substrate formation. Cell number and ALP expression level were improved in the group administered ruxolitinib, a JAK-STAT inhibitor. Additionally, ruxolitinib significantly suppressed IL-6 and pMLKL levels.<br>
Conclusion: Ruxolitinib interfered with the IFN-β-mediated necroptosis and osteogenic differentiation via the JAK-STAT pathway.
en-copyright=
kn-copyright=

en-aut-name=TanakaAtsuko
en-aut-sei=Tanaka
en-aut-mei=Atsuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HayanoSatoru
en-aut-sei=Hayano
en-aut-mei=Satoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NagataMasayo
en-aut-sei=Nagata
en-aut-mei=Masayo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KosamiTakahiro
en-aut-sei=Kosami
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=WangZiyi
en-aut-sei=Wang
en-aut-mei=Ziyi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KamiokaHiroshi
en-aut-sei=Kamioka
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Department of Orthodontics, Okayama University Hospital
kn-affil=

affil-num=2
en-affil=Department of Orthodontics, Okayama University Hospital
kn-affil=

affil-num=3
en-affil=Department of Orthodontics, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Orthodontics, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Orthodontics, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Type-I interferon
kn-keyword=Type-I interferon
en-keyword=Janus kinase/signal transducers and activators of transcription pathway
kn-keyword=Janus kinase/signal transducers and activators of transcription pathway
en-keyword=Osteoblast
kn-keyword=Osteoblast
en-keyword=Necroptosis
kn-keyword=Necroptosis
en-keyword=Singleton-Merten Syndrome
kn-keyword=Singleton-Merten Syndrome
END

start-ver=1.4
cd-journal=joma
no-vol=65
cd-vols=
no-issue=8
article-no=
start-page=6039
end-page=6055
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220411
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Identification of a Vitamin-D Receptor Antagonist, MeTC7, which Inhibits the Growth of Xenograft and Transgenic Tumors In Vivo
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Vitamin-D receptor (VDR) mRNA is overexpressed in neuroblastoma and carcinomas of lung, pancreas, and ovaries and predicts poor prognoses. VDR antagonists may be able to inhibit tumors that overexpress VDR. However, the current antagonists are arduous to synthesize and are only partial antagonists, limiting their use. Here, we show that the VDR antagonist MeTC7 (5), which can be synthesized from 7-dehydrocholesterol (6) in two steps, inhibits VDR selectively, suppresses the viability of cancer cell-lines, and reduces the growth of the spontaneous transgenic TH-MYCN neuroblastoma and xenografts in vivo. The VDR selectivity of 5 against RXRα and PPAR-γ was confirmed, and docking studies using VDR-LBD indicated that 5 induces major changes in the binding motifs, which potentially result in VDR antagonistic effects. These data highlight the therapeutic benefits of targeting VDR for the treatment of malignancies and demonstrate the creation of selective VDR antagonists that are easy to synthesize.
en-copyright=
kn-copyright=

en-aut-name=KhazanNegar
en-aut-sei=Khazan
en-aut-mei=Negar
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KimKyu Kwang
en-aut-sei=Kim
en-aut-mei=Kyu Kwang
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HansenJeanne N.
en-aut-sei=Hansen
en-aut-mei=Jeanne N.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SinghNiloy A.
en-aut-sei=Singh
en-aut-mei=Niloy A.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MooreTaylor
en-aut-sei=Moore
en-aut-mei=Taylor
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SnyderCameron W. A.
en-aut-sei=Snyder
en-aut-mei=Cameron W. A.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=PanditaRavina
en-aut-sei=Pandita
en-aut-mei=Ravina
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=StrawdermanMyla
en-aut-sei=Strawderman
en-aut-mei=Myla
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=FujiharaMichiko
en-aut-sei=Fujihara
en-aut-mei=Michiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=TakamuraYuta
en-aut-sei=Takamura
en-aut-mei=Yuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=JianYe
en-aut-sei=Jian
en-aut-mei=Ye
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=BattagliaNicholas
en-aut-sei=Battaglia
en-aut-mei=Nicholas
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=YanoNaohiro
en-aut-sei=Yano
en-aut-mei=Naohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=TeramotoYuki
en-aut-sei=Teramoto
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=ArnoldLeggy A.
en-aut-sei=Arnold
en-aut-mei=Leggy A.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=HopsonRussell
en-aut-sei=Hopson
en-aut-mei=Russell
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=KishorKeshav
en-aut-sei=Kishor
en-aut-mei=Keshav
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=NayakSneha
en-aut-sei=Nayak
en-aut-mei=Sneha
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=OjhaDebasmita
en-aut-sei=Ojha
en-aut-mei=Debasmita
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=SharonAshoke
en-aut-sei=Sharon
en-aut-mei=Ashoke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

en-aut-name=AshtonJohn M.
en-aut-sei=Ashton
en-aut-mei=John M.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=21
ORCID=

en-aut-name=WangJian
en-aut-sei=Wang
en-aut-mei=Jian
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=22
ORCID=

en-aut-name=MilanoMichael T.
en-aut-sei=Milano
en-aut-mei=Michael T.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=23
ORCID=

en-aut-name=MiyamotoHiroshi
en-aut-sei=Miyamoto
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=24
ORCID=

en-aut-name=LinehanDavid C.
en-aut-sei=Linehan
en-aut-mei=David C.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=25
ORCID=

en-aut-name=GerberScott A.
en-aut-sei=Gerber
en-aut-mei=Scott A.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=26
ORCID=

en-aut-name=KawarNada
en-aut-sei=Kawar
en-aut-mei=Nada
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=27
ORCID=

en-aut-name=SinghAjay P.
en-aut-sei=Singh
en-aut-mei=Ajay P.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=28
ORCID=

en-aut-name=TabdanovErdem D.
en-aut-sei=Tabdanov
en-aut-mei=Erdem D.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=29
ORCID=

en-aut-name=DokholyanNikolay V.
en-aut-sei=Dokholyan
en-aut-mei=Nikolay V.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=30
ORCID=

en-aut-name=KakutaHiroki
en-aut-sei=Kakuta
en-aut-mei=Hiroki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=31
ORCID=

en-aut-name=JurutkaPeter W.
en-aut-sei=Jurutka
en-aut-mei=Peter W.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=32
ORCID=

en-aut-name=SchorNina F.
en-aut-sei=Schor
en-aut-mei=Nina F.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=33
ORCID=

en-aut-name=Rowswell-TurnerRachael B.
en-aut-sei=Rowswell-Turner
en-aut-mei=Rachael B.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=34
ORCID=

en-aut-name=SinghRakesh K.
en-aut-sei=Singh
en-aut-mei=Rakesh K.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=35
ORCID=

en-aut-name=MooreRichard G.
en-aut-sei=Moore
en-aut-mei=Richard G.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=36
ORCID=

affil-num=1
en-affil=Wilmot Cancer Institute and Division of Gynecologic Oncology, Department of Obstetrics and Gynecology, University of Rochester Medical Center
kn-affil=

affil-num=2
en-affil=Wilmot Cancer Institute and Division of Gynecologic Oncology, Department of Obstetrics and Gynecology, University of Rochester Medical Center
kn-affil=

affil-num=3
en-affil=Department of Pediatrics, University of Rochester Medical Center
kn-affil=

affil-num=4
en-affil=Wilmot Cancer Institute and Division of Gynecologic Oncology, Department of Obstetrics and Gynecology, University of Rochester Medical Center
kn-affil=

affil-num=5
en-affil=Wilmot Cancer Institute and Division of Gynecologic Oncology, Department of Obstetrics and Gynecology, University of Rochester Medical Center
kn-affil=

affil-num=6
en-affil=Wilmot Cancer Institute and Division of Gynecologic Oncology, Department of Obstetrics and Gynecology, University of Rochester Medical Center
kn-affil=

affil-num=7
en-affil=Wilmot Cancer Institute and Division of Gynecologic Oncology, Department of Obstetrics and Gynecology, University of Rochester Medical Center
kn-affil=

affil-num=8
en-affil=Department of Biostatistics and Computational Biology, University of Rochester Medical Center
kn-affil=

affil-num=9
en-affil=Division of Pharmaceutical Sciences, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Division of Pharmaceutical Sciences, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Division of Surgery and of Microbiology and Immunology, University of Rochester Medical Center
kn-affil=

affil-num=12
en-affil=Division of Surgery and of Microbiology and Immunology, University of Rochester Medical Center
kn-affil=

affil-num=13
en-affil=Department of Surgery, Division of Surgical Research, Rhode Island Hospital, Alpert Medical School of Brown University
kn-affil=

affil-num=14
en-affil=Department of Pathology and Laboratory Medicine, University of Rochester Medical Center
kn-affil=

affil-num=15
en-affil=Department of Chemistry and Biochemistry, University of Wisconsin Milwaukee
kn-affil=

affil-num=16
en-affil=Department of Chemistry, Brown University
kn-affil=

affil-num=17
en-affil=Department of Chemistry, Birla Institute of Technology
kn-affil=

affil-num=18
en-affil=Department of Chemistry, Birla Institute of Technology
kn-affil=

affil-num=19
en-affil=Department of Chemistry, Birla Institute of Technology
kn-affil=

affil-num=20
en-affil=Department of Chemistry, Birla Institute of Technology
kn-affil=

affil-num=21
en-affil=Genomics Core Facility, Wilmot Cancer Center, University of Rochester Medical Center
kn-affil=

affil-num=22
en-affil=Department of Pharmacology and Department of Biochemistry and Molecular Biology, Penn State College of Medicine, Penn State University
kn-affil=

affil-num=23
en-affil=Department of Radiation Oncology, University of Rochester Medical Center
kn-affil=

affil-num=24
en-affil=Department of Pathology and Laboratory Medicine, University of Rochester Medical Center
kn-affil=

affil-num=25
en-affil=Division of Surgery and of Microbiology and Immunology, University of Rochester Medical Center
kn-affil=

affil-num=26
en-affil=Division of Surgery and of Microbiology and Immunology, University of Rochester Medical Center
kn-affil=

affil-num=27
en-affil=Center for Breast Health and Gynecologic Oncology, Mercy Medical Center
kn-affil=

affil-num=28
en-affil=Rutgers, The State University of New Jersey
kn-affil=

affil-num=29
en-affil=CytoMechanobiology Laboratory, Department of Pharmacology, Penn State College of Medicine, Pennsylvania State University
kn-affil=

affil-num=30
en-affil=Department of Pharmacology and Department of Biochemistry and Molecular Biology, Penn State College of Medicine, Penn State University
kn-affil=

affil-num=31
en-affil=Division of Pharmaceutical Sciences, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=32
en-affil=School of Mathematical and Natural Sciences, Arizona State University, Health Futures Center
kn-affil=

affil-num=33
en-affil=Departments of Pediatrics, Neurology, and Neuroscience, University of Rochester Medical Center
kn-affil=

affil-num=34
en-affil=Wilmot Cancer Institute and Division of Gynecologic Oncology, Department of Obstetrics and Gynecology, University of Rochester Medical Center
kn-affil=

affil-num=35
en-affil=Wilmot Cancer Institute and Division of Gynecologic Oncology, Department of Obstetrics and Gynecology, University of Rochester Medical Center
kn-affil=

affil-num=36
en-affil=Wilmot Cancer Institute and Division of Gynecologic Oncology, Department of Obstetrics and Gynecology, University of Rochester Medical Center
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=71
cd-vols=
no-issue=2
article-no=
start-page=154
end-page=164
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230201
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Identification of a Functionally Efficient and Thermally Stable Outward Sodium-Pumping Rhodopsin (BeNaR) from a Thermophilic Bacterium
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Rhodopsins are transmembrane proteins with retinal chromophores that are involved in photo-energy conversion and photo-signal transduction in diverse organisms. In this study, we newly identified and characterized a rhodopsin from a thermophilic bacterium, Bellilinea sp. Recombinant Escherichia coli cells expressing the rhodopsin showed light-induced alkalization of the medium only in the presence of sodium ions (Na+), and the alkalization signal was enhanced by addition of a protonophore, indicating an outward Na+ pump function across the cellular membrane. Thus, we named the protein Bellilinea Na+-pumping rhodopsin, BeNaR. Of note, its Na+-pumping activity is significantly greater than that of the known Na+-pumping rhodopsin, KR2. We further characterized its photochemical properties as follows: (i) Visible spectroscopy and HPLC revealed that BeNaR has an absorption maximum at 524 nm with predominantly (>96%) the all-trans retinal conformer. (ii) Time-dependent thermal denaturation experiments revealed that BeNaR showed high thermal stability. (iii) The time-resolved flash-photolysis in the nanosecond to millisecond time domains revealed the presence of four kinetically distinctive photointermediates, K, L, M and O. (iv) Mutational analysis revealed that Asp101, which acts as a counterion, and Asp230 around the retinal were essential for the Na+-pumping activity. From the results, we propose a model for the outward Na+-pumping mechanism of BeNaR. The efficient Na+-pumping activity of BeNaR and its high stability make it a useful model both for ion transporters and optogenetics tools.
en-copyright=
kn-copyright=

en-aut-name=KuriharaMarie
en-aut-sei=Kurihara
en-aut-mei=Marie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ThielVera
en-aut-sei=Thiel
en-aut-mei=Vera
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TakahashiHirona
en-aut-sei=Takahashi
en-aut-mei=Hirona
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KojimaKeiichi
en-aut-sei=Kojima
en-aut-mei=Keiichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=WardDavid M.
en-aut-sei=Ward
en-aut-mei=David M.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=BryantDonald A.
en-aut-sei=Bryant
en-aut-mei=Donald A.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SakaiMakoto
en-aut-sei=Sakai
en-aut-mei=Makoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YoshizawaSusumu
en-aut-sei=Yoshizawa
en-aut-mei=Susumu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=SudoYuki
en-aut-sei=Sudo
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Biological Sciences, Tokyo Metropolitan University
kn-affil=

affil-num=3
en-affil=Department of Chemistry, Graduate School of Science, Okayama University of Science
kn-affil=

affil-num=4
en-affil=Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Land Resources and Environmental Sciences, Montana State University
kn-affil=

affil-num=6
en-affil=Department of Biochemistry and Molecular Biology, The Pennsylvania State University
kn-affil=

affil-num=7
en-affil=Department of Chemistry, Graduate School of Science, Okayama University of Science
kn-affil=

affil-num=8
en-affil=Atmosphere and Ocean Research Institute, The University of Tokyo
kn-affil=

affil-num=9
en-affil=Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=rhodopsin
kn-keyword=rhodopsin
en-keyword=ion transport
kn-keyword=ion transport
en-keyword=retinal
kn-keyword=retinal
en-keyword=isomerization
kn-keyword=isomerization
en-keyword=optogenetics
kn-keyword=optogenetics
END

start-ver=1.4
cd-journal=joma
no-vol=154
cd-vols=
no-issue=1
article-no=
start-page=169
end-page=179
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230823
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Low frequency of intracranial progression in advanced NSCLC patients treated with cancer immunotherapies
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Intracranial metastases are common in nonsmall-cell lung cancer (NSCLC) patients, whose prognosis is very poor. In addition, intracranial progression is common during systemic treatments due to the inability to penetrate central nervous system (CNS) barriers, whereas the intracranial effects of cancer immunotherapies remain unclear. We analyzed clinical data to evaluate the frequency of intracranial progression in advanced NSCLC patients treated with PD-1 blockade therapies compared with those treated without PD-1 blockade therapies, and found that the frequency of intracranial progression in advanced NSCLC patients treated with PD-1 blockade therapies was significantly lower than that in patients treated with cytotoxic chemotherapies. In murine models, intracranial rechallenged tumors after initial rejection by PD-1 blockade were suppressed. Accordingly, long-lived memory precursor effector T cells and antigen-specific T cells were increased by PD-1 blockade in intracranial lesions. However, intracranial rechallenged different tumors are not suppressed. Our results indicate that cancer immunotherapies can prevent intracranial progression, maintaining long-term effects intracranially as well as systemically. If intracranial recurrence occurs during the treatment with PD-1 blockade therapies, aggressive local therapies could be worthwhile.
en-copyright=
kn-copyright=

en-aut-name=KemmotsuNaoya
en-aut-sei=Kemmotsu
en-aut-mei=Naoya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NinomiyaKiichiro
en-aut-sei=Ninomiya
en-aut-mei=Kiichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KunimasaKei
en-aut-sei=Kunimasa
en-aut-mei=Kei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=IshinoTakamasa
en-aut-sei=Ishino
en-aut-mei=Takamasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NagasakiJoji
en-aut-sei=Nagasaki
en-aut-mei=Joji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OtaniYoshihiro
en-aut-sei=Otani
en-aut-mei=Yoshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MichiueHiroyuki
en-aut-sei=Michiue
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=IchiharaEiki
en-aut-sei=Ichihara
en-aut-mei=Eiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=OhashiKadoaki
en-aut-sei=Ohashi
en-aut-mei=Kadoaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=InoueTakako
en-aut-sei=Inoue
en-aut-mei=Takako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=TamiyaMotohiro
en-aut-sei=Tamiya
en-aut-mei=Motohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=SakaiKazuko
en-aut-sei=Sakai
en-aut-mei=Kazuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=UedaYouki
en-aut-sei=Ueda
en-aut-mei=Youki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=DansakoHiromichi
en-aut-sei=Dansako
en-aut-mei=Hiromichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=NishioKazuto
en-aut-sei=Nishio
en-aut-mei=Kazuto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=KiuraKatsuyuki
en-aut-sei=Kiura
en-aut-mei=Katsuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=DateIsao
en-aut-sei=Date
en-aut-mei=Isao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=TogashiYosuke
en-aut-sei=Togashi
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

affil-num=1
en-affil=Department of Tumor Microenvironment, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Respiratory Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Thoracic Oncology, Osaka International Cancer Institute
kn-affil=

affil-num=4
en-affil=Department of Tumor Microenvironment, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Tumor Microenvironment, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Neurological Surgery, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Neurological Surgery, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Respiratory Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Respiratory Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=10
en-affil=Department of Thoracic Oncology, Osaka International Cancer Institute
kn-affil=

affil-num=11
en-affil=Department of Thoracic Oncology, Osaka International Cancer Institute
kn-affil=

affil-num=12
en-affil=Department of Genome Biology, Kindai University Faculty of Medicine
kn-affil=

affil-num=13
en-affil=Department of Tumor Microenvironment, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=14
en-affil=Department of Tumor Microenvironment, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=15
en-affil=Department of Genome Biology, Kindai University Faculty of Medicine
kn-affil=

affil-num=16
en-affil=Department of Respiratory Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=17
en-affil=Department of Neurological Surgery, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=18
en-affil=Department of Tumor Microenvironment, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=cancer immunotherapy
kn-keyword=cancer immunotherapy
en-keyword=intracranial metastasis
kn-keyword=intracranial metastasis
en-keyword=intracranial progression
kn-keyword=intracranial progression
en-keyword=memory precursor effector T cell
kn-keyword=memory precursor effector T cell
en-keyword=nonsmall-cell lung cancer
kn-keyword=nonsmall-cell lung cancer
END

start-ver=1.4
cd-journal=joma
no-vol=2
cd-vols=
no-issue=7
article-no=
start-page=739
end-page=753
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220728
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Mixed Response to Cancer Immunotherapy is Driven by Intratumor Heterogeneity and Differential Interlesion Immune Infiltration
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Some patients experience mixed response to immunotherapy, whose biological mechanisms and clinical impact have been obscure. We obtained two tumor samples from lymph node (LN) metastatic lesions in a same patient. Whole exome sequencing for the both tumors and single-cell sequencing for the both tumor-infiltrating lymphocytes (TIL) demonstrated a significant difference in tumor clonality and TILs' characteristics, especially exhausted T-cell clonotypes, although a close relationship between the tumor cell and T-cell clones were observed as a response of an overlapped exhausted T-cell clone to an overlapped neoantigen. To mimic the clinical setting, we generated a mouse model of several clones from a same tumor cell line. Similarly, differential tumor clones harbored distinct TILs, and one responded to programmed cell death protein 1 (PD-1) blockade but the other did not in this model. We further conducted cohort study (n = 503) treated with PD-1 blockade monotherapies to investigate the outcome of mixed response. Patients with mixed responses to PD-1 blockade had a poor prognosis in our cohort. Particularly, there were significant differences in both tumor and T-cell clones between the primary and LN lesions in a patient who experienced tumor response to anti-PD-1 mAb followed by disease progression in only LN metastasis. Our results underscore that intertumoral heterogeneity alters characteristics of TILs even in the same patient, leading to mixed response to immunotherapy and significant difference in the outcome.<br>
Significance: Several patients experience mixed responses to immunotherapies, but the biological mechanisms and clinical significance remain unclear. Our results from clinical and mouse studies underscore that intertumoral heterogeneity alters characteristics of TILs even in the same patient, leading to mixed response to immunotherapy and significant difference in the outcome.
en-copyright=
kn-copyright=

en-aut-name=MorinagaTakao
en-aut-sei=Morinaga
en-aut-mei=Takao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=InozumeTakashi
en-aut-sei=Inozume
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KawazuMasahito
en-aut-sei=Kawazu
en-aut-mei=Masahito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=UedaYouki
en-aut-sei=Ueda
en-aut-mei=Youki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SaxNicolas
en-aut-sei=Sax
en-aut-mei=Nicolas
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YamashitaKazuo
en-aut-sei=Yamashita
en-aut-mei=Kazuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KawashimaShusuke
en-aut-sei=Kawashima
en-aut-mei=Shusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NagasakiJoji
en-aut-sei=Nagasaki
en-aut-mei=Joji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=UenoToshihide
en-aut-sei=Ueno
en-aut-mei=Toshihide
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=LinJason
en-aut-sei=Lin
en-aut-mei=Jason
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=OharaYuuki
en-aut-sei=Ohara
en-aut-mei=Yuuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=KuwataTakeshi
en-aut-sei=Kuwata
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=YukamiHiroki
en-aut-sei=Yukami
en-aut-mei=Hiroki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=KawazoeAkihito
en-aut-sei=Kawazoe
en-aut-mei=Akihito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=ShitaraKohei
en-aut-sei=Shitara
en-aut-mei=Kohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=Honobe-TabuchiAkiko
en-aut-sei=Honobe-Tabuchi
en-aut-mei=Akiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=OhnumaTakehiro
en-aut-sei=Ohnuma
en-aut-mei=Takehiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=KawamuraTatsuyoshi
en-aut-sei=Kawamura
en-aut-mei=Tatsuyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=UmedaYoshiyasu
en-aut-sei=Umeda
en-aut-mei=Yoshiyasu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=KawaharaYu
en-aut-sei=Kawahara
en-aut-mei=Yu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

en-aut-name=NakamuraYasuhiro
en-aut-sei=Nakamura
en-aut-mei=Yasuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=21
ORCID=

en-aut-name=KiniwaYukiko
en-aut-sei=Kiniwa
en-aut-mei=Yukiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=22
ORCID=

en-aut-name=MoritaAyako
en-aut-sei=Morita
en-aut-mei=Ayako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=23
ORCID=

en-aut-name=IchiharaEiki
en-aut-sei=Ichihara
en-aut-mei=Eiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=24
ORCID=

en-aut-name=KiuraKatsuyuki
en-aut-sei=Kiura
en-aut-mei=Katsuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=25
ORCID=

en-aut-name=EnokidaTomohiro
en-aut-sei=Enokida
en-aut-mei=Tomohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=26
ORCID=

en-aut-name=TaharaMakoto
en-aut-sei=Tahara
en-aut-mei=Makoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=27
ORCID=

en-aut-name=HasegawaYoshinori
en-aut-sei=Hasegawa
en-aut-mei=Yoshinori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=28
ORCID=

en-aut-name=ManoHiroyuki
en-aut-sei=Mano
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=29
ORCID=

