FullText URL EpilepsyRes105_1_220.pdf
Author Ohmori, Iori| Hayashi, Keiichiro| Wang, Haijiao| Ouchida, Mamoru| Fujita, Naohiro| Inoue, Takushi| Michiue, Hiroyuki| Nishiki, Teiichi| Matsui, Hideki|
Published Date 2013-07
Publication Title Epilepsy Research
Volume volume105
Issue issue1-2
Publisher Elsevier Science
Start Page 220
End Page 224
ISSN 09201211
NCID AA10726642
Content Type Journal Article
language 英語
OAI-PMH Set 岡山大学
File Version author
PubMed ID 23375560
DOI 10.1016/j.eplepsyres.2013.01.003
Web of Science KeyUT 000320737500027
Related Url isVersionOf https://doi.org/10.1016/j.eplepsyres.2013.01.003
FullText URL NeurobiolDis_50_209.pdf
Author Ohmori, Iori| Ouchida, Mamoru| Kobayashi, Katsuhiro| Jitsumori, Yoshimi| Mori, Akiko| Michiue, Hiroyuki| Nishiki, Teiichi| Ohtsuka, Yoko| Matsui, Hideki|
Note CACNA1A variants contribute to severity of seizures in Dravet syndrome|
Published Date 2013-02
Publication Title Neurobiology of disease
Volume volume50
Publisher Academic Press
Start Page 209
End Page 217
ISSN 09699961
NCID AA11645502
Content Type Journal Article
language 英語
OAI-PMH Set 岡山大学
File Version author
PubMