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=197
cd-vols=
no-issue=
article-no=
start-page=115301
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=Fraglide-1 from traditional Chinese aromatic vinegar: A natural AhR antagonist for atopic dermatitis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Traditional Chinese Zhenjiang aromatic vinegar (Kozu) contains Fraglide-1 (FG1), a bioactive lactone with demonstrated peroxisome proliferator-activated receptor gamma (PPARγ) agonist and antioxidant activities. This study explored FG1's novel ability to antagonize the aryl hydrocarbon receptor (AhR) signaling pathway, which regulates artemin expression and contributes to itching and inflammation in atopic dermatitis. Through molecular docking simulations and cell-based assays in human keratinocytes, we demonstrated FG1's potent antagonistic activity against AhR signaling. FG1 effectively suppressed FICZ-induced inflammatory responses, including artemin expression, with potency (half maximal inhibitory concentration, IC50 = 5.1 μM) comparable to the synthetic antagonist StemRegenin 1 (SR1) while demonstrating a superior safety profile (median lethal concentration, LC50 > 100 μM vs. 27.5 μM for SR1). These findings expand our understanding of bioactive compounds from traditional fermented foods and their regulatory effects on AhR signaling, providing a foundation for future studies on FG1's role in modulating skin inflammation.
en-copyright=
kn-copyright=

en-aut-name=KatoKosuke
en-aut-sei=Kato
en-aut-mei=Kosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=AkamatsuMiki
en-aut-sei=Akamatsu
en-aut-mei=Miki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KakimaruSaya
en-aut-sei=Kakimaru
en-aut-mei=Saya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KoreishiMayuko
en-aut-sei=Koreishi
en-aut-mei=Mayuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TakagiMasahiro
en-aut-sei=Takagi
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MiyashitaMasahiro
en-aut-sei=Miyashita
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
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=7
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=8
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=9
ORCID=

en-aut-name=TsujinoYoshio
en-aut-sei=Tsujino
en-aut-mei=Yoshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
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 Environmental and Life Science, 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=School of Materials Science, Japan Advanced Institute of Science and Technology
kn-affil=

affil-num=6
en-affil=Graduate School of Agriculture, Kyoto University
kn-affil=

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

affil-num=8
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=9
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=10
en-affil=Graduate School of Science, Technology and Innovation, Kobe University
kn-affil=
en-keyword=AhR
kn-keyword=AhR
en-keyword=Xenobiotic responsive element
kn-keyword=Xenobiotic responsive element
en-keyword=StemRegenin 1
kn-keyword=StemRegenin 1
en-keyword=ARNT
kn-keyword=ARNT
en-keyword=Atopic dermatitis
kn-keyword=Atopic dermatitis
en-keyword=Artemin
kn-keyword=Artemin
END

start-ver=1.4
cd-journal=joma
no-vol=125
cd-vols=
no-issue=
article-no=
start-page=106672
end-page=
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=Resveratrol, a food-derived polyphenol, promotes Melanosomal degradation in skin fibroblasts through coordinated activation of autophagy, lysosomal, and antioxidant pathways
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Resveratrol, a polyphenol found in grapes and peanuts, is known for diverse biological activities, yet its effects on dermal hyperpigmentation (so-called dark spots) remain unexplored. We investigated resveratrol's ability to enhance melanosomal degradation in human dermal fibroblasts. At concentrations of 25-50 mu M, resveratrol increased autophagy as measured by microtubule-associated protein 1A/1B-light chain 3 (LC3)-II/LC3-I ratio and enhanced lysosomal activity as assessed by a lysosomal activity reporter system. RNA sequencing revealed upregulation of lysosomal and autophagy-related genes, including cathepsins. Furthermore, reporter assays showed resveratrol's activation of antioxidant response via nuclear factor erythroid 2-related factor 2 (NRF2)mediated, leading to upregulation of transcription factor EB/transcription factor E3 (TFEB/TFE3), master regulators of lysosomal function. In fibroblasts pre-loaded with melanosomes, resveratrol reduced melanosome content compared to control by day 3. The findings reveal the activation of interconnected autophagy, lysosomal, and antioxidant pathways by resveratrol, suggesting potential applications in functional foods targeting dermal hyperpigmentation.
en-copyright=
kn-copyright=

en-aut-name=OkamotoSaki
en-aut-sei=Okamoto
en-aut-mei=Saki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KakimaruSaya
en-aut-sei=Kakimaru
en-aut-mei=Saya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KoreishiMayuko
en-aut-sei=Koreishi
en-aut-mei=Mayuko
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=NakamuraYoshimasa
en-aut-sei=Nakamura
en-aut-mei=Yoshimasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=AndoHideya
en-aut-sei=Ando
en-aut-mei=Hideya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TsujinoYoshio
en-aut-sei=Tsujino
en-aut-mei=Yoshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
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=8
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=National Institute of Genetics, ROIS
kn-affil=

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

affil-num=6
en-affil=Department of Applied Chemistry and Biotechnology, Okayama University of Science
kn-affil=

affil-num=7
en-affil=Graduate School of Science, Technology, and Innovation, Kobe University
kn-affil=

affil-num=8
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
en-keyword=Antioxidant
kn-keyword=Antioxidant
en-keyword=Lysosomes
kn-keyword=Lysosomes
en-keyword=Autophagy
kn-keyword=Autophagy
en-keyword=Resveratrol
kn-keyword=Resveratrol
en-keyword=Skin fibroblasts
kn-keyword=Skin fibroblasts
en-keyword=Bioactive compounds
kn-keyword=Bioactive compounds
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=
aut-affil-num=6
ORCID=

en-aut-name=TadaNatsume
en-aut-sei=Tada
en-aut-mei=Natsume
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=GotohAkira
en-aut-sei=Gotoh
en-aut-mei=Akira
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
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=9
ORCID=

en-aut-name=HatanoNaoya
en-aut-sei=Hatano
en-aut-mei=Naoya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
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=11
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=12
ORCID=

en-aut-name=SunatsukiYukinari
en-aut-sei=Sunatsuki
en-aut-mei=Yukinari
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=NilssonUlf J.
en-aut-sei=Nilsson
en-aut-mei=Ulf J.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
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=15
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=16
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=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=19
cd-vols=
no-issue=1
article-no=
start-page=e0296408
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240105
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Aromatic oil from lavender as an atopic dermatitis suppressant
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=In atopic dermatitis (AD), nerves are abnormally stretched near the surface of the skin, making it sensitive to itching. Expression of neurotrophic factor Artemin (ARTN) involved in such nerve stretching is induced by the xenobiotic response (XRE) to air pollutants and UV radiation products. Therefore, AD can be monitored by the XRE response. Previously, we established a human keratinocyte cell line stably expressing a NanoLuc reporter gene downstream of XRE. We found that 6-formylindolo[3,2-b]carbazole (FICZ), a tryptophan metabolite and known inducer of the XRE, increased reporter and Artemin mRNA expression, indicating that FICZ-treated cells could be a model for AD. Lavender essential oil has been used in folk medicine to treat AD, but the scientific basis for its use is unclear. In the present study, we investigated the efficacy of lavender essential oil and its major components, linalyl acetate and linalool, to suppress AD and sensitize skin using the established AD model cell line, and keratinocyte and dendritic cell activation assays. Our results indicated that lavender essential oil from L. angustifolia and linalyl acetate exerted a strong AD inhibitory effect and almost no skin sensitization. Our model is useful in that it can circumvent the practice of using animal studies to evaluate AD medicines.
en-copyright=
kn-copyright=

en-aut-name=SatoHaruna
en-aut-sei=Sato
en-aut-mei=Haruna
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KatoKosuke
en-aut-sei=Kato
en-aut-mei=Kosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KoreishiMayuko
en-aut-sei=Koreishi
en-aut-mei=Mayuko
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=TsujinoYoshio
en-aut-sei=Tsujino
en-aut-mei=Yoshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
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=6
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 Environmental and Life Science, Okayama University
kn-affil=

affil-num=5
en-affil=Graduate School of Science, Technology, and Innovation, Kobe University
kn-affil=

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

start-ver=1.4
cd-journal=joma
no-vol=16
cd-vols=
no-issue=1
article-no=
start-page=3
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20211108
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Evaluation of skin sensitization based on interleukin‑2 promoter activation in Jurkat cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Skin sensitization is an allergic reaction caused by certain chemical substances, and is an important factor to be taken into consideration when evaluating the safety of numerous types of products. Although animal testing has long been used to evaluate skin sensitization, the recent trend to regulate such testing has led to the development and use of alternative methods. Skin sensitization reactions are summarized in the form of an adverse outcome pathway consisting of four key events (KE), including covalent binding to skin proteins (KE1), keratinocyte activation (KE2), and dendritic cell activation (KE3). Equivalent alternative methods have been developed for KE1 to KE3, but no valid alternative has yet been developed for the evaluation of KE4 and T‑cell activation. Current alternative methods rely on data from KE1 to KE3 to predict the effect of chemicals on skin sensitization. The addition of KE4 data is expected to improve the accuracy and reproducibility of such predictions. The aim of this study was to establish an assay to evaluate KE4 T‑cell activation to supplement data on skin sensitization related to KE4. To evaluate T‑cell activation, the Jurkat T‑cell line stably expressing luciferase downstream of the pro‑inflammatory cytokine interleukin‑2 promoter was used. After exposure to known skin sensitizing agents and control substances, luciferase activity measurements revealed that this assay was valid for evaluating skin sensitization. However, two skin sensitizers known to have immunosuppressive effects on T‑cells reacted negatively in this assay. The results revealed that this assay simultaneously allows for monitoring of the skin sensitization and immuno‑suppressiveness of chemical substances and supplements KE4 T‑cell activation data, and may thus contribute to reducing the use of animal experiments.
en-copyright=
kn-copyright=

en-aut-name=NagahataTaichi
en-aut-sei=Nagahata
en-aut-mei=Taichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TsujinoYoshio
en-aut-sei=Tsujino
en-aut-mei=Yoshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TakayamaEiji
en-aut-sei=Takayama
en-aut-mei=Eiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HikasaHaruka
en-aut-sei=Hikasa
en-aut-mei=Haruka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
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=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 Science, Technology and Innovation, Kobe University
kn-affil=

affil-num=3
en-affil=Department of Oral Biochemistry, Asahi University School of Dentistry
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=skin sensitization
kn-keyword=skin sensitization
en-keyword=immunotoxicity
kn-keyword=immunotoxicity
en-keyword=interleukin-2 promoter
kn-keyword=interleukin-2 promoter
en-keyword=Jurkat
kn-keyword=Jurkat
en-keyword=T-cell activation
kn-keyword=T-cell activation
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=235
end-page=246
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20221214
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=An Electron Tomographic Analysis of Giantin-Deficient Golgi Proposes a New Function of the Golgin Protein Family
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The Golgi apparatus is an organelle that mediates modifications, sorting, and transport of proteins and lipids. Golgins are a group of proteins with coiled-coil structures that localize to the Golgi and are thought to function as tethers to facilitate the docking of vesicles, Rab GTPases, and cytoskeleton components to the Golgi stack. Giantin is the longest golgin and has been thought to function as a tether for COPI vesicles along with other golgins, such as p115 and GM130. Contrary to our expectation that the loss of the tether will result in an increase in untethered COPI vesicles in the cytoplasm, our electron microscopy observations showed that the fenestrae normally present in Golgi cisternae were reduced upon Giantin knockdown. We also found that this structural change is accompanied by altered secretion of cargo proteins and cell surface glycosylation. These results indicate that there exists a correlation between Golgi structural changes caused by the loss of Giantin and Golgi function. Here, we describe electron tomography methods for the detection of structural changes in the Golgi.
en-copyright=
kn-copyright=

en-aut-name=SatohAyano
en-aut-sei=Satoh
en-aut-mei=Ayano
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=Hayashi-NishinoMitsuko
en-aut-sei=Hayashi-Nishino
en-aut-mei=Mitsuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NishinoKunihiko
en-aut-sei=Nishino
en-aut-mei=Kunihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=Institute of Scientific and Industrial Research, Osaka University
kn-affil=

affil-num=3
en-affil=Institute of Scientific and Industrial Research, Osaka University
kn-affil=
en-keyword=Golgi
kn-keyword=Golgi
en-keyword=Golgin
kn-keyword=Golgin
en-keyword=Giantin
kn-keyword=Giantin
en-keyword=Electron tomography
kn-keyword=Electron tomography
en-keyword=3D modeling
kn-keyword=3D modeling
en-keyword=Vesicles
kn-keyword=Vesicles
END

start-ver=1.4
cd-journal=joma
no-vol=18
cd-vols=
no-issue=2
article-no=
start-page=e0281516
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230213
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Fucosyltransferase 8 (FUT8) and core fucose expression in oxidative stress response
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=GlycoMaple is a new tool to predict glycan structures based on the expression levels of 950 genes encoding glycan biosynthesis-related enzymes and proteins using RNA-seq data. The antioxidant response, protecting cells from oxidative stress, has been focused on because its activation may relieve pathological conditions, such as neurodegenerative diseases. Genes involved in the antioxidant response are defined within the GO:0006979 category, including 441 human genes. Fifteen genes overlap between the glycan biosynthesis-related genes defined by GlycoMaple and the antioxidant response genes defined by GO:0006979, one of which is FUT8. 5-Hydroxy-4-phenyl-butenolide (5H4PB) extracted from Chinese aromatic vinegar induces the expression of a series of antioxidant response genes that protect cells from oxidative stress via activation of the nuclear factor erythroid 2-related factor 2-antioxidant response element pathway. Here, we show that FUT8 is upregulated in both our RNA-seq data set of 5H4PB-treated cells and publicly available RNA-seq data set of cells treated with another antioxidant, sulforaphane. Applying our RNA-seq data set to GlycoMaple led to a prediction of an increase in the core fucose of N-glycan that was confirmed by flow cytometry using a fucose-binding lectin. These results suggest that FUT8 and core fucose expression may increase upon the antioxidant response.
en-copyright=
kn-copyright=

en-aut-name=KyunaiYuki
en-aut-sei=Kyunai
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
ORCID=

en-aut-name=KoreishiMayuko
en-aut-sei=Koreishi
en-aut-mei=Mayuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TsujinoYoshio
en-aut-sei=Tsujino
en-aut-mei=Yoshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
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=5
ORCID=

affil-num=1
en-affil=Department of Applied Chemistry and Biotechnology, Faculty of Engineering, Okayama University
kn-affil=

affil-num=2
en-affil=National Institute of Genetics, ROIS
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 Science, Technology, and Innovation, Kobe University
kn-affil=

affil-num=5
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=23
cd-vols=
no-issue=19
article-no=
start-page=11035
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220920
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Immune State Conversion of the Mesenteric Lymph Node in a Mouse Breast Cancer Model
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Secondary lymphoid tissues, such as the spleen and lymph nodes (LNs), contribute to breast cancer development and metastasis in both anti- and pro-tumoral directions. Although secondary lymphoid tissues have been extensively studied, very little is known about the immune conversion in mesenteric LNs (mLNs) during breast cancer development. Here, we demonstrate inflammatory immune conversion of mLNs in a metastatic 4T1 breast cancer model. Splenic T cells were significantly decreased and continuously suppressed IFN-gamma production during tumor development, while myeloid-derived suppressor cells (MDSCs) were dramatically enriched. However, T cell numbers in the mLN did not decrease, and the MDSCs only moderately increased. T cells in the mLN exhibited conversion from a pro-inflammatory state with high IFN-gamma expression to an anti-inflammatory state with high expression of IL-4 and IL-10 in early- to late-stages of breast cancer development. Interestingly, increased migration of CD103(+)CD11b(+) dendritic cells (DCs) into the mLN, along with increased (1 -> 3)-beta-D-glucan levels in serum, was observed even in late-stage breast cancer. This suggests that CD103(+)CD11b(+) DCs could prime cancer-reactive T cells. Together, the data indicate that the mLN is an important lymphoid tissue contributing to breast cancer development.
en-copyright=
kn-copyright=

en-aut-name=ShigehiroTsukasa
en-aut-sei=Shigehiro
en-aut-mei=Tsukasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=UenoMaho
en-aut-sei=Ueno
en-aut-mei=Maho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KijihiraMayumi
en-aut-sei=Kijihira
en-aut-mei=Mayumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TakahashiRyotaro
en-aut-sei=Takahashi
en-aut-mei=Ryotaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=UmemuraChiho
en-aut-sei=Umemura
en-aut-mei=Chiho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
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=6
ORCID=

en-aut-name=KurosakaChisaki
en-aut-sei=Kurosaka
en-aut-mei=Chisaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=AsayamaMegumi
en-aut-sei=Asayama
en-aut-mei=Megumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MurakamiHiroshi
en-aut-sei=Murakami
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
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=10
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=11
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=12
ORCID=

en-aut-name=MasudaJunko
en-aut-sei=Masuda
en-aut-mei=Junko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

affil-num=1
en-affil=Research Institute for Biomedical Sciences, Tokyo University of Science
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=Department of Applied Chemistry and Biotechnology, Faculty of Engineering, 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=Division of Medical Bioengineering, Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=6
en-affil=Division of Medical Bioengineering, Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Applied Chemistry and Biotechnology, Faculty of Engineering, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Applied Chemistry and Biotechnology, Faculty of Engineering, Okayama University
kn-affil=

affil-num=9
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=10
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=11
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=12
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=13
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
en-keyword=breast cancer cells
kn-keyword=breast cancer cells
en-keyword=dendritic cells
kn-keyword=dendritic cells
en-keyword=mesenteric lymph node
kn-keyword=mesenteric lymph node
en-keyword=myeloid-derived suppressor cells
kn-keyword=myeloid-derived suppressor cells
END

start-ver=1.4
cd-journal=joma
no-vol=28
cd-vols=
no-issue=37
article-no=
start-page=e202201253
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220523
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Design and Synthesis of Glycosylated Cholera Toxin B Subunit as a Tracer of Glycoprotein Trafficking in Organelles of Living Cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Glycosylation of proteins is known to be essential for changing biological activity and stability of glycoproteins on the cell surfaces and in body fluids. Delivering of homogeneous glycoproteins into the endoplasmic reticulum (ER) and the Golgi apparatus would enable us to investigate the function of asparagine-linked (N-) glycans in the organelles. In this work, we designed and synthesized an intentionally glycosylated cholera toxin B-subunit (CTB) to be transported to the organelles of mammalian cells. The heptasaccharide, the intermediate structure of various complex-type N-glycans, was introduced to the CTB. The synthesized monomeric glycosyl-CTB successfully entered mammalian cells and was transported to the Golgi and the ER, suggesting the potential use of synthetic CTB to deliver and investigate the functions of homogeneous N-glycans in specific organelles of living cells.
en-copyright=
kn-copyright=

en-aut-name=MakiYuta
en-aut-sei=Maki
en-aut-mei=Yuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KawataKazuki
en-aut-sei=Kawata
en-aut-mei=Kazuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=LiuYanbo
en-aut-sei=Liu
en-aut-mei=Yanbo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=GooKang‐Ying
en-aut-sei=Goo
en-aut-mei=Kang‐Ying
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=OkamotoRyo
en-aut-sei=Okamoto
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KajiharaYasuhiro
en-aut-sei=Kajihara
en-aut-mei=Yasuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
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=7
ORCID=

affil-num=1
en-affil=Department of Chemistry, Graduate School of Science, Osaka University
kn-affil=

affil-num=2
en-affil=Department of Chemistry, Graduate School of Science, Osaka University
kn-affil=

affil-num=3
en-affil=Department of Chemistry, Graduate School of Science, Osaka University
kn-affil=

affil-num=4
en-affil=Department of Chemistry, Graduate School of Science, Osaka University
kn-affil=

affil-num=5
en-affil=Department of Chemistry, Graduate School of Science, Osaka University
kn-affil=

affil-num=6
en-affil=Department of Chemistry, Graduate School of Science, Osaka University
kn-affil=

affil-num=7
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
en-keyword=glycoprotein
kn-keyword=glycoprotein
en-keyword=N-glycan
kn-keyword=N-glycan
en-keyword=cholera toxin
kn-keyword=cholera toxin
en-keyword=native chemical ligation
kn-keyword=native chemical ligation
en-keyword=live imaging
kn-keyword=live imaging
END

start-ver=1.4
cd-journal=joma
no-vol=23
cd-vols=
no-issue=3
article-no=
start-page=1762
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220203
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A Major Intestinal Catabolite of Quercetin Glycosides, 3-Hydroxyphenylacetic Acid, Protects the Hepatocytes from the Acetaldehyde-Induced Cytotoxicity through the Enhancement of the Total Aldehyde Dehydrogenase Activity
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Aldehyde dehydrogenases (ALDHs) are the major enzyme superfamily for the aldehyde metabolism. Since the ALDH polymorphism leads to the accumulation of acetaldehyde, we considered that the enhancement of the liver ALDH activity by certain food ingredients could help prevent alcohol-induced chronic diseases. Here, we evaluated the modulating effects of 3-hydroxyphenylacetic acid (OPAC), the major metabolite of quercetin glycosides, on the ALDH activity and acetaldehyde-induced cytotoxicity in the cultured cell models. OPAC significantly enhanced the total ALDH activity not only in mouse hepatoma Hepa1c1c7 cells, but also in human hepatoma HepG2 cells. OPAC significantly increased not only the nuclear level of aryl hydrocarbon receptor (AhR), but also the AhR-dependent reporter gene expression, though not the nuclear factor erythroid-2-related factor 2 (Nrf2)-dependent one. The pretreatment of OPAC at the concentration required for the ALDH upregulation completely inhibited the acetaldehyde-induced cytotoxicity. Silencing AhR impaired the resistant effect of OPAC against acetaldehyde. These results strongly suggested that OPAC protects the cells from the acetaldehyde-induced cytotoxicity, mainly through the AhR-dependent and Nrf2-independent enhancement of the total ALDH activity. Our findings suggest that OPAC has a protective potential in hepatocyte models and could offer a new preventive possibility of quercetin glycosides for targeting alcohol-induced chronic diseases.
en-copyright=
kn-copyright=

en-aut-name=LiuYujia
en-aut-sei=Liu
en-aut-mei=Yujia
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MyojinTakumi
en-aut-sei=Myojin
en-aut-mei=Takumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=LiKexin
en-aut-sei=Li
en-aut-mei=Kexin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KuritaAyuki
en-aut-sei=Kurita
en-aut-mei=Ayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SetoMasayuki
en-aut-sei=Seto
en-aut-mei=Masayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MotoyamaAyano
en-aut-sei=Motoyama
en-aut-mei=Ayano
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=LiuXiaoyang
en-aut-sei=Liu
en-aut-mei=Xiaoyang
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
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=8
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=9
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=10
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=11
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=12
ORCID=

affil-num=1
en-affil=School of Biological Engineering, Dalian Polytechnic 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=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=9
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

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

affil-num=11
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=12
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
en-keyword=3-hydroxyphenylacetic acid
kn-keyword=3-hydroxyphenylacetic acid
en-keyword=aldehyde dehydrogenase
kn-keyword=aldehyde dehydrogenase
en-keyword=quercetin metabolites
kn-keyword=quercetin metabolites
en-keyword=aryl hydrocarbon receptor
kn-keyword=aryl hydrocarbon receptor
en-keyword=acetaldehyde
kn-keyword=acetaldehyde
END

start-ver=1.4
cd-journal=joma
no-vol=24
cd-vols=
no-issue=1
article-no=
start-page=18
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20211023
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Synthesis and characterization of conductive flexible cellulose carbon nanohorn sheets for human tissue applications
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background<br>
Conductive sheets of cellulose and carbon nanomaterials and its human skin applications are an interesting research aspect as they have potential for applications for skin compatibility. Hence it is needed to explore the effects and shed light on these applications.<br>
Method<br>
To fabricate wearable, portable, flexible, lightweight, inexpensive, and biocompatible composite materials, carbon nanohorns (CNHs) and hydroxyethylcellulose (HEC) were used as precursors to prepare CNH-HEC (Cnh-cel) composite sheets. Cnh-cel sheets were prepared with different loading concentrations of CNHs (10, 20 50,100mg) in 200mg cellulose. To fabricate the bio-compatible sheets, a pristine composite of CNHs and HEC was prepared without any pretreatment of the materials.<br>
Results<br>
The obtained sheets possess a conductivity of 1.83x10(-10)S/m and bio-compatible with human skin. Analysis for skin-compatibility was performed for Cnh-cel sheets by h-CLAT in vitro skin sensitization tests to evaluate the activation of THP-1 cells. It was found that THP-1 cells were not activated by Cnh-cel; hence Cnh-cel is a safe biomaterial for human skin. It was also found that the composite allowed only a maximum loading of 100mg to retain the consistent geometry of free-standing sheets of <100<mu>m thickness. Since CNHs have a unique arrangement of aggregates (dahlia structure), the composite is homogeneous, as verified by transmission electron microscopy (TEM) and, scanning electron microscopy (SEM), and other functional properties investigated by Raman spectroscopy, Fourier transform infrared spectroscopy (FT-IR), conductivity measurement, tensile strength measurement, and skin sensitization.<br>
Conclusion<br>
It can be concluded that cellulose and CNHs sheets are conductive and compatible to human skin applications.
en-copyright=
kn-copyright=

en-aut-name=SelvamKarthik Paneer
en-aut-sei=Selvam
en-aut-mei=Karthik Paneer
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NagahataTaichi
en-aut-sei=Nagahata
en-aut-mei=Taichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KatoKosuke
en-aut-sei=Kato
en-aut-mei=Kosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KoreishiMayuko
en-aut-sei=Koreishi
en-aut-mei=Mayuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
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=5
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=6
ORCID=

en-aut-name=NishikawaTakeshi
en-aut-sei=Nishikawa
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
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=8
ORCID=

en-aut-name=HayashiYasuhiko
en-aut-sei=Hayashi
en-aut-mei=Yasuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
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 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 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 Natural Science and Technology, Okayama University
kn-affil=

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

affil-num=9
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=
en-keyword=Carbon Nanohorns
kn-keyword=Carbon Nanohorns
en-keyword=Cellulose
kn-keyword=Cellulose
en-keyword=Skin sensitization
kn-keyword=Skin sensitization
en-keyword=Composites
kn-keyword=Composites
en-keyword=Bio-compatible
kn-keyword=Bio-compatible
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=2021
dt-pub=2021
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=3D model of control Golgi
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=SatohAyano
en-aut-sei=Satoh
en-aut-mei=Ayano
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
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=2021
dt-pub=2021
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title= 3D model of Giantin deficient Golgi
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=SatohAyano
en-aut-sei=Satoh
en-aut-mei=Ayano
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
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=2021
dt-pub=2021
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Cover slide rack
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=KyunaiYuki M
en-aut-sei=Kyunai
en-aut-mei=Yuki M
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
ORCID=

affil-num=1
en-affil=Faculty of Engineering, Department of Applied Chemistry and Biotechnology, Okayama University
kn-affil=

affil-num=2
en-affil=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=1
article-no=
start-page=4798
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200316
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Development of an experimental method of systematically estimating protein expression limits in HEK293 cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Protein overexpression sometimes causes cellular defects, although the underlying mechanism is still unknown. A protein's expression limit, which triggers cellular defects, is a useful indication of the underlying mechanism. In this study, we developed an experimental method of estimating the expression limits of target proteins in the human embryonic kidney cell line HEK293 by measuring the proteins' expression levels in cells that survived after the high-copy introduction of plasmid DNA by which the proteins were expressed under a strong cytomegalovirus promoter. The expression limits of nonfluorescent target proteins were indirectly estimated by measuring the levels of green fluorescent protein (GFP) connected to the target proteins with the self-cleaving sequence P2A. The expression limit of a model GFP was similar to 5.0% of the total protein, and sustained GFP overexpression caused cell death. The expression limits of GFPs with mitochondria-targeting signals and endoplasmic reticulum localization signals were 1.6% and 0.38%, respectively. The expression limits of four proteins involved in vesicular trafficking were far lower compared to a red fluorescent protein. The protein expression limit estimation method developed will be valuable for defining toxic proteins and consequences of protein overexpression.
en-copyright=
kn-copyright=

en-aut-name=MoriYoshihiro
en-aut-sei=Mori
en-aut-mei=Yoshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YoshidaYuki
en-aut-sei=Yoshida
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
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=3
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=4
ORCID=

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

affil-num=2
en-affil=Sony Computer Science Laboratories
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=Research Core for Interdisciplinary Sciences, Okayama University
kn-affil=
en-keyword=Biological techniques
kn-keyword=Biological techniques
en-keyword=Cell biology
kn-keyword=Cell biology
en-keyword=Gene expression analysis
kn-keyword=Gene expression analysis
en-keyword=Molecular biology
kn-keyword=Molecular biology
en-keyword=Protein translocation
kn-keyword=Protein translocation
en-keyword=Protein transport
kn-keyword=Protein transport
END

start-ver=1.4
cd-journal=joma
no-vol=12
cd-vols=
no-issue=5
article-no=
start-page=1260
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200516
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Knockout of MMP3 Weakens Solid Tumor Organoids and Cancer Extracellular Vesicles
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The tumor organoid (tumoroid) model in three-dimensional (3D) culture systems has been developed to reflect more closely the in vivo tumors than 2D-cultured tumor cells. Notably, extracellular vesicles (EVs) are efficiently collectible from the culture supernatant of gel-free tumoroids. Matrix metalloproteinase (MMP) 3 is a multi-functional factor playing crucial roles in tumor progression. However, roles of MMP3 within tumor growth and EVs have not unveiled. Here, we investigated the protumorigenic roles of MMP3 on integrities of tumoroids and EVs. We generated MMP3-knockout (KO) cells using the CRISPR/Cas9 system from rapidly metastatic LuM1 tumor cells. Moreover, we established fluorescent cell lines with palmitoylation signal-fused fluorescent proteins (tdTomato and enhanced GFP). Then we confirmed the exchange of EVs between cellular populations and tumoroids. LuM1-tumoroids released large EVs (200-1000 nm) and small EVs (50-200 nm) while the knockout of MMP3 resulted in the additional release of broken EVs from tumoroids. The loss of MMP3 led to a significant reduction in tumoroid size and the development of the necrotic area within tumoroids. MMP3 and CD9 (a category-1 EV marker tetraspanin protein) were significantly down-regulated in MMP3-KO cells and their EV fraction. Moreover, CD63, another member of the tetraspanin family, was significantly reduced only in the EVs fractions of the MMP3-KO cells compared to their counterpart. These weakened phenotypes of MMP3-KO were markedly rescued by the addition of MMP3-rich EVs or conditioned medium (CM) collected from LuM1-tumoroids, which caused a dramatic rise in the expression of MMP3, CD9, and Ki-67 (a marker of proliferating cells) in the MMP3-null/CD9-low tumoroids. Notably, MMP3 enriched in tumoroids-derived EVs and CM deeply penetrated recipient MMP3-KO tumoroids, resulting in a remarkable enlargement of solid tumoroids, while MMP3-null EVs did not. These data demonstrate that EVs can mediate molecular transfer of MMP3, resulting in increasing the proliferation and tumorigenesis, indicating crucial roles of MMP3 in tumor progression.
en-copyright=
kn-copyright=