en-aut-name=SuzukiYutaka
en-aut-sei=Suzuki
en-aut-mei=Yutaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=30
ORCID=

en-aut-name=NishikawaHiroyoshi
en-aut-sei=Nishikawa
en-aut-mei=Hiroyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=31
ORCID=

en-aut-name=TogashiYosuke
en-aut-sei=Togashi
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=32
ORCID=

affil-num=1
en-affil=Chiba Cancer Center, Research Institute
kn-affil=

affil-num=2
en-affil=Chiba Cancer Center, Research Institute
kn-affil=

affil-num=3
en-affil=Chiba Cancer Center, Research Institute
kn-affil=

affil-num=4
en-affil=Department of Tumor Microenvironment, Okayama University Graduate School of Medicine Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=KOTAI Biotechnologies Inc
kn-affil=

affil-num=6
en-affil=KOTAI Biotechnologies Inc
kn-affil=

affil-num=7
en-affil=Chiba Cancer Center, Research Institute
kn-affil=

affil-num=8
en-affil=Department of Tumor Microenvironment, Okayama University Graduate School of Medicine Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Division of Cellular Signaling, National Cancer Center Research Institute
kn-affil=

affil-num=10
en-affil=Chiba Cancer Center, Research Institute
kn-affil=

affil-num=11
en-affil=Department of Pathology, National Cancer Center Hospital East
kn-affil=

affil-num=12
en-affil=Department of Genetic Medicineand Services, National Cancer Center Hospital East
kn-affil=

affil-num=13
en-affil=Department of Gastroenterology and Gastrointestinal Oncology, National Cancer Center Hospital East
kn-affil=

affil-num=14
en-affil=Department of Gastroenterology and Gastrointestinal Oncology, National Cancer Center Hospital East
kn-affil=

affil-num=15
en-affil=Department of Gastroenterology and Gastrointestinal Oncology, National Cancer Center Hospital East
kn-affil=

affil-num=16
en-affil=Department of Dermatology, University of Yamanashi
kn-affil=

affil-num=17
en-affil=Department of Dermatology, University of Yamanashi
kn-affil=

affil-num=18
en-affil=Department of Dermatology, University of Yamanashi
kn-affil=

affil-num=19
en-affil=Department of Skin Oncology/Dermatology, Saitama Medical University International Medical Center
kn-affil=

affil-num=20
en-affil=Department of Skin Oncology/Dermatology, Saitama Medical University International Medical Center
kn-affil=

affil-num=21
en-affil=Department of Skin Oncology/Dermatology, Saitama Medical University International Medical Center
kn-affil=

affil-num=22
en-affil=Department of Dermatology, Shinshu University School of Medicine 
kn-affil=

affil-num=23
en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital
kn-affil=

affil-num=24
en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital
kn-affil=

affil-num=25
en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital
kn-affil=

affil-num=26
en-affil=Department of Head and Neck Medical Oncology, National Cancer Center Hospital East
kn-affil=

affil-num=27
en-affil=Department of Head and Neck Medical Oncology, National Cancer Center Hospital East
kn-affil=

affil-num=28
en-affil=Department of Applied Genomics, Kazusa DNA Research Institute
kn-affil=

affil-num=29
en-affil=Division of Cellular Signaling, National Cancer Center Research Institute
kn-affil=

affil-num=30
en-affil=Department of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo
kn-affil=

affil-num=31
en-affil=Division of Cancer Immunology, Research Institute/Exploratory Oncology Research and Clinical Trial Center (EPOC), National Cancer Center
kn-affil=

affil-num=32
en-affil=Department of Tumor Microenvironment, Okayama University Graduate School of Medicine Dentistry and Pharmaceutical Sciences
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=81
cd-vols=
no-issue=1
article-no=
start-page=58
end-page=67
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220309
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Improvement of anterior disc displacement on the mandibular deviated side after intraoral vertical ramus osteotomy in a patient with facial asymmetry: a case report
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Purpose: We present the orthognathic treatment of an adult skeletal Class III patient with facial asymmetry, mandibular rightward deviation, and anterior disc displacement without reduction (ADDwoR) at the right temporomandibular joint (TMJ) by intraoral vertical ramus osteotomy (IVRO).<br>
Materials and methods: The patient was a 23-year-old man with complaints of mandibular deviation and crowded lower anterior teeth, resulting in facial asymmetry. The maxillary position was normal with protrusion and rightward deviation of the mandible. There was no cant of the maxilla. He experienced pain in the right TMJ during mastication, and Magnetic resonance imaging (MRI) revealed an ADDwoR on the right side. The patient was diagnosed with Class III malocclusion, skeletal Class III prognathism with mandibular deviation, and ADDwoR on the right side. Orthognathic surgery was proposed for jaw deformity, and IVRO was performed to correct mandibular deviation.<br>
Results: One year and 2 months after treatment onset, IVRO was performed with differential setback: 2 mm on the right and 8 mm on the left side of the mandible. The midline of the lower dentition was rotated by 6 mm to coincide with the facial midline. Symptoms of temporomandibular disorders were not observed post-operatively. Active-treatment period was for 31 months. MRI findings showed improvement in anterior disc displacement on the right side during the post-retention.<br>
Conclusion: In the case of facial asymmetry with anterior disc displacement on the mandibular deviated side, IVRO was suggested to have a potential effect on the positional relationship between the mandibular head and temporomandibular disc.
en-copyright=
kn-copyright=

en-aut-name=UedaHirotaka
en-aut-sei=Ueda
en-aut-mei=Hirotaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OkaNaoki
en-aut-sei=Oka
en-aut-mei=Naoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ShimoTsuyoshi
en-aut-sei=Shimo
en-aut-mei=Tsuyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SasakiAkira
en-aut-sei=Sasaki
en-aut-mei=Akira
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YamashiroTakashi
en-aut-sei=Yamashiro
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KamiokaHiroshi
en-aut-sei=Kamioka
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Department of Orthodontics, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Orthodontics, Okayama University Hospital
kn-affil=

affil-num=3
en-affil=Division of Reconstructive Surgery for Oral and Maxillofacial Region, Department of Human Biology and Pathophysiology, School of Dentistry, Health Sciences University of Hokkaido
kn-affil=

affil-num=4
en-affil=Department of Oral and Maxillofacial Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Orthodontics and Dentofacial Orthopedics, Osaka University Graduate School of Dentistry
kn-affil=

affil-num=6
en-affil=Department of Orthodontics, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Facial asymmetry
kn-keyword=Facial asymmetry
en-keyword=mandibular deviation
kn-keyword=mandibular deviation
en-keyword=anterior disc displacement
kn-keyword=anterior disc displacement
en-keyword=temporomandibular disorders
kn-keyword=temporomandibular disorders
en-keyword=intraoral vertical ramus osteotomy
kn-keyword=intraoral vertical ramus osteotomy
END

start-ver=1.4
cd-journal=joma
no-vol=26
cd-vols=
no-issue=3
article-no=
start-page=394
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230727
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=An imaging‑based diagnostic approach to vascular anomalies of the oral and maxillofacial region
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The accurate diagnosis of vascular anomalies (VAs) is considered a challenging endeavor. Misdiagnosis of VAs can lead clinicians in the wrong direction, such as the performance of an unnecessary biopsy or inappropriate surgical procedures, which can potentially lead to unforeseen consequences and increase the risk of patient injury. The purpose of the present study was to develop an approach for the diagnosis of VAs of the oral and maxillofacial region based on computed tomography (CT), magnetic resonance imaging (MRI) and dynamic contrast‑enhanced MRI (DCE‑MRI). In the present study, the CT and MR images of 87 VAs were examined, and the following imaging features were evaluated: Detectability of the lesion, the periphery of the lesion, the inner nature of the lesion, the density of the lesion on CT, the signal intensity of the lesion on MRI, the detectability of phleboliths and the shape of the lesion. A total of 29 lesions were further evaluated using the contrast index (CI) curves created from the DCE‑MRI images. A diagnostic diagram, which is based on the imaging features of VAs and CI curve patterns, was subsequently extrapolated. The results obtained demonstrated that the VAs were detected more readily by MRI compared with CT, whereas the detectability of phleboliths was superior when using CT compared with MRI. VAs showed a propensity for homogeneous isodensity on CT, whereas, by contrast, they exhibited a propensity for heterogeneous hyperdensity on CE‑CT. VAs also showed a propensity for homogeneous intermediate signal intensity when performing T1‑weighted imaging (T1WI), heterogeneous high signal intensity when performing short tau inversion recovery MRI, and heterogeneous high signal intensity when performing fat‑saturated CE‑T1WI. The CI curves of VAs were found to exhibit a specific pattern: Of the 29 CI curves, 23 (79.3%) showed early weak enhancement, followed by a plateau leading up to 400‑600 sec. An imaging‑based diagnostic diagram was ultimately formulated. This diagram can act as an aid for radiologists when they are expecting to find a VA, and hopefully serve the purpose of simplifying the diagnostic process. Taken together, the findings of the present study indicated that DCE‑MRI may be considered a useful tool for the diagnosis of VAs.
en-copyright=
kn-copyright=

en-aut-name=Al‑HammadWlla
en-aut-sei=Al‑Hammad
en-aut-mei=Wlla
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=FujikuraMamiko
en-aut-sei=Fujikura
en-aut-mei=Mamiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HisatomiMiki
en-aut-sei=Hisatomi
en-aut-mei=Miki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OkadaShunsuke
en-aut-sei=Okada
en-aut-mei=Shunsuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MunhozLuciana
en-aut-sei=Munhoz
en-aut-mei=Luciana
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KawazuToshiyuki
en-aut-sei=Kawazu
en-aut-mei=Toshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TakeshitaYohei
en-aut-sei=Takeshita
en-aut-mei=Yohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=FujitaMariko
en-aut-sei=Fujita
en-aut-mei=Mariko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=YanagiYoshinobu
en-aut-sei=Yanagi
en-aut-mei=Yoshinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=AsaumiJun-Ichi
en-aut-sei=Asaumi
en-aut-mei=Jun-Ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of Oral and Maxillofacial Radiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Oral Diagnosis and Dentomaxillofacial Radiology, Okayama University Hospital
kn-affil=

affil-num=3
en-affil=Department of Oral Diagnosis and Dentomaxillofacial Radiology, Okayama University Hospital
kn-affil=

affil-num=4
en-affil=Department of Oral Diagnosis and Dentomaxillofacial Radiology, Okayama University Hospital
kn-affil=

affil-num=5
en-affil=Department of Stomatology, School of Dentistry, University of São Paulo
kn-affil=

affil-num=6
en-affil=Department of Oral and Maxillofacial Radiology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Oral and Maxillofacial Radiology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Oral and Maxillofacial Radiology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Dental Informatics, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=10
en-affil=Department of Oral Diagnosis and Dentomaxillofacial Radiology, Okayama University Hospital
kn-affil=
en-keyword=vascular anomalies
kn-keyword=vascular anomalies
en-keyword=magnetic resonance imaging
kn-keyword=magnetic resonance imaging
en-keyword=computed tomography
kn-keyword=computed tomography
en-keyword=dynamic contrast-enhanced magnetic resonance imaging
kn-keyword=dynamic contrast-enhanced magnetic resonance imaging
en-keyword=contrast index curve
kn-keyword=contrast index curve
END

start-ver=1.4
cd-journal=joma
no-vol=77
cd-vols=
no-issue=4
article-no=
start-page=341
end-page=345
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=202308
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Biological Roles of Hepatitis B Viral X Protein in the Viral Replication and Hepatocarcinogenesis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Hepatitis B virus is a pathogenic virus that infects 300 million people worldwide and causes chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma. Hepatitis B virus encodes four proteins. Among them, the HBx protein plays a central role in the HBV pathogenesis. Because the HBx protein is considered to play a central role in the induction of viral replication and hepatocarcinogenesis, the regulation of its function could be a key factor in the development of new interventions against hepatitis B. In this review, HBx protein-related viral replication and hepatocarcinogenesis mechanisms are described, with a focus on the recently reported viral replication mechanisms related to degradation of the Smc5/6 protein complex. We also discuss our recent discovery of a compound that inhibits HBx protein-induced degradation of the Smc5/6 protein complex, and that exerts inhibitory effects on both viral replication and hepatocarcinogenesis. Finally, prospects for future research on the HBx protein are described.
en-copyright=
kn-copyright=

en-aut-name=OtsukaMotoyuki
en-aut-sei=Otsuka
en-aut-mei=Motoyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Department of Gastroenterology and Hepatology, Academic Field of Medicine, Density and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=HBx
kn-keyword=HBx
en-keyword=Smc5/6
kn-keyword=Smc5/6
en-keyword=DDB1
kn-keyword=DDB1
en-keyword=nitazoxianide
kn-keyword=nitazoxianide
en-keyword=DNA repair
kn-keyword=DNA repair
END

start-ver=1.4
cd-journal=joma
no-vol=14
cd-vols=
no-issue=1
article-no=
start-page=621
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230204
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Pivotal role for S-nitrosylation of DNA methyltransferase 3B in epigenetic regulation of tumorigenesis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=DNA methyltransferases (DNMTs) catalyze methylation at the C5 position of cytosine with S-adenosyl-l-methionine. Methylation regulates gene expression, serving a variety of physiological and pathophysiological roles. The chemical mechanisms regulating DNMT enzymatic activity, however, are not fully elucidated. Here, we show that protein S-nitrosylation of a cysteine residue in DNMT3B attenuates DNMT3B enzymatic activity and consequent aberrant upregulation of gene expression. These genes include Cyclin D2 (Ccnd2), which is required for neoplastic cell proliferation in some tumor types. In cell-based and in vivo cancer models, only DNMT3B enzymatic activity, and not DNMT1 or DNMT3A, affects Ccnd2 expression. Using structure-based virtual screening, we discovered chemical compounds that specifically inhibit S-nitrosylation without directly affecting DNMT3B enzymatic activity. The lead compound, designated DBIC, inhibits S-nitrosylation of DNMT3B at low concentrations (IC50 <= 100nM). Treatment with DBIC prevents nitric oxide (NO)-induced conversion of human colonic adenoma to adenocarcinoma in vitro. Additionally, in vivo treatment with DBIC strongly attenuates tumor development in a mouse model of carcinogenesis triggered by inflammation-induced generation of NO. Our results demonstrate that de novo DNA methylation mediated by DNMT3B is regulated by NO, and DBIC protects against tumor formation by preventing aberrant S-nitrosylation of DNMT3B.
en-copyright=
kn-copyright=

en-aut-name=OkudaKosaku
en-aut-sei=Okuda
en-aut-mei=Kosaku
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakaharaKengo
en-aut-sei=Nakahara
en-aut-mei=Kengo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ItoAkihiro
en-aut-sei=Ito
en-aut-mei=Akihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=IijimaYuta
en-aut-sei=Iijima
en-aut-mei=Yuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NomuraRyosuke
en-aut-sei=Nomura
en-aut-mei=Ryosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KumarAshutosh
en-aut-sei=Kumar
en-aut-mei=Ashutosh
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=FujikawaKana
en-aut-sei=Fujikawa
en-aut-mei=Kana
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=AdachiKazuya
en-aut-sei=Adachi
en-aut-mei=Kazuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=ShimadaYuki
en-aut-sei=Shimada
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=FujioSatoshi
en-aut-sei=Fujio
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=YamamotoReina
en-aut-sei=Yamamoto
en-aut-mei=Reina
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=TakasugiNobumasa
en-aut-sei=Takasugi
en-aut-mei=Nobumasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=OnumaKunishige
en-aut-sei=Onuma
en-aut-mei=Kunishige
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=OsakiMitsuhiko
en-aut-sei=Osaki
en-aut-mei=Mitsuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=OkadaFutoshi
en-aut-sei=Okada
en-aut-mei=Futoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=UkegawaTaichi
en-aut-sei=Ukegawa
en-aut-mei=Taichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=TakeuchiYasuo
en-aut-sei=Takeuchi
en-aut-mei=Yasuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=YasuiNorihisa
en-aut-sei=Yasui
en-aut-mei=Norihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=YamashitaAtsuko
en-aut-sei=Yamashita
en-aut-mei=Atsuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=MarusawaHiroyuki
en-aut-sei=Marusawa
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

en-aut-name=MatsushitaYosuke
en-aut-sei=Matsushita
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=21
ORCID=

en-aut-name=KatagiriToyomasa
en-aut-sei=Katagiri
en-aut-mei=Toyomasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=22
ORCID=

en-aut-name=ShibataTakahiro
en-aut-sei=Shibata
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=23
ORCID=

en-aut-name=UchidaKoji
en-aut-sei=Uchida
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=24
ORCID=

en-aut-name=NiuSheng-Yong
en-aut-sei=Niu
en-aut-mei=Sheng-Yong
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=25
ORCID=

en-aut-name=LangNhi B.
en-aut-sei=Lang
en-aut-mei=Nhi B.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=26
ORCID=

en-aut-name=NakamuraTomohiro
en-aut-sei=Nakamura
en-aut-mei=Tomohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=27
ORCID=

en-aut-name=ZhangKam Y. J.
en-aut-sei=Zhang
en-aut-mei=Kam Y. J.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=28
ORCID=

en-aut-name=LiptonStuart A.
en-aut-sei=Lipton
en-aut-mei=Stuart A.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=29
ORCID=

en-aut-name=UeharaTakashi
en-aut-sei=Uehara
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=30
ORCID=

affil-num=1
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Chemical Genomics Research Group, RIKEN Center for Sustainable Resource Science
kn-affil=

affil-num=4
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Laboratory for Structural Bioinformatics, Center for Biosystems Dynamics Research, RIKEN
kn-affil=

affil-num=7
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=10
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=11
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=12
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=13
en-affil=Division of Experimental Pathology, Faculty of Medicine, Tottori University
kn-affil=

affil-num=14
en-affil=Division of Experimental Pathology, Faculty of Medicine, Tottori University
kn-affil=

affil-num=15
en-affil=Division of Experimental Pathology, Faculty of Medicine, Tottori University
kn-affil=

affil-num=16
en-affil=Department of Synthetic and Medicinal Chemistry, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=17
en-affil=Department of Synthetic and Medicinal Chemistry, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=18
en-affil=Laboratory of Structural Biology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=19
en-affil=Laboratory of Structural Biology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=20
en-affil=Department of Gastroenterology and Hepatology, Graduate School of Medicine, Kyoto University
kn-affil=

affil-num=21
en-affil=Division of Genome Medicine, Institute of Advanced Medical Sciences, Tokushima University
kn-affil=

affil-num=22
en-affil=Division of Genome Medicine, Institute of Advanced Medical Sciences, Tokushima University
kn-affil=

affil-num=23
en-affil=Graduate School of Bioagricultural Sciences, Nagoya University
kn-affil=

affil-num=24
en-affil=Laboratory of Food Chemistry, Department of Applied Biological Chemistry, Graduate School of Agricultural and Life Sciences, The University of Tokyo
kn-affil=

affil-num=25
en-affil=Broad Institute of MIT and Harvard
kn-affil=

affil-num=26
en-affil=Neurodegeneration New Medicines Center, and Departments of Molecular Medicine and Neuroscience, The Scripps Research Institute
kn-affil=

affil-num=27
en-affil=Neurodegeneration New Medicines Center, and Departments of Molecular Medicine and Neuroscience, The Scripps Research Institute
kn-affil=

affil-num=28
en-affil=Laboratory for Structural Bioinformatics, Center for Biosystems Dynamics Research, RIKEN
kn-affil=

affil-num=29
en-affil=Neurodegeneration New Medicines Center, and Departments of Molecular Medicine and Neuroscience, The Scripps Research Institute
kn-affil=

affil-num=30
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=45
cd-vols=
no-issue=7
article-no=
start-page=5263
end-page=5275
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230621
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Update in Molecular Aspects and Diagnosis of Autoimmune Gastritis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Recent studies have advanced our understanding of the pathophysiology of autoimmune gastritis, particularly its molecular aspects. The most noteworthy recent advancement lies in the identification of several candidate genes implicated in the pathogenesis of pernicious anemia through genome-wide association studies. These genes include PTPN22, PNPT1, HLA-DQB1, and IL2RA. Recent studies have also directed attention towards other genes such as ATP4A, ATP4B, AIRE, SLC26A7, SLC26A9, and BACH2 polymorphism. In-depth investigations have been conducted on lymphocytes and cytokines, including T helper 17 cells, interleukin (IL)-17A, IL-17E, IL-17F, IL-21, IL-19, tumor necrosis factor-α, IL-15, transforming growth factor-β1, IL-13, and diminished levels of IL-27. Animal studies have explored the involvement of roseolovirus and H. pylori in relation to the onset of the disease and the process of carcinogenesis, respectively. Recent studies have comprehensively examined the involvement of autoantibodies, serum pepsinogen, and esophagogastroduodenoscopy in the diagnosis of autoimmune gastritis. The current focus lies on individuals demonstrating atypical presentations of the disease, including those diagnosed in childhood, those yielding negative results for autoantibodies, and those lacking the typical endoscopic characteristics of mucosal atrophy. Here, we discuss the recent developments in this field, focusing on genetic predisposition, epigenetic modifications, lymphocytes, cytokines, oxidative stress, infectious agents, proteins, microRNAs, autoantibodies, serum pepsinogen, gastrin, esophagogastroduodenoscopy and microscopic findings, and the risk of gastric neoplasm.
en-copyright=
kn-copyright=

en-aut-name=IwamuroMasaya
en-aut-sei=Iwamuro
en-aut-mei=Masaya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TanakaTakehiro
en-aut-sei=Tanaka
en-aut-mei=Takehiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OtsukaMotoyuki
en-aut-sei=Otsuka
en-aut-mei=Motoyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Pathology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Gastroenterology and Hepatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=autoimmune gastritis
kn-keyword=autoimmune gastritis
en-keyword=esophagogastroduodenoscopy
kn-keyword=esophagogastroduodenoscopy
en-keyword=genetic predisposition
kn-keyword=genetic predisposition
en-keyword=lymphocyte
kn-keyword=lymphocyte
en-keyword=oxidative stress
kn-keyword=oxidative stress
END

start-ver=1.4
cd-journal=joma
no-vol=40
cd-vols=
no-issue=7
article-no=
start-page=msad151
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230707
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Ongoing Rapid Evolution of a Post-Y Region Revealed by Chromosome-Scale Genome Assembly of a Hexaploid Monoecious Persimmon (Diospyros kaki)
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Plants have evolved sex chromosomes independently in many lineages, and loss of separate sexes can also occur. In this study, we assembled a monoecious recently hexaploidized persimmon (Diospyros kaki), in which the Y chromosome has lost the maleness-determining function. Comparative genomic analysis of D. kaki and its dioecious relatives uncovered the evolutionary process by which the nonfunctional Y chromosome (or Y-monoecy) was derived, which involved silencing of the sex-determining gene, OGI, approximately 2 million years ago. Analyses of the entire X and Y-monoecy chromosomes suggested that D. kaki's nonfunctional male-specific region of the Y chromosome (MSY), which we call a post-MSY, has conserved some characteristics of the original functional MSY. Specifically, comparing the functional MSY in Diospyros lotus and the nonfunctional "post-MSY" in D. kaki indicated that both have been rapidly rearranged, mainly via ongoing transposable element bursts, resembling structural changes often detected in Y-linked regions, some of which can enlarge the nonrecombining regions. The recent evolution of the post-MSY (and possibly also MSYs in dioecious Diospyros species) therefore probably reflects these regions' ancestral location in a pericentromeric region, rather than the presence of male-determining genes and/or genes controlling sexually dimorphic traits.
en-copyright=
kn-copyright=