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=1
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=2
ORCID=

en-aut-name=OkushaYuka
en-aut-sei=Okusha
en-aut-mei=Yuka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KawaiHotaka
en-aut-sei=Kawai
en-aut-mei=Hotaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=OoMay Wathone
en-aut-sei=Oo
en-aut-mei=May Wathone
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ElseoudiAbdellatif
en-aut-sei=Elseoudi
en-aut-mei=Abdellatif
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=LuYanyin
en-aut-sei=Lu
en-aut-mei=Yanyin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NagatsukaHitoshi
en-aut-sei=Nagatsuka
en-aut-mei=Hitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
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=9
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=10
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=11
ORCID=

en-aut-name=EguchiTakanori
en-aut-sei=Eguchi
en-aut-mei=Takanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
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=Department of Dental Pharmacology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

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

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

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

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

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

affil-num=8
en-affil=Department of Oral Pathology and Medicine, 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=

affil-num=10
en-affil=Department of Medical Bioengineering, Okayama University Graduate School of Natural Science and Technology
kn-affil=

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

affil-num=12
en-affil=Department of Dental Pharmacology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=matrix metalloproteinase 3 (MMP3)
kn-keyword=matrix metalloproteinase 3 (MMP3)
en-keyword=extracellular vesicles (EVs)
kn-keyword=extracellular vesicles (EVs)
en-keyword=tumoroid
kn-keyword=tumoroid
en-keyword=tumor organoid
kn-keyword=tumor organoid
en-keyword=tumorigenesis
kn-keyword=tumorigenesis
en-keyword=three-dimensional (3D) culture system
kn-keyword=three-dimensional (3D) culture system
END

start-ver=1.4
cd-journal=joma
no-vol=12
cd-vols=
no-issue=1
article-no=
start-page=82
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=20191229
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Hematopoietic Cells Derived from Cancer Stem Cells Generated from Mouse Induced Pluripotent Stem Cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Cancer stem cells (CSCs) represent the subpopulation of cancer cells with the ability to differentiate into other cell phenotypes and initiated tumorigenesis. Previously, we reported generating CSCs from mouse induced pluripotent stem cells (miPSCs). Here, we investigated the ability of the CSCs to differentiate into hematopoietic cells. First, the primary cells were isolated from malignant tumors that were formed by the CSCs. Non-adherent cells (NACs) that arose from adherent cells were collected and their viability, as well as the morphology and expression of hematopoietic cell markers, were analyzed. Moreover, NACs were injected into the tail vein of busulfan conditioned Balb/c nude mice. Finally, CSCs were induced to differentiate to macrophages while using IL3 and SCF. The round nucleated NACs were found to be viable, positive for hematopoietic lineage markers and CD34, and expressed hematopoietic markers, just like homing to the bone marrow. When NACs were injected into mice, Wright-Giemsa staining showed that the number of white blood cells got higher than those in the control mice after four weeks. CSCs also showed the ability to differentiate toward macrophages. CSCs were demonstrated to have the potential to provide progenies with hematopoietic markers, morphology, and homing ability to the bone marrow, which could give new insight into the tumor microenvironment according to the plasticity of CSCs.
en-copyright=
kn-copyright=

en-aut-name=HassanGhmkin
en-aut-sei=Hassan
en-aut-mei=Ghmkin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=AfifySaid M.
en-aut-sei=Afify
en-aut-mei=Said M.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NairNeha
en-aut-sei=Nair
en-aut-mei=Neha
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KumonKazuki
en-aut-sei=Kumon
en-aut-mei=Kazuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=OsmanAmira
en-aut-sei=Osman
en-aut-mei=Amira
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=DuJuan
en-aut-sei=Du
en-aut-mei=Juan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MansourHager
en-aut-sei=Mansour
en-aut-mei=Hager
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=Abu QuoraHagar A.
en-aut-sei=Abu Quora
en-aut-mei=Hagar A.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=NawaraHend M.
en-aut-sei=Nawara
en-aut-mei=Hend M.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
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=10
ORCID=

en-aut-name=ZahraMaram H.
en-aut-sei=Zahra
en-aut-mei=Maram H.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=OkadaNobuhiro
en-aut-sei=Okada
en-aut-mei=Nobuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=SenoAkimasa
en-aut-sei=Seno
en-aut-mei=Akimasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=SenoMasaharu
en-aut-sei=Seno
en-aut-mei=Masaharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
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 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 Interdisciplinary Science and Engineering in Health Systems, 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=
kn-affil=Graduate School of Natural Science and Technology, Okayama University

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

affil-num=11
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=12
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=13
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=14
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
en-keyword=Induced pluripotent stem cells
kn-keyword=Induced pluripotent stem cells
en-keyword=Cancer stem cells differentiation
kn-keyword=Cancer stem cells differentiation
en-keyword=tumor microenvironment
kn-keyword=tumor microenvironment
en-keyword=hematopoietic cells
kn-keyword=hematopoietic cells
END

start-ver=1.4
cd-journal=joma
no-vol=9
cd-vols=
no-issue=
article-no=
start-page=8866
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=2019620
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Yeast screening system reveals the inhibitory mechanism of cancer cell proliferation by benzyl isothiocyanate through down-regulation of Mis12
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Benzyl isothiocyanate (BITC) is a naturally-occurring isothiocyanate derived from cruciferous vegetables. BITC has been reported to inhibit the proliferation of various cancer cells, which is believed to be important for the inhibition of tumorigenesis. However, the detailed mechanisms of action remain unclear. In this study, we employed a budding yeast Saccharomyces cerevisiae as a model organism for screening. Twelve genes including MTW1 were identified as the overexpression suppressors for the antiproliferative effect of BITC using the genome-wide multi-copy plasmid collection for S. cerevisiae. Overexpression of the kinetochore protein Mtw1 counteracts the antiproliferative effect of BITC in yeast. The inhibitory effect of BITC on the proliferation of human colon cancer HCT-116 cells was consistently suppressed by the overexpression of Mis12, a human orthologue of Mtw1, and enhanced by the knockdown of Mis12. We also found that BITC increased the phosphorylated and ubiquitinated Mis12 level with consequent reduction of Mis12, suggesting that BITC degrades Mis12 through an ubiquitin-proteasome system. Furthermore, cell cycle analysis showed that the change in the Mis12 level affected the cell cycle distribution and the sensitivity to the BITC-induced apoptosis. These results provide evidence that BITC suppresses cell proliferation through the post-transcriptional regulation of the kinetochore protein Mis12.
en-copyright=
kn-copyright=

en-aut-name=Abe-KanohNaomi
en-aut-sei=Abe-Kanoh
en-aut-mei=Naomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KunisueNarumi
en-aut-sei=Kunisue
en-aut-mei=Narumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MyojinTakumi
en-aut-sei=Myojin
en-aut-mei=Takumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ChinoAyako
en-aut-sei=Chino
en-aut-mei=Ayako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
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=5
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=6
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=7
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=8
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=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=Research Core for Interdisciplinary Sciences, 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 Natural Science and Technology, Okayama University
kn-affil=

affil-num=8
en-affil=Research Core for Interdisciplinary Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Graduate School of Environmental and Life Science, Okayama University, Okayama
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=7
cd-vols=
no-issue=
article-no=
start-page=160
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2019
dt-pub=20190827
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The Golgin Protein Giantin Regulates Interconnections Between Golgi Stacks
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract= Golgins are a family of Golgi-localized long coiled-coil proteins. The major golgin function is thought to be the tethering of vesicles, membranes, and cytoskeletal elements to the Golgi. We previously showed that knockdown of one of the longest golgins, Giantin, altered the glycosylation patterns of cell surfaces and the kinetics of cargo transport, suggesting that Giantin maintains correct glycosylation through slowing down transport within the Golgi. Giantin knockdown also altered the sizes and numbers of mini Golgi stacks generated by microtubule de-polymerization, suggesting that it maintains the independence of individual Golgi stacks. Therefore, it is presumed that Golgi stacks lose their independence following Giantin knockdown, allowing easier and possibly increased transport among stacks and abnormal glycosylation. To gain structural insights into the independence of Golgi stacks, we herein performed electron tomography and 3D modeling of Golgi stacks in Giantin knockdown cells. Compared with control cells, Giantin-knockdown cells had fewer and smaller fenestrae within each cisterna. This was supported by data showing that the diffusion rate of Golgi membrane proteins is faster in Giantin-knockdown Golgi, indicating that Giantin knockdown structurally and functionally increases connectivity among Golgi cisternae and stacks. This increased connectivity suggests that contrary to the cis-golgin tether model, Giantin instead inhibits the tether and fusion of nearby Golgi cisternae and stacks, resulting in transport difficulties between stacks that may enable the correct glycosylation of proteins and lipids passing through the Golgi.
en-copyright=
kn-copyright=