en-aut-name=HoriuchiAyano
en-aut-sei=Horiuchi
en-aut-mei=Ayano
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MasudaKanae
en-aut-sei=Masuda
en-aut-mei=Kanae
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ShirasawaKenta
en-aut-sei=Shirasawa
en-aut-mei=Kenta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OnoueNoriyuki
en-aut-sei=Onoue
en-aut-mei=Noriyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=FujitaNaoko
en-aut-sei=Fujita
en-aut-mei=Naoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=UshijimaKoichiro
en-aut-sei=Ushijima
en-aut-mei=Koichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=AkagiTakashi
en-aut-sei=Akagi
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Frontier Research and Development, Kazusa DNA Research Institute
kn-affil=

affil-num=4
en-affil=Institute of Fruit Tree and Tea Science, NARO
kn-affil=

affil-num=5
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=6
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=7
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
en-keyword=sex chromosome
kn-keyword=sex chromosome
en-keyword=genome assembly
kn-keyword=genome assembly
en-keyword=monoecy
kn-keyword=monoecy
en-keyword=transposable elements
kn-keyword=transposable elements
END

start-ver=1.4
cd-journal=joma
no-vol=189
cd-vols=
no-issue=1
article-no=
start-page=329
end-page=343
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220214
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Photosystem I light-harvesting proteins regulate photosynthetic electron transfer and hydrogen production
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Linear electron flow (LEF) and cyclic electron flow (CEF) compete for light-driven electrons transferred from the acceptor side of photosystem I (PSI). Under anoxic conditions, such highly reducing electrons also could be used for hydrogen (H2) production via electron transfer between ferredoxin and hydrogenase in the green alga Chlamydomonas reinhardtii. Partitioning between LEF and CEF is regulated through PROTON-GRADIENT REGULATION5 (PGR5). There is evidence that partitioning of electrons also could be mediated via PSI remodeling processes. This plasticity is linked to the dynamics of PSI-associated light-harvesting proteins (LHCAs) LHCA2 and LHCA9. These two unique light-harvesting proteins are distinct from all other LHCAs because they are loosely bound at the PSAL pole. Here, we investigated photosynthetic electron transfer and H2 production in single, double, and triple mutants deficient in PGR5, LHCA2, and LHCA9. Our data indicate that lhca2 and lhca9 mutants are efficient in photosynthetic electron transfer, that LHCA2 impacts the pgr5 phenotype, and that pgr5/lhca2 is a potent H2 photo-producer. In addition, pgr5/lhca2 and pgr5/lhca9 mutants displayed substantially different H2 photo-production kinetics. This indicates that the absence of LHCA2 or LHCA9 impacts H2 photo-production independently, despite both being attached at the PSAL pole, pointing to distinct regulatory capacities.
en-copyright=
kn-copyright=

en-aut-name=HoThi Thu Hoai
en-aut-sei=Ho
en-aut-mei=Thi Thu Hoai
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SchwierChris
en-aut-sei=Schwier
en-aut-mei=Chris
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ElmanTamar
en-aut-sei=Elman
en-aut-mei=Tamar
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=FleuterVera
en-aut-sei=Fleuter
en-aut-mei=Vera
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ZinziusKaren
en-aut-sei=Zinzius
en-aut-mei=Karen
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ScholzMartin
en-aut-sei=Scholz
en-aut-mei=Martin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YacobyIftach
en-aut-sei=Yacoby
en-aut-mei=Iftach
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=BuchertFelix
en-aut-sei=Buchert
en-aut-mei=Felix
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=HipplerMichael
en-aut-sei=Hippler
en-aut-mei=Michael
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Institute of Plant Biology and Biotechnology, University of Münster
kn-affil=

affil-num=2
en-affil=Institute of Plant Biology and Biotechnology, University of Münster
kn-affil=

affil-num=3
en-affil=School of Plant Sciences and Food Security, The George S. Wise Faculty of Life Sciences, Tel Aviv University
kn-affil=

affil-num=4
en-affil=Institute of Plant Biology and Biotechnology, University of Münster
kn-affil=

affil-num=5
en-affil=Institute of Plant Biology and Biotechnology, University of Münster
kn-affil=

affil-num=6
en-affil=Institute of Plant Biology and Biotechnology, University of Münster
kn-affil=

affil-num=7
en-affil=School of Plant Sciences and Food Security, The George S. Wise Faculty of Life Sciences, Tel Aviv University
kn-affil=

affil-num=8
en-affil=Institute of Plant Biology and Biotechnology, University of Münster
kn-affil=

affil-num=9
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=13
cd-vols=
no-issue=1
article-no=
start-page=8826
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230531
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Effects of the order of exposure to antimicrobials on the incidence of multidrug-resistant Pseudomonas aeruginosa
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Multidrug-resistant Pseudomonas aeruginosa (MDRP) is one of the most important pathogens in clinical practice. To clarify the mechanisms contributing to its emergence, we isolated MDRPs using the P. aeruginosa PAO1, the whole genome sequence of which has already been elucidated. Mutant strains resistant to carbapenems, aminoglycosides, and new quinolones, which are used to treat P. aeruginosa infections, were isolated; however, none met the criteria for MDRPs. Then, PAO1 strains were exposed to these antimicrobial agents in various orders and the appearance rate of MDRP varied depending on the order of exposure; MDRPs more frequently appeared when gentamicin was applied before ciprofloxacin, but were rarely isolated when ciprofloxacin was applied first. Exposure to ciprofloxacin followed by gentamicin increased the expression of MexCD-OprJ, an RND-type multidrug efflux pump, due to the NfxB mutation. In contrast, exposure to gentamicin followed by ciprofloxacin resulted in more mutations in DNA gyrase. These results suggest that the type of quinolone resistance mechanism is related to the frequency of MDRP and that the risk of MDRP incidence is highly dependent on the order of exposure to gentamicin and ciprofloxacin.
en-copyright=
kn-copyright=

en-aut-name=YasudaNami
en-aut-sei=Yasuda
en-aut-mei=Nami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=FujitaTomoko
en-aut-sei=Fujita
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=FujiokaTakahiro
en-aut-sei=Fujioka
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TagawaMei
en-aut-sei=Tagawa
en-aut-mei=Mei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KohiraNaoki
en-aut-sei=Kohira
en-aut-mei=Naoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TorimaruKensho
en-aut-sei=Torimaru
en-aut-mei=Kensho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=ShiotaSumiko
en-aut-sei=Shiota
en-aut-mei=Sumiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KumagaiTakanori
en-aut-sei=Kumagai
en-aut-mei=Takanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MoritaDaichi
en-aut-sei=Morita
en-aut-mei=Daichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=OgawaWakano
en-aut-sei=Ogawa
en-aut-mei=Wakano
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=TsuchiyaTomofusa
en-aut-sei=Tsuchiya
en-aut-mei=Tomofusa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=KurodaTeruo
en-aut-sei=Kuroda
en-aut-mei=Teruo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

affil-num=1
en-affil=Department of Microbiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Microbiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Microbiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Microbiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Microbiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Microbiology, Graduate  School of Biomedical and Health Sciences, Hiroshima University
kn-affil=

affil-num=7
en-affil=Department of Molecular Biology, School of Pharmacy, Shujitsu University
kn-affil=

affil-num=8
en-affil=Department of Microbiology, Graduate  School of Biomedical and Health Sciences, Hiroshima University
kn-affil=

affil-num=9
en-affil=Department of Microbiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama  University
kn-affil=

affil-num=10
en-affil=Department of Microbiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama  University
kn-affil=

affil-num=11
en-affil=Department of Microbiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama  University
kn-affil=

affil-num=12
en-affil=Department of Microbiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama  University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=119
cd-vols=
no-issue=43
article-no=
start-page=e2122641119
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20221017
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Structures and mechanisms of actin ATP hydrolysis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The major cytoskeleton protein actin undergoes cyclic transitions between the monomeric G-form and the filamentous F-form, which drive organelle transport and cell motility. This mechanical work is driven by the ATPase activity at the catalytic site in the F-form. For deeper understanding of the actin cellular functions, the reaction mechanism must be elucidated. Here, we show that a single actin molecule is trapped in the F-form by fragmin domain-1 binding and present their crystal structures in the ATP analog-, ADP-Pi-, and ADP-bound forms, at 1.15-Å resolutions. The G-to-F conformational transition shifts the side chains of Gln137 and His161, which relocate four water molecules including W1 (attacking water) and W2 (helping water) to facilitate the hydrolysis. By applying quantum mechanics/molecular mechanics calculations to the structures, we have revealed a consistent and comprehensive reaction path of ATP hydrolysis by the F-form actin. The reaction path consists of four steps: 1) W1 and W2 rotations; 2) PG–O3B bond cleavage; 3) four concomitant events: W1–PO3− formation, OH− and proton cleavage, nucleophilic attack by the OH− against PG, and the abstracted proton transfer; and 4) proton relocation that stabilizes the ADP-Pi–bound F-form actin. The mechanism explains the slow rate of ATP hydrolysis by actin and the irreversibility of the hydrolysis reaction. While the catalytic strategy of actin ATP hydrolysis is essentially the same as those of motor proteins like myosin, the process after the hydrolysis is distinct and discussed in terms of Pi release, F-form destabilization, and global conformational changes.
en-copyright=
kn-copyright=

en-aut-name=KanematsuYusuke
en-aut-sei=Kanematsu
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NaritaAkihiro
en-aut-sei=Narita
en-aut-mei=Akihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OdaToshiro
en-aut-sei=Oda
en-aut-mei=Toshiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KoikeRyotaro
en-aut-sei=Koike
en-aut-mei=Ryotaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=OtaMotonori
en-aut-sei=Ota
en-aut-mei=Motonori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TakanoYu
en-aut-sei=Takano
en-aut-mei=Yu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MoritsuguKei
en-aut-sei=Moritsugu
en-aut-mei=Kei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=FujiwaraIkuko
en-aut-sei=Fujiwara
en-aut-mei=Ikuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TanakaKotaro
en-aut-sei=Tanaka
en-aut-mei=Kotaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=KomatsuHideyuki
en-aut-sei=Komatsu
en-aut-mei=Hideyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=NagaeTakayuki
en-aut-sei=Nagae
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=WatanabeNobuhisa
en-aut-sei=Watanabe
en-aut-mei=Nobuhisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=IwasaMitsusada
en-aut-sei=Iwasa
en-aut-mei=Mitsusada
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=MaédaYuichiro
en-aut-sei=Maéda
en-aut-mei=Yuichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=TakedaShuichi
en-aut-sei=Takeda
en-aut-mei=Shuichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

affil-num=1
en-affil=Graduate School of Information Sciences, Hiroshima City University
kn-affil=

affil-num=2
en-affil=Structural Biology Research Center, Graduate School of Science, Nagoya University
kn-affil=

affil-num=3
en-affil=Faculty of Health and Welfare, Tokai Gakuin University
kn-affil=

affil-num=4
en-affil=Graduate School of Informatics, Nagoya University
kn-affil=

affil-num=5
en-affil=Graduate School of Informatics, Nagoya University
kn-affil=

affil-num=6
en-affil=Graduate School of Information Sciences, Hiroshima City University
kn-affil=

affil-num=7
en-affil=Graduate School of Medical Life Science, Yokohama City University
kn-affil=

affil-num=8
en-affil=Graduate School of Science, Osaka City University
kn-affil=

affil-num=9
en-affil=Structural Biology Research Center, Graduate School of Science, Nagoya University
kn-affil=

affil-num=10
en-affil=Department of Bioscience and Bioinformatics, Graduate School of Computer Science and Systems Engineering, Kyushu Institute of Technology
kn-affil=

affil-num=11
en-affil=Synchrotron Radiation Research Center, Nagoya University
kn-affil=

affil-num=12
en-affil=Synchrotron Radiation Research Center, Nagoya University
kn-affil=

affil-num=13
en-affil=Graduate School of Informatics, Nagoya University
kn-affil=

affil-num=14
en-affil=Research Institute for Interdisciplinary Science, Okayama University
kn-affil=

affil-num=15
en-affil=Research Institute for Interdisciplinary Science, Okayama University
kn-affil=
en-keyword=actin
kn-keyword=actin
en-keyword=ATP hydrolysis
kn-keyword=ATP hydrolysis
en-keyword=protein crystallography
kn-keyword=protein crystallography
en-keyword=QM
kn-keyword=QM
en-keyword=MM simulation
kn-keyword=MM simulation
END