en-aut-name=SatohAyano
en-aut-sei=Satoh
en-aut-mei=Ayano
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=Hayashi-NishinoMitsuko
en-aut-sei=Hayashi-Nishino
en-aut-mei=Mitsuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ShakunoTakuto
en-aut-sei=Shakuno
en-aut-mei=Takuto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MasudaJunko
en-aut-sei=Masuda
en-aut-mei=Junko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KoreishiMayuko
en-aut-sei=Koreishi
en-aut-mei=Mayuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MurakamiRuna
en-aut-sei=Murakami
en-aut-mei=Runa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
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=7
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=8
ORCID=

en-aut-name=Abe-KanohNaomi
en-aut-sei=Abe-Kanoh
en-aut-mei=Naomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
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=10
ORCID=

en-aut-name=MalsamJoerg
en-aut-sei=Malsam
en-aut-mei=Joerg
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=YuSidney
en-aut-sei=Yu
en-aut-mei=Sidney
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=ishinoKunihiko 
en-aut-sei=ishino
en-aut-mei=Kunihiko 
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
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=Institute of Scientific and Industrial Research, Osaka 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 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=

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

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

affil-num=8
en-affil=raduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=9
en-affil=raduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=10
en-affil=esearch Institute for Radiation Biology and Medicine, Hiroshima University
kn-affil=

affil-num=11
en-affil=Center for Biochemistry (BZH), Heidelberg University
kn-affil=

affil-num=12
en-affil=School of Biomedical Sciences, The Chinese University of Hong Kong
kn-affil=

affil-num=13
en-affil=Institute of Scientific and Industrial Research, Osaka University
kn-affil=
en-keyword=Golgi
kn-keyword=Golgi
en-keyword=golgins
kn-keyword=golgins
en-keyword=glycosylation
kn-keyword=glycosylation
en-keyword=endoplasmic reticulum
kn-keyword=endoplasmic reticulum
en-keyword=electron tomography
kn-keyword=electron tomography
END

start-ver=1.4
cd-journal=joma
no-vol=25
cd-vols=
no-issue=146
article-no=
start-page=241
end-page=244
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=201311
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=ゴルジ体内の輸送：糖タンパク質の移動に関する研究
kn-title=Transport within the Golgi: for the Study of Glycoprotein Movement
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=SatohAyano
en-aut-sei=Satoh
en-aut-mei=Ayano
kn-aut-name=佐藤あやの
kn-aut-sei=佐藤
kn-aut-mei=あやの
aut-affil-num=1
ORCID=

en-aut-name=IwakiriYasuko
en-aut-sei=Iwakiri
en-aut-mei=Yasuko
kn-aut-name=岩切泰子
kn-aut-sei=岩切
kn-aut-mei=泰子
aut-affil-num=2
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院自然科学研究科

affil-num=2
en-affil=
kn-affil=エール大学医学部内科消化器科
en-keyword=Golgi
kn-keyword=Golgi
en-keyword=glycosylation
kn-keyword=glycosylation
en-keyword=intracellular trafficking
kn-keyword=intracellular trafficking
END

start-ver=1.4
cd-journal=joma
no-vol=182
cd-vols=
no-issue=3
article-no=
start-page=786
end-page=795
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=201303
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Absence of Nogo-B (Reticulon 4B) Facilitates Hepatic Stellate Cell Apoptosis and Diminishes Hepatic Fibrosis in Mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Nogo-B (reticulon 4B) accentuates hepatic fibrosis and cirrhosis, but the mechanism remains unclear. The aim of this study was to identify the role of Nogo-B in hepatic stellate cell (HSC) apoptosis in cirrhotic livers. Cirrhosis was generated by carbon tetrachloride inhalation in wild-type (WT) and Nogo-A/B knockout (Nogo-B KO) mice. HSCs were isolated from WT and Nogo-B KO mice and cultured for activation and transformation to myofibroblasts (MF-HSCs). Human hepatic stellate cells (LX2 cells) were used to assess apoptotic responses of activated HSCs after silencing or overexpressing Nogo-B. Livers from cirrhotic Nogo-B KO mice showed significantly reduced fibrosis (P < 0.05) compared with WT mice. Apoptotic cells were more prominent in fibrotic areas of cirrhotic Nogo-B KO livers. Nogo-B KO MF-HSCs showed significantly increased Levels of apoptotic markers, cleaved poly (ADP-ribose) polymerase, and caspase-3 and -8 (P < 0.05) compared with WT MF-HSCs in response to staurosporine. Treatment with tunicamycin, an endoplasmic reticulum stress inducer, increased cleaved caspase-3 and -8 levels in Nogo-B KO MF-HSCs compared with WT MF-HSCs (P < 0.01). In LX2 cells, Nogo-B knockdown enhanced apoptosis in response to staurosporine, whereas Nogo-B overexpression inhibited apoptosis. The absence of Nogo-B enhances apoptosis of HSCs in experimental cirrhosis. Selective blockade of Nogo-B in HSCs may represent a potential therapeutic strategy to mitigate liver fibrosis. (Am J Pathol 2013, 182: 786-795; http://dx.doLorg/10.1016Aajpath.2012.11.032)
en-copyright=
kn-copyright=

en-aut-name=TashiroKeitaro
en-aut-sei=Tashiro
en-aut-mei=Keitaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
ORCID=

en-aut-name=UtsumiTeruo
en-aut-sei=Utsumi
en-aut-mei=Teruo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ChungChuhan
en-aut-sei=Chung
en-aut-mei=Chuhan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=IwakiriYasuko
en-aut-sei=Iwakiri
en-aut-mei=Yasuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=
kn-affil=Yale Univ, Sch Med, Sect Digest Dis, Dept Internal Med

affil-num=2
en-affil=
kn-affil=Okayama Univ, Grad Sch Nat Sci

affil-num=3
en-affil=
kn-affil=Yale Univ, Sch Med, Sect Digest Dis, Dept Internal Med

affil-num=4
en-affil=
kn-affil=Yale Univ, Sch Med, Sect Digest Dis, Dept Internal Med

affil-num=5
en-affil=
kn-affil=Yale Univ, Sch Med, Sect Digest Dis, Dept Internal Med
END

start-ver=1.4
cd-journal=joma
no-vol=8
cd-vols=
no-issue=3
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=20130521
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The Golgin Tether Giantin Regulates the Secretory Pathway by Controlling Stack Organization within Golgi Apparatus
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Golgins are coiled-coil proteins that play a key role in the regulation of Golgi architecture and function. Giantin, the largest golgin in mammals, forms a complex with p115, rab1, GM130, and soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs), thereby facilitating vesicle tethering and fusion processes around the Golgi apparatus. Treatment with the microtubule destabilizing drug nocodazole transforms the Golgi ribbon into individual Golgi stacks. Here we show that siRNA-mediated depletion of giantin resulted in more dispersed Golgi stacks after nocodazole treatment than by control treatment, without changing the average cisternal length. Furthermore, depletion of giantin caused an increase in cargo transport that was associated with altered cell surface protein glycosylation. Drosophila S2 cells are known to have dispersed Golgi stacks and no giantin homolog. The exogenous expression of mammalian giantin cDNA in S2 cells resulted in clustered Golgi stacks, similar to the Golgi ribbon in mammalian cells. These results suggest that the spatial organization of the Golgi ribbon is mediated by giantin, which also plays a role in cargo transport and sugar modifications.
en-copyright=
kn-copyright=