start-ver=1.4
cd-journal=joma
no-vol=13
cd-vols=
no-issue=1
article-no=
start-page=8954
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230602
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Refining the evolutionary tree of the horse Y chromosome
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The Y chromosome carries information about the demography of paternal lineages, and thus, can prove invaluable for retracing both the evolutionary trajectory of wild animals and the breeding history of domesticates. In horses, the Y chromosome shows a limited, but highly informative, sequence diversity, supporting the increasing breeding influence of Oriental lineages during the last 1500 years. Here, we augment the primary horse Y-phylogeny, which is currently mainly based on modern horse breeds of economic interest, with haplotypes (HT) segregating in remote horse populations around the world. We analyze target enriched sequencing data of 5 Mb of the Y chromosome from 76 domestic males, together with 89 whole genome sequenced domestic males and five Przewalski's horses from previous studies. The resulting phylogeny comprises 153 HTs defined by 2966 variants and offers unprecedented resolution into the history of horse paternal lineages. It reveals the presence of a remarkable number of previously unknown haplogroups in Mongolian horses and insular populations. Phylogenetic placement of HTs retrieved from 163 archaeological specimens further indicates that most of the present-day Y-chromosomal variation evolved after the domestication process that started around 4200 years ago in the Western Eurasian steppes. Our comprehensive phylogeny significantly reduces ascertainment bias and constitutes a robust evolutionary framework for analyzing horse population dynamics and diversity.
en-copyright=
kn-copyright=

en-aut-name=BozlakElif
en-aut-sei=Bozlak
en-aut-mei=Elif
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=RadovicLara
en-aut-sei=Radovic
en-aut-mei=Lara
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=RemerViktoria
en-aut-sei=Remer
en-aut-mei=Viktoria
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=RiglerDoris
en-aut-sei=Rigler
en-aut-mei=Doris
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=AllenLucy
en-aut-sei=Allen
en-aut-mei=Lucy
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=BremGottfried
en-aut-sei=Brem
en-aut-mei=Gottfried
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=StalderGabrielle
en-aut-sei=Stalder
en-aut-mei=Gabrielle
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=CastanedaCaitlin
en-aut-sei=Castaneda
en-aut-mei=Caitlin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=CothranGus
en-aut-sei=Cothran
en-aut-mei=Gus
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=RaudseppTerje
en-aut-sei=Raudsepp
en-aut-mei=Terje
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=OkudaYu
en-aut-sei=Okuda
en-aut-mei=Yu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=MoeKyaw Kyaw
en-aut-sei=Moe
en-aut-mei=Kyaw Kyaw
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=MoeHla Hla
en-aut-sei=Moe
en-aut-mei=Hla Hla
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=KounnavongsaBounthavone
en-aut-sei=Kounnavongsa
en-aut-mei=Bounthavone
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=KeonouchanhSoukanh
en-aut-sei=Keonouchanh
en-aut-mei=Soukanh
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=VanNguyen Huu
en-aut-sei=Van
en-aut-mei=Nguyen Huu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=VuVan Hai
en-aut-sei=Vu
en-aut-mei=Van Hai
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=ShahManoj Kumar
en-aut-sei=Shah
en-aut-mei=Manoj Kumar
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=NishiboriMasahide
en-aut-sei=Nishibori
en-aut-mei=Masahide
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=KazymbetPolat
en-aut-sei=Kazymbet
en-aut-mei=Polat
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

en-aut-name=BakhtinMeirat
en-aut-sei=Bakhtin
en-aut-mei=Meirat
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=21
ORCID=

en-aut-name=ZhunushovAsankadyr
en-aut-sei=Zhunushov
en-aut-mei=Asankadyr
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=22
ORCID=

en-aut-name=PaulRipon Chandra
en-aut-sei=Paul
en-aut-mei=Ripon Chandra
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=23
ORCID=

en-aut-name=DashnyamBumbein
en-aut-sei=Dashnyam
en-aut-mei=Bumbein
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=24
ORCID=

en-aut-name=NozawaKen
en-aut-sei=Nozawa
en-aut-mei=Ken
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=25
ORCID=

en-aut-name=AlmarzookSaria
en-aut-sei=Almarzook
en-aut-mei=Saria
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=26
ORCID=

en-aut-name=BrockmannGudrun A.
en-aut-sei=Brockmann
en-aut-mei=Gudrun A.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=27
ORCID=

en-aut-name=ReissmannMonika
en-aut-sei=Reissmann
en-aut-mei=Monika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=28
ORCID=

en-aut-name=AntczakDouglas F.
en-aut-sei=Antczak
en-aut-mei=Douglas F.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=29
ORCID=

en-aut-name=MillerDonald C.
en-aut-sei=Miller
en-aut-mei=Donald C.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=30
ORCID=

en-aut-name=SadeghiRaheleh
en-aut-sei=Sadeghi
en-aut-mei=Raheleh
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=31
ORCID=

en-aut-name=Butler-WemkenInes von
en-aut-sei=Butler-Wemken
en-aut-mei=Ines von
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=32
ORCID=

en-aut-name=KostarasNikos
en-aut-sei=Kostaras
en-aut-mei=Nikos
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=33
ORCID=

en-aut-name=HanHaige
en-aut-sei=Han
en-aut-mei=Haige
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=34
ORCID=

en-aut-name=ManglaiDugarjaviin
en-aut-sei=Manglai
en-aut-mei=Dugarjaviin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=35
ORCID=

en-aut-name=AbdurasulovAbdugani
en-aut-sei=Abdurasulov
en-aut-mei=Abdugani
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=36
ORCID=

en-aut-name=SukhbaatarBoldbaatar
en-aut-sei=Sukhbaatar
en-aut-mei=Boldbaatar
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=37
ORCID=

en-aut-name=Ropka-MolikKatarzyna
en-aut-sei=Ropka-Molik
en-aut-mei=Katarzyna
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=38
ORCID=

en-aut-name=Stefaniuk-SzmukierMonika
en-aut-sei=Stefaniuk-Szmukier
en-aut-mei=Monika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=39
ORCID=

en-aut-name=LopesMaria Susana
en-aut-sei=Lopes
en-aut-mei=Maria Susana
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=40
ORCID=

en-aut-name=MachadoArtur da Câmara
en-aut-sei=Machado
en-aut-mei=Artur da Câmara
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=41
ORCID=

en-aut-name=KalashnikovValery V.
en-aut-sei=Kalashnikov
en-aut-mei=Valery V.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=42
ORCID=

en-aut-name=KalinkovaLiliya
en-aut-sei=Kalinkova
en-aut-mei=Liliya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=43
ORCID=

en-aut-name=ZaitevAlexander M.
en-aut-sei=Zaitev
en-aut-mei=Alexander M.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=44
ORCID=

en-aut-name=Novoa-BravoMiguel
en-aut-sei=Novoa-Bravo
en-aut-mei=Miguel
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=45
ORCID=

en-aut-name=LindgrenGabriella
en-aut-sei=Lindgren
en-aut-mei=Gabriella
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=46
ORCID=

en-aut-name=BrooksSamantha
en-aut-sei=Brooks
en-aut-mei=Samantha
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=47
ORCID=

en-aut-name=RosaLaura Patterson
en-aut-sei=Rosa
en-aut-mei=Laura Patterson
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=48
ORCID=

en-aut-name=OrlandoLudovic
en-aut-sei=Orlando
en-aut-mei=Ludovic
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=49
ORCID=

en-aut-name=JurasRytis
en-aut-sei=Juras
en-aut-mei=Rytis
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=50
ORCID=

en-aut-name=KuniedaTetsuo
en-aut-sei=Kunieda
en-aut-mei=Tetsuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=51
ORCID=

en-aut-name=WallnerBarbara
en-aut-sei=Wallner
en-aut-mei=Barbara
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=52
ORCID=

affil-num=1
en-affil=Institute of Animal Breeding and Genetics, University of Veterinary Medicine Vienna
kn-affil=

affil-num=2
en-affil=Institute of Animal Breeding and Genetics, University of Veterinary Medicine Vienna
kn-affil=

affil-num=3
en-affil=Institute of Animal Breeding and Genetics, University of Veterinary Medicine Vienna
kn-affil=

affil-num=4
en-affil=Institute of Animal Breeding and Genetics, University of Veterinary Medicine Vienna
kn-affil=

affil-num=5
en-affil=Institute of Animal Breeding and Genetics, University of Veterinary Medicine Vienna
kn-affil=

affil-num=6
en-affil=Institute of Animal Breeding and Genetics, University of Veterinary Medicine Vienna
kn-affil=

affil-num=7
en-affil=Research Institute of Wildlife Ecology, University of Veterinary Medicine Vienna
kn-affil=

affil-num=8
en-affil=School of Veterinary Medicine and Biomedical Sciences, Texas A&M University
kn-affil=

affil-num=9
en-affil=School of Veterinary Medicine and Biomedical Sciences, Texas A&M University
kn-affil=

affil-num=10
en-affil=School of Veterinary Medicine and Biomedical Sciences, Texas A&M University
kn-affil=

affil-num=11
en-affil=Museum of Dinosaur Research, Okayama University of Science
kn-affil=

affil-num=12
en-affil=Department of Pathology and Microbiology, University of Veterinary Science
kn-affil=

affil-num=13
en-affil=Department of Genetics and Animal Breeding, University of Veterinary Science
kn-affil=

affil-num=14
en-affil=National Agriculture and Forestry Research Institute (Lao) Resources, Livestock Research Center
kn-affil=

affil-num=15
en-affil=Faculty of Animal Science and Veterinary Medicine, University of Agriculture and Forestry, Hue University
kn-affil=

affil-num=16
en-affil=Faculty of Animal Science and Veterinary Medicine, University of Agriculture and Forestry, Hue University
kn-affil=

affil-num=17
en-affil=Faculty of Animal Science and Veterinary Medicine, University of Agriculture and Forestry, Hue University
kn-affil=

affil-num=18
en-affil=Faculty of Animal Science, Veterinary Science and Fisheries, Agriculture and Forestry University
kn-affil=

affil-num=19
en-affil=Graduate School of Integrated Sciences for Life, Hiroshima University
kn-affil=

affil-num=20
en-affil=Radiobiological Research Institute, JSC Astana Medical University
kn-affil=

affil-num=21
en-affil=Institute of Biotechnology, National Academy of Sciences of the Kyrgyz Republic
kn-affil=

affil-num=22
en-affil=Institute of Biotechnology, National Academy of Sciences of the Kyrgyz Republic
kn-affil=

affil-num=23
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=24
en-affil=Institute of Biological Sciences, Mongolian Academy of Sciences
kn-affil=

affil-num=25
en-affil=Primate Research Institute, Kyoto University
kn-affil=

affil-num=26
en-affil=Albrecht Daniel Thaer‑Institut, Humboldt-Universität zu Berlin
kn-affil=

affil-num=27
en-affil=Albrecht Daniel Thaer‑Institut, Humboldt-Universität zu Berlin
kn-affil=

affil-num=28
en-affil=Baker Institute for Animal Health, College of Veterinary Medicine, Cornell University
kn-affil=

affil-num=29
en-affil=Baker Institute for Animal Health, College of Veterinary Medicine, Cornell University
kn-affil=

affil-num=30
en-affil=Baker Institute for Animal Health, College of Veterinary Medicine, Cornell University
kn-affil=

affil-num=31
en-affil=Baker Institute for Animal Health, College of Veterinary Medicine, Cornell University
kn-affil=

affil-num=32
en-affil=Barb Horse Breeding Organisation VFZB E. V., Verein der Freunde und Züchter Des Berberpferdes E.V.
kn-affil=

affil-num=33
en-affil=Amaltheia
kn-affil=

affil-num=34
en-affil=Inner Mongolia Key Laboratory of Equine Genetics, Breeding and Reproduction, College of Animal Science, Equine Research Center, Inner Mongolia Agricultural University
kn-affil=