en-aut-name=KoreishiMayuko
en-aut-sei=Koreishi
en-aut-mei=Mayuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=GniadekThomas J.
en-aut-sei=Gniadek
en-aut-mei=Thomas J.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YuSidney
en-aut-sei=Yu
en-aut-mei=Sidney
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MasudaJunko
en-aut-sei=Masuda
en-aut-mei=Junko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
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=5
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=6
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama Univ, Grad Sch Nat Sci & Technol

affil-num=2
en-affil=
kn-affil=Johns Hopkins Univ, Sch Med, Dept Pathol

affil-num=3
en-affil=
kn-affil=Chinese Univ Hong Kong, Sch Biomed Sci, Shatin

affil-num=4
en-affil=
kn-affil=NIAID, Mucosal Immun Sect, Lab Host Def

affil-num=5
en-affil=
kn-affil=Okayama Univ, RCIS

affil-num=6
en-affil=
kn-affil=Okayama Univ, Grad Sch Nat Sci & Technol
END

start-ver=1.4
cd-journal=joma
no-vol=8
cd-vols=
no-issue=1
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=20130118
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=CK2 Phosphorylates Sec31 and Regulates ER-To-Golgi Trafficking
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Protein export from the endoplasmic reticulum (ER) is an initial and rate-limiting step of molecular trafficking and secretion. This is mediated by coat protein II (COPII)-coated vesicles, whose formation requires small GTPase Sar1 and 6 Sec proteins including Sec23 and Sec31. Sec31 is a component of the outer layer of COPII coat and has been identified as a phosphoprotein. The initiation and promotion of COPII vesicle formation is regulated by Sar1; however, the mechanism regulating the completion of COPII vesicle formation followed by vesicle release is largely unknown. Hypothesizing that the Sec31 phosphorylation may be such a mechanism, we identified phosphorylation sites in the middle linker region of Sec31. Sec31 phosphorylation appeared to decrease its association with ER membranes and Sec23. Non-phosphorylatable mutant of Sec31 stayed longer at ER exit sites and bound more strongly to Sec23. We also found that CK2 is one of the kinases responsible for Sec31 phosphorylation because CK2 knockdown decreased Sec31 phosphorylation, whereas CK2 overexpression increased Sec31 phosphorylation. Furthermore, CK2 knockdown increased affinity of Sec31 for Sec23 and inhibited ER-to-Golgi trafficking. These results suggest that Sec31 phosphorylation by CK2 controls the duration of COPII vesicle formation, which regulates ER-to-Golgi trafficking.
en-copyright=
kn-copyright=

en-aut-name=KoreishiMayuko
en-aut-sei=Koreishi
en-aut-mei=Mayuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YuSidney
en-aut-sei=Yu
en-aut-mei=Sidney
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OdaMayumi
en-aut-sei=Oda
en-aut-mei=Mayumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
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=4
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=5
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama Univ, Grad Sch Nat Sci & Technol

affil-num=2
en-affil=
kn-affil=Chinese Univ Hong Kong, Sch Biomed Sci

affil-num=3
en-affil=
kn-affil=Okayama Univ, Grad Sch Nat Sci & Technol

affil-num=4
en-affil=
kn-affil=Okayama Univ, Res Core Interdisciplinary Sci RCIS

affil-num=5
en-affil=
kn-affil=Okayama Univ, Grad Sch Nat Sci & Technol
END

start-ver=1.4
cd-journal=joma
no-vol=7
cd-vols=
no-issue=4
article-no=
start-page=e33544
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2012
dt-pub=20120412
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A Model of Cancer Stem Cells Derived from Mouse Induced Pluripotent Stem Cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Cancer stem cells (CSCs) are capable of continuous proliferation and self-renewal and are proposed to play significant roles in oncogenesis, tumor growth, metastasis and cancer recurrence. CSCs are considered derived from normal stem cells affected by the tumor microenvironment although the mechanism of development is not clear yet. In 2007, Yamanaka's group succeeded in generating Nanog mouse induced pluripotent stem (miPS) cells, in which green fluorescent protein (GFP) has been inserted into the 5'-untranslated region of the Nanog gene. Usually, iPS cells, just like embryonic stem cells, are considered to be induced into progenitor cells, which differentiate into various normal phenotypes depending on the normal niche. We hypothesized that CSCs could be derived from Nanog miPS cells in the conditioned culture medium of cancer cell lines, which is a mimic of carcinoma microenvironment. As a result, the Nanog miPS cells treated with the conditioned medium of mouse Lewis lung carcinoma acquired characteristics of CSCs, in that they formed spheroids expressing GFP in suspension culture, and had a high tumorigenicity in Balb/c nude mice exhibiting angiogenesis in vivo. In addition, these iPS-derived CSCs had a capacity of self-renewal and expressed the marker genes, Nanog, Rex1, Eras, Esg1 and Cripto, associated with stem cell properties and an undifferentiated state. Thus we concluded that a model of CSCs was originally developed from miPS cells and proposed the conditioned culture medium of cancer cell lines might perform as niche for producing CSCs. The model of CSCs and the procedure of their establishment will help study the genetic alterations and the secreted factors in the tumor microenvironment which convert miPS cells to CSCs. Furthermore, the identification of potentially bona fide markers of CSCs, which will help the development of novel anti-cancer therapies, might be possible though the CSC model.
en-copyright=
kn-copyright=

en-aut-name=ChenLing
en-aut-sei=Chen
en-aut-mei=Ling
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KasaiTomonari
en-aut-sei=Kasai
en-aut-mei=Tomonari
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=LiYueguang
en-aut-sei=Li
en-aut-mei=Yueguang
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SugiiYuh
en-aut-sei=Sugii
en-aut-mei=Yuh
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=JinGuoliang
en-aut-sei=Jin
en-aut-mei=Guoliang
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OkadaMasashi
en-aut-sei=Okada
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=VaidyanathArun
en-aut-sei=Vaidyanath
en-aut-mei=Arun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MizutaniAkifumi
en-aut-sei=Mizutani
en-aut-mei=Akifumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
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=9
ORCID=

en-aut-name=KudohTakayuki
en-aut-sei=Kudoh
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=HendrixMary J. C.
en-aut-sei=Hendrix
en-aut-mei=Mary J. C.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=SalomonDavid S
en-aut-sei=Salomon
en-aut-mei=David S
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=FuLi
en-aut-sei=Fu
en-aut-mei=Li
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=SenoMasaharu
en-aut-sei=Seno
en-aut-mei=Masaharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama Univ

affil-num=2
en-affil=
kn-affil=Okayama Univ

affil-num=3
en-affil=
kn-affil=Tianjin 4th Ctr Hosp

affil-num=4
en-affil=
kn-affil=Okayama Univ

affil-num=5
en-affil=
kn-affil=Okayama Univ

affil-num=6
en-affil=
kn-affil=Okayama Univ

affil-num=7
en-affil=
kn-affil=Okayama Univ

affil-num=8
en-affil=
kn-affil=Okayama Univ

affil-num=9
en-affil=
kn-affil=Okayama Univ

affil-num=10
en-affil=
kn-affil=Okayama Univ

affil-num=11
en-affil=
kn-affil=Northwestern Univ

affil-num=12
en-affil=
kn-affil=NCI

affil-num=13
en-affil=
kn-affil=Tianjin Med Univ

affil-num=14
en-affil=
kn-affil=Okayama Univ
END

start-ver=1.4
cd-journal=joma
no-vol=2011
cd-vols=
no-issue=1
article-no=
start-page=5
end-page=11
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2011
dt-pub=20110809
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Detection of in situ cleaved p115 with the cut specific antibodies in rapid protein inactivation system by tobacco etch viral protease cleavage
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Gene perturbation methods are commonly used in the study of gene and protein function. The authors of this paper recently developed a rapid protein inactivation technique utilizing tobacco etch virus (TEV)-derived protease. TEV protease recognizes the ENLYFQG (Glu-Asn-Leu-Tyr-Phe-Gln-Gly) amino acid sequence and specifically cleaves between Q and G. The authors developed antibodies that recognize the cleaved TEV (ENLYFQ) sequence, both in vitro and in vivo, but do not bind to uncleaved TEV (ENLYFQG). Using these antibodies, in situ protein cleavage was successfully detected. These antibodies used in combination with the TEV protease may be a useful complement to other perturbation methods.
en-copyright=
kn-copyright=