affil-num=35
en-affil=Inner Mongolia Key Laboratory of Equine Genetics, Breeding and Reproduction, College of Animal Science, Equine Research Center, Inner Mongolia Agricultural University
kn-affil=

affil-num=36
en-affil=Department of Agriculture, Faculty of Natural Sciences and Geography, Osh State University
kn-affil=

affil-num=37
en-affil=Sector of Surveillance and Diagnosis of Infectious Diseases, State Central Veterinary Laboratory
kn-affil=

affil-num=38
en-affil=National Research Institute of Animal Production, Animal Molecular Biology
kn-affil=

affil-num=39
en-affil=National Research Institute of Animal Production, Animal Molecular Biology
kn-affil=

affil-num=40
en-affil=Biotechnology Centre of Azores, University of Azores
kn-affil=

affil-num=41
en-affil=Biotechnology Centre of Azores, University of Azores
kn-affil=

affil-num=42
en-affil=All-Russian Research Institute for Horse Breeding
kn-affil=

affil-num=43
en-affil=All-Russian Research Institute for Horse Breeding
kn-affil=

affil-num=44
en-affil=All-Russian Research Institute for Horse Breeding
kn-affil=

affil-num=45
en-affil=Genética Animal de Colombia SAS.
kn-affil=

affil-num=46
en-affil=Department of Animal Breeding and Genetics, Swedish University of Agricultural Sciences
kn-affil=

affil-num=47
en-affil=Department of Animal Science, UF Genetics Institute, University of Florida
kn-affil=

affil-num=48
en-affil=Department of Agriculture and Industry, Sul Ross State University
kn-affil=

affil-num=49
en-affil=Centre d’Anthropobiologie et de Génomique de Toulouse, Université Paul Sabatier
kn-affil=

affil-num=50
en-affil=School of Veterinary Medicine and Biomedical Sciences, Texas A&M University
kn-affil=

affil-num=51
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=52
en-affil=Institute of Animal Breeding and Genetics, University of Veterinary Medicine Vienna
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=108
cd-vols=
no-issue=
article-no=
start-page=110717
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=202308
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=STAT1/3 signaling suppresses axon degeneration and neuronal cell death through regulation of NAD+-biosynthetic and consuming enzymes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Nicotinamide adenine dinucleotide (NAD)+-biosynthetic and consuming enzymes are involved in various intracellular events through the regulation of NAD+ metabolism. Recently, it has become clear that alterations in the expression of NAD+-biosynthetic and consuming enzymes contribute to the axonal stability of neurons. We explored soluble bioactive factor(s) that alter the expression of NAD+-metabolizing enzymes and found that cytokine interferon (IFN)-γ increased the expression of nicotinamide nucleotide adenylyltransferase 2 (NMNAT2), an NAD+-biosynthetic enzyme. IFN-γ activated signal transducers and activators of transcription 1 and 3 (STAT1/3) followed by c-Jun N-terminal kinase (JNK) suppression. As a result, STAT1/3 increased the expression of NMNAT2 at both mRNA and protein levels in a dose- and time-dependent manner and, at the same time, suppressed activation of sterile alpha and Toll/interleukin receptor motif-containing 1 (SARM1), an NAD+-consuming enzyme, and increased intracellular NAD+ levels. We examined the protective effect of STAT1/3 signaling against vincristine-mediated cell injury as a model of chemotherapy-induced peripheral neuropathy (CIPN), in which axonal degeneration is involved in disease progression. We found that IFN-γ-mediated STAT1/3 activation inhibited vincristine-induced downregulation of NMNAT2 and upregulation of SARM1 phosphorylation, resulting in modest suppression of subsequent neurite degradation and cell death. These results indicate that STAT1/3 signaling induces NMNAT2 expression while simultaneously suppressing SARM1 phosphorylation, and that both these actions contribute to suppression of axonal degeneration and cell death.
en-copyright=
kn-copyright=

en-aut-name=MurataHitoshi
en-aut-sei=Murata
en-aut-mei=Hitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YasuiYu
en-aut-sei=Yasui
en-aut-mei=Yu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OisoKazuma
en-aut-sei=Oiso
en-aut-mei=Kazuma
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OchiToshiki
en-aut-sei=Ochi
en-aut-mei=Toshiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TomonobuNahoko
en-aut-sei=Tomonobu
en-aut-mei=Nahoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YamamotoKen-ichi
en-aut-sei=Yamamoto
en-aut-mei=Ken-ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KinoshitaRie
en-aut-sei=Kinoshita
en-aut-mei=Rie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=SakaguchiMasakiyo
en-aut-sei=Sakaguchi
en-aut-mei=Masakiyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=NMNAT2
kn-keyword=NMNAT2
en-keyword=SARM1
kn-keyword=SARM1
en-keyword=NAD+
kn-keyword=NAD+
en-keyword=STAT1/3
kn-keyword=STAT1/3
en-keyword=IFN-γ
kn-keyword=IFN-γ
END

start-ver=1.4
cd-journal=joma
no-vol=148
cd-vols=
no-issue=11
article-no=
start-page=2626
end-page=2632
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=2023
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=FRET probe for detecting two mutations in one EGFR mRNA
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Technologies for visualizing and tracking RNA are essential in molecular biology, including in disease-related fields. In this study, we propose a novel probe set (DAt-probe and T-probe) that simultaneously detects two mutations in the same RNA using fluorescence resonance energy transfer (FRET). The DAt-probe carrying the fluorophore Atto488 and the quencher Dabcyl were used to detect a cancer mutation (exon19del), and the T-probe carrying the fluorophore Tamra was used to detect drug resistance mutations (T790M) in epidermal growth factor receptor (EGFR) mRNA. These probes were designed to induce FRET when both mutations were present in the mRNA. Gel electrophoresis confirmed that the two probes could efficiently bind to the mutant mRNA. We measured the FRET ratios using wild-type and double-mutant RNAs and found a significant difference between them. Even in living cells, the FRET probe could visualize mutant RNA. As a result, we conclude that this probe set provides a method for detecting two mutations in the single EGFR mRNA via FRET.
en-copyright=
kn-copyright=

en-aut-name=ThuMyat
en-aut-sei=Thu
en-aut-mei=Myat
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YanaiKouta
en-aut-sei=Yanai
en-aut-mei=Kouta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ShigetoHajime
en-aut-sei=Shigeto
en-aut-mei=Hajime
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YamamuraShohei
en-aut-sei=Yamamura
en-aut-mei=Shohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=WatanabeKazunori
en-aut-sei=Watanabe
en-aut-mei=Kazunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OhtsukiTakashi
en-aut-sei=Ohtsuki
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=3
en-affil=Health and Medical Research Institute, National Institute of Advanced Industrial Science and Technology (AIST)
kn-affil=

affil-num=4
en-affil=Health and Medical Research Institute, National Institute of Advanced Industrial Science and Technology (AIST)
kn-affil=

affil-num=5
en-affil=Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=6
cd-vols=
no-issue=1
article-no=
start-page=596
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230602
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=NFYA promotes malignant behavior of triple-negative breast cancer in mice through the regulation of lipid metabolism
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Two splicing variants exist in NFYA that exhibit high expression in many human tumour types. The balance in their expression correlates with prognosis in breast cancer, but functional differences remain unclear. Here, we demonstrate that NFYAv1, a long-form variant, upregulates the transcription of essential lipogenic enzymes ACACA and FASN to enhance the malignant behavior of triple-negative breast cancer (TNBC). Loss of the NFYAv1-lipogenesis axis strongly suppresses malignant behavior in vitro and in vivo, indicating that the NFYAv1-lipogenesis axis is essential for TNBC malignant behavior and that the axis might be a potential therapeutic target for TNBC. Furthermore, mice deficient in lipogenic enzymes, such as Acly, Acaca, and Fasn, exhibit embryonic lethality; however, Nfyav1-deficient mice exhibited no apparent developmental abnormalities. Our results indicate that the NFYAv1-lipogenesis axis has tumour-promoting effects and that NFYAv1 may be a safe therapeutic target for TNBC.
en-copyright=
kn-copyright=

en-aut-name=OkadaNobuhiro
en-aut-sei=Okada
en-aut-mei=Nobuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=UekiChihiro
en-aut-sei=Ueki
en-aut-mei=Chihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ShimazakiMasahiro
en-aut-sei=Shimazaki
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TsujimotoGoki
en-aut-sei=Tsujimoto
en-aut-mei=Goki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KohnoSusumu
en-aut-sei=Kohno
en-aut-mei=Susumu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MuranakaHayato
en-aut-sei=Muranaka
en-aut-mei=Hayato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YoshikawaKiyotsugu
en-aut-sei=Yoshikawa
en-aut-mei=Kiyotsugu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TakahashiChiaki
en-aut-sei=Takahashi
en-aut-mei=Chiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Graduate School of Interdisciplinary Science & Engineering in Health Systems, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Interdisciplinary Science & Engineering in Health Systems, Okayama University
kn-affil=

affil-num=3
en-affil=Laboratory for Malignancy Control Research, Medical Innovation Center, Kyoto University
kn-affil=

affil-num=4
en-affil=Graduate School of Interdisciplinary Science & Engineering in Health Systems, Okayama University
kn-affil=

affil-num=5
en-affil=Division of Oncology and Molecular Biology, Cancer Research Institute, Kanazawa University
kn-affil=

affil-num=6
en-affil=Division of Oncology and Molecular Biology, Cancer Research Institute, Kanazawa University
kn-affil=

affil-num=7
en-affil=Faculty of Pharmaceutical Sciences, Doshisha Women’s College of Liberal Arts
kn-affil=

affil-num=8
en-affil=Division of Oncology and Molecular Biology, Cancer Research Institute, Kanazawa University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=77
cd-vols=
no-issue=3
article-no=
start-page=273
end-page=280
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=202306
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Usefulness of Simple Diffusion Kurtosis Imaging for Head and Neck Tumors: An Early Clinical Study
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Diffusion kurtosis (DK) imaging (DKI), a type of restricted diffusion-weighted imaging, has been reported to be useful for tumor diagnoses in clinical studies. We developed a software program to simultaneously create DK images with apparent diffusion coefficient (ADC) maps and conducted an initial clinical study. Multi-shot echo-planar diffusion-weighted images were obtained at b-values of 0, 400, and 800 sec/mm2 for simple DKI, and DK images were created simultaneously with the ADC map. The usefulness of the DK image and ADC map was evaluated using a pixel analysis of all pixels and a median analysis of the pixels of each case. Tumor and normal tissues differed significantly in both pixel and median analyses. In the pixel analysis, the area under the curve was 0.64 for the mean kurtosis (MK) value and 0.77 for the ADC value. In the median analysis, the MK value was 0.74, and the ADC value was 0.75. The MK and ADC values correlated moderately in the pixel analysis and strongly in the median analysis. Our simple DKI system created DK images simultaneously with ADC maps, and the obtained MK and ADC values were useful for differentiating head and neck tumors from normal tissue.
en-copyright=
kn-copyright=

en-aut-name=ShimizuYudai
en-aut-sei=Shimizu
en-aut-mei=Yudai
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KurodaMasahiro
en-aut-sei=Kuroda
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NakamitsuYuki
en-aut-sei=Nakamitsu
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=Al-HammadWlla E.
en-aut-sei=Al-Hammad
en-aut-mei=Wlla E.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YoshidaSuzuka
en-aut-sei=Yoshida
en-aut-mei=Suzuka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=FukumuraYuka
en-aut-sei=Fukumura
en-aut-mei=Yuka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NakamuraYoshihide
en-aut-sei=Nakamura
en-aut-mei=Yoshihide
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KurodaKazuhiro
en-aut-sei=Kuroda
en-aut-mei=Kazuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KamizakiRyo
en-aut-sei=Kamizaki
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=ImajohSatoshi
en-aut-sei=Imajoh
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=TanabeYoshinori
en-aut-sei=Tanabe
en-aut-mei=Yoshinori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=SugimotoKohei
en-aut-sei=Sugimoto
en-aut-mei=Kohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=OitaMasataka
en-aut-sei=Oita
en-aut-mei=Masataka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=SugiantoIrfan
en-aut-sei=Sugianto
en-aut-mei=Irfan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=BamgboseBabatunde O.
en-aut-sei=Bamgbose
en-aut-mei=Babatunde O.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=YanagiYoshinobu
en-aut-sei=Yanagi
en-aut-mei=Yoshinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=AsaumiJunichi
en-aut-sei=Asaumi
en-aut-mei=Junichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

affil-num=1
en-affil=Department of Oral and Maxillofacial Radiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Radiological Technology, Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Radiological Technology, Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Oral and Maxillofacial Radiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Oral and Maxillofacial Radiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Oral and Maxillofacial Radiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Oral and Maxillofacial Radiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Radiological Technology, Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Radiological Technology, Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=10
en-affil=Radiological Technology, Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=11
en-affil=Radiological Technology, Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=12
en-affil=Graduate School of Interdisciplinary Sciences and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=13
en-affil=Graduate School of Interdisciplinary Sciences and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=14
en-affil=Department of Oral Radiology, Faculty of Dentistry, Hasanuddin University
kn-affil=

affil-num=15
en-affil=Department of Oral Diagnostic Sciences, Faculty of Dentistry, Bayero University
kn-affil=

affil-num=16
en-affil=Department of Dental Informatics, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=17
en-affil=Department of Oral and Maxillofacial Radiology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=simple diffusion kurtosis imaging
kn-keyword=simple diffusion kurtosis imaging
en-keyword=mean kurtosis
kn-keyword=mean kurtosis
en-keyword=clinical trial
kn-keyword=clinical trial
en-keyword=head and neck tumor
kn-keyword=head and neck tumor
en-keyword=magnetic resonance imaging
kn-keyword=magnetic resonance imaging
END

start-ver=1.4
cd-journal=joma
no-vol=48
cd-vols=
no-issue=
article-no=
start-page=109071
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=202306
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The dataset of de novo assembly and inferred functional annotation of the transcriptome of Heterosigma akashiwo, a bloom-forming, cosmopolitan raphidophyte
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Heterosigma akashiwo is a eukaryotic, cosmopolitan, and uni-cellular alga (class: Raphidophyceae), and produces fish -killing blooms. There is a substantial scientific and practical interest in its ecophysiological characteristics that determine bloom dynamics and its adaptation to broad climate zones. A well-annotated genomic/genetic sequence information en-ables researchers to characterize organisms using modern molecular technology. In the present study, we conducted H. akashiwo RNA sequencing, a de novo transcriptome assem-bly of 84,693,530 high-quality deduplicated short-read se-quences. <br>
Obtained RNA reads were assembled by Trinity assembler and 144,777 contigs were identified with N 50 values of 1085. Total 60,877 open reading frames with the length of 150 bp or greater were predicted. For further analy-ses, top Gene Ontology terms, pfam hits, and blast hits were annotated for all the predicted genes. The raw data were deposited in the NCBI SRA database (BioProject PR - JDB6241 and PRJDB15108), and the assemblies are available in NCBI TSA database (ICRV01). The annotation information can be obtained in Dryad and can be accessed via doi: 10.5061/dryad.m0cfxpp56.
en-copyright=
kn-copyright=

en-aut-name=SatoMasanao
en-aut-sei=Sato
en-aut-mei=Masanao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SekiMasahide
en-aut-sei=Seki
en-aut-mei=Masahide
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SuzukiYutaka
en-aut-sei=Suzuki
en-aut-mei=Yutaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=UekiShoko
en-aut-sei=Ueki
en-aut-mei=Shoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=Division of Applied Bioscience, Graduate School of Agriculture, Hokkaido University
kn-affil=

affil-num=2
en-affil=Department of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo
kn-affil=

affil-num=3
en-affil=Department of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo
kn-affil=

affil-num=4
en-affil=Institute of Plant Science and Resources, Okayama University
kn-affil=
en-keyword=Harmful alga
kn-keyword=Harmful alga
en-keyword=Nuclear gene
kn-keyword=Nuclear gene
en-keyword=Gene prediction
kn-keyword=Gene prediction
en-keyword=Gene ontology
kn-keyword=Gene ontology
en-keyword=Stramenopile
kn-keyword=Stramenopile
en-keyword=Heterokont
kn-keyword=Heterokont
END

start-ver=1.4
cd-journal=joma
no-vol=19
cd-vols=
no-issue=4
article-no=
start-page=e1010732
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230428
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Overexpression profiling reveals cellular requirements in the context of genetic backgrounds and environments
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Overexpression can help life adapt to stressful environments, making an examination of overexpressed genes valuable for understanding stress tolerance mechanisms. However, a systematic study of genes whose overexpression is functionally adaptive (GOFAs) under stress has yet to be conducted. We developed a new overexpression profiling method and systematically identified GOFAs in Saccharomyces cerevisiae under stress (heat, salt, and oxidative). Our results show that adaptive overexpression compensates for deficiencies and increases fitness under stress, like calcium under salt stress. We also investigated the impact of different genetic backgrounds on GOFAs, which varied among three S. cerevisiae strains reflecting differing calcium and potassium requirements for salt stress tolerance. Our study of a knockout collection also suggested that calcium prevents mitochondrial outbursts under salt stress. Mitochondria-enhancing GOFAs were only adaptive when adequate calcium was available and non-adaptive when calcium was deficient, supporting this idea. Our findings indicate that adaptive overexpression meets the cell's needs for maximizing the organism's adaptive capacity in the given environment and genetic context. Author summaryThe study aimed to investigate how overexpression of genes can aid organisms in adapting to stress. The researchers utilized a new method to identify genes in yeast that demonstrated functional adaptability when overexpressed under stress such as heat, salt, and oxidative stress. The results indicated that overexpressing specific genes, like calcium, during salt stress could counteract deficiencies and improve the organism's ability to withstand stress. The study also examined the effect of different genetic backgrounds on these genes and discovered that the impact differed among various yeast strains. Additionally, the study revealed that calcium could play a key role in adapting to salt stress by preventing mitochondrial outbursts. These findings suggest that overexpressing certain genes can help the organism maximize its adaptability to stress in a given environment and genetic context.
en-copyright=
kn-copyright=

en-aut-name=SaekiNozomu
en-aut-sei=Saeki
en-aut-mei=Nozomu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YamamotoChie
en-aut-sei=Yamamoto
en-aut-mei=Chie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=EguchiYuichi
en-aut-sei=Eguchi
en-aut-mei=Yuichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SekitoTakayuki
en-aut-sei=Sekito
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ShigenobuShuji
en-aut-sei=Shigenobu
en-aut-mei=Shuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YoshimuraMami
en-aut-sei=Yoshimura
en-aut-mei=Mami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YashirodaYoko
en-aut-sei=Yashiroda
en-aut-mei=Yoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=BooneCharles
en-aut-sei=Boone
en-aut-mei=Charles
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MoriyaHisao
en-aut-sei=Moriya
en-aut-mei=Hisao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=3
en-affil=Biomedical Business Center, RICOH Futures BU
kn-affil=

affil-num=4
en-affil=Graduate School of Agriculture, Ehime University
kn-affil=

affil-num=5
en-affil=National Institute for Basic Biology
kn-affil=

affil-num=6
en-affil=RIKEN Center for Sustainable Resource Science
kn-affil=

affil-num=7
en-affil=RIKEN Center for Sustainable Resource Science
kn-affil=

affil-num=8
en-affil=RIKEN Center for Sustainable Resource Science
kn-affil=

affil-num=9
en-affil=Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=13
cd-vols=
no-issue=
article-no=
start-page=1142907
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230404
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Lysyl oxidase-like 4 exerts an atypical role in breast cancer progression that is dependent on the enzymatic activity that targets the cell-surface annexin A2
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: LOX family members are reported to play pivotal roles in cancer. Unlike their enzymatic activities in collagen cross-linking, their precise cancer functions are unclear. We revealed that LOXL4 is highly upregulated in breast cancer cells, and we thus sought to define an unidentified role of LOXL4 in breast cancer.<br>
Methods: We established the MDA-MB-231 sublines MDA-MB-231-LOXL4 mutCA and -LOXL4 KO, which stably overexpress mutant LOXL4 that loses its catalytic activity and genetically ablates the intrinsic LOXL4 gene, respectively. In vitro and in vivo evaluations of these cells’ activities of cancer outgrowth were conducted by cell-based assays in cultures and an orthotopic xenograft model, respectively. The new target (s) of LOXL4 were explored by the MS/MS analytic approach.<br>
Results: Our in vitro results revealed that both the overexpression of mutCA and the KO of LOXL4 in cells resulted in a marked reduction of cell growth and invasion. Interestingly, the lowered cellular activities observed in the engineered cells were also reflected in the mouse model. We identified a novel binding partner of LOXL4, i.e., annexin A2. LOXL4 catalyzes cell surface annexin A2 to achieve a cross-linked multimerization of annexin A2, which in turn prevents the internalization of integrin β-1, resulting in the locking of integrin β-1 on the cell surface. These events enhance the promotion of cancer cell outgrowth.<br>
Conclusions: LOXL4 has a new role in breast cancer progression that occurs via an interaction with annexin A2 and integrin β-1 on the cell surface.<br>
en-copyright=
kn-copyright=

en-aut-name=KomalasariNi Luh Gede Yoni
en-aut-sei=Komalasari
en-aut-mei=Ni Luh Gede Yoni
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TomonobuNahoko
en-aut-sei=Tomonobu
en-aut-mei=Nahoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KinoshitaRie
en-aut-sei=Kinoshita
en-aut-mei=Rie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ChenYouyi
en-aut-sei=Chen
en-aut-mei=Youyi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SakaguchiYoshihiko
en-aut-sei=Sakaguchi
en-aut-mei=Yoshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=GoharaYuma
en-aut-sei=Gohara
en-aut-mei=Yuma
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=JiangFan
en-aut-sei=Jiang
en-aut-mei=Fan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YamamotoKen-Ich
en-aut-sei=Yamamoto
en-aut-mei=Ken-Ich
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MurataHitoshi
en-aut-sei=Murata
en-aut-mei=Hitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=RumaI Made Winarsa
en-aut-sei=Ruma
en-aut-mei=I Made Winarsa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=SumardikaI Wayan
en-aut-sei=Sumardika
en-aut-mei=I Wayan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=ZhouJin
en-aut-sei=Zhou
en-aut-mei=Jin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=YamauchiAkira
en-aut-sei=Yamauchi
en-aut-mei=Akira
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=KuribayashiFutoshi
en-aut-sei=Kuribayashi
en-aut-mei=Futoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=InoueYusuke
en-aut-sei=Inoue
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=ToyookaShinichi
en-aut-sei=Toyooka
en-aut-mei=Shinichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=SakaguchiMasakiyo
en-aut-sei=Sakaguchi
en-aut-mei=Masakiyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

affil-num=1
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of General Surgery & Bio-Bank of General Surgery, TheFourth Affiliated Hospital of Harbin Medical University
kn-affil=

affil-num=5
en-affil=Department of Microbiology, Kitasato University School of Medicine
kn-affil=

affil-num=6
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Faculty of Medicine, Udayana University
kn-affil=

affil-num=11
en-affil=Faculty of Medicine, Udayana University
kn-affil=

affil-num=12
en-affil=Medical Oncology Department of Gastrointestinal Tumors, Liaoning Cancer Hospital & Institute, Cancer Hospital of Dalian University of Technology
kn-affil=

affil-num=13
en-affil=Department of Biochemistry, Kawasaki Medical School
kn-affil=

affil-num=14
en-affil=Department of Biochemistry, Kawasaki Medical School
kn-affil=

affil-num=15
en-affil=Faculty of Science and Technology, Division of Molecular Science, Gunma University
kn-affil=

affil-num=16
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=17
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=breast cancer
kn-keyword=breast cancer
en-keyword=lysyl oxidase
kn-keyword=lysyl oxidase
en-keyword=annexin A2
kn-keyword=annexin A2
en-keyword=integrin
kn-keyword=integrin
en-keyword=cancer microenvironment
kn-keyword=cancer microenvironment
END