en-aut-name=KoreishiMayuko
en-aut-sei=Koreishi
en-aut-mei=Mayuko
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=SatohAyano
en-aut-sei=Satoh
en-aut-mei=Ayano
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=The Research Core for Interdisciplinary Sciences (RCIS), Okayama University
kn-affil=

affil-num=2
en-affil=The Research Core for Interdisciplinary Sciences (RCIS), Okayama University
kn-affil=

affil-num=3
en-affil=The Research Core for Interdisciplinary Sciences (RCIS), Okayama University
kn-affil=
en-keyword=TEV protease
kn-keyword=TEV protease
en-keyword=Golgi
kn-keyword=Golgi
en-keyword=golgins
kn-keyword=golgins
en-keyword=microinjection
kn-keyword=microinjection
en-keyword=recombinant proteins
kn-keyword=recombinant proteins
END

start-ver=1.4
cd-journal=joma
no-vol=7
cd-vols=
no-issue=1
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2012
dt-pub=20120118
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=TRAPPC9 Mediates the Interaction between p150<sup>Glued</sup> and COPII Vesicles at the Target Membrane
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: The transport of endoplasmic reticulum (ER)-derived COPII vesicles toward the ER-Golgi intermediate
compartment (ERGIC) requires cytoplasmic dynein and is dependent on microtubules. p150<sup>Glued</sup>, a subunit of dynactin, has
been implicated in the transport of COPII vesicles via its interaction with COPII coat components Sec23 and Sec24. However,
whether and how COPII vesicle tether, TRAPP (Transport protein particle), plays a role in the interaction between COPII
vesicles and microtubules is currently unknown.
Principle Findings: We address the functional relationship between COPII tether TRAPP and dynactin. Overexpressed TRAPP
subunits interfered with microtubule architecture by competing p150<sup>Glued</sup> away from the MTOC. TRAPP subunit TRAPPC9
bound directly to p150<sup>Glued</sup> via the same carboxyl terminal domain of p150<sup>Glued</sup> that binds Sec23 and Sec24. TRAPPC9 also
inhibited the interaction between p150<sup>Glued</sup> and Sec23/Sec24 both in vitro and in vivo, suggesting that TRAPPC9 serves to
uncouple p150<sup>Glued</sup> from the COPII coat, and to relay the vesicle-dynactin interaction at the target membrane.
Conclusions: These findings provide a new perspective on the function of TRAPP as an adaptor between the ERGIC
membrane and dynactin. By preserving the connection between dynactin and the tethered and/or fused vesicles, TRAPP
allows nascent ERGIC to continue the movement along the microtubules as they mature into the cis-Golgi.
en-copyright=
kn-copyright=

en-aut-name=ZongMin
en-aut-sei=Zong
en-aut-mei=Min
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
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=2
ORCID=

en-aut-name=YuMei Kuen
en-aut-sei=Yu
en-aut-mei=Mei Kuen
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SiuKa Yu
en-aut-sei=Siu
en-aut-mei=Ka Yu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NgWing Yan
en-aut-sei=Ng
en-aut-mei=Wing Yan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ChaｎHsiao Chang
en-aut-sei=Chaｎ
en-aut-mei=Hsiao Chang
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TannerJulian A.
en-aut-sei=Tanner
en-aut-mei=Julian A.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YuSidney
en-aut-sei=Yu
en-aut-mei=Sidney
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=
kn-affil=School of Biomedical Sciences, The Chinese University of Hong Kong

affil-num=2
en-affil=
kn-affil=The Research Core for Interdisciplinary Science, Okayama University

affil-num=3
en-affil=
kn-affil=Epithelial Cell Biology Research Center, The Chinese University of Hong Kong,

affil-num=4
en-affil=
kn-affil=School of Biomedical Sciences, The Chinese University of Hong Kong

affil-num=5
en-affil=
kn-affil=School of Biomedical Sciences, The Chinese University of Hong Kong

affil-num=6
en-affil=
kn-affil=School of Biomedical Sciences, The Chinese University of Hong Kong

affil-num=7
en-affil=
kn-affil=Department of Biochemistry, The University of Hong Kong

affil-num=8
en-affil=
kn-affil=School of Biomedical Sciences, The Chinese University of Hong Kong
END

start-ver=1.4
cd-journal=joma
no-vol=20
cd-vols=
no-issue=19
article-no=
start-page=4205
end-page=4215
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2009
dt-pub=20091001
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=mTrs130 Is a Component of a Mammalian TRAPPII Complex, a Rab1 GEF That Binds to COPI-coated Vesicles
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The GTPase Rab1 regulates endoplasmic reticulum-Golgi and early Golgi traffic. The guanine nucleotide exchange factor (GEF) or factors that activate Rab1 at these stages of the secretory pathway are currently unknown. Trs130p is a subunit of the yeast TRAPPII (transport protein particle II) complex, a multisubunit tethering complex that is a GEF for the Rab1 homologue Ypt1p. Here, we show that mammalian Trs130 (mTrs130) is a component of an analogous TRAPP complex in mammalian cells, and we describe for the first time the role that this complex plays in membrane traffic. mTRAPPII is enriched on COPI (Coat Protein I)-coated vesicles and buds, but not Golgi cisternae, and it specifically activates Rab1. In addition, we find that mTRAPPII binds to γ1COP, a COPI coat adaptor subunit. The depletion of mTrs130 by short hairpin RNA leads to an increase of vesicles in the vicinity of the Golgi and the accumulation of cargo in an early Golgi compartment. We propose that mTRAPPII is a Rab1 GEF that tethers COPI-coated vesicles to early Golgi membranes.
en-copyright=
kn-copyright=

en-aut-name=YamasakiAkinori
en-aut-sei=Yamasaki
en-aut-mei=Akinori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MenonShekar
en-aut-sei=Menon
en-aut-mei=Shekar
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YuSidney
en-aut-sei=Yu
en-aut-mei=Sidney
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=BarrowmanJemima
en-aut-sei=Barrowman
en-aut-mei=Jemima
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MeerlooTimo
en-aut-sei=Meerloo
en-aut-mei=Timo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OorschotViola
en-aut-sei=Oorschot
en-aut-mei=Viola
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KlumpermanJudith
en-aut-sei=Klumperman
en-aut-mei=Judith
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
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=8
ORCID=

en-aut-name=Ferro-NovickSusan
en-aut-sei=Ferro-Novick
en-aut-mei=Susan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Cell Biology, Howard Hughes Medical Institute, Yale University School of Medicine

affil-num=2
en-affil=
kn-affil=Department of Cell Biology, Howard Hughes Medical Institute, Yale University School of Medicine

affil-num=3
en-affil=
kn-affil=Department of Cell Biology, Howard Hughes Medical Institute, Yale University School of Medicine

affil-num=4
en-affil=
kn-affil=Department of Cell Biology, Howard Hughes Medical Institute, Yale University School of Medicine

affil-num=5
en-affil=
kn-affil=Department of Cellular and Molecular Medicine, University of California at San Diego

affil-num=6
en-affil=
kn-affil=Cell Microscopy Center, Department of Cell Biology, University Medical Center Utrecht

affil-num=7
en-affil=
kn-affil=Cell Microscopy Center, Department of Cell Biology, University Medical Center Utrecht

affil-num=8
en-affil=
kn-affil=Department of Cell Biology, Yale University School of Medicine

affil-num=9
en-affil=
kn-affil=Department of Cell Biology, Howard Hughes Medical Institute, Yale University School of Medicine
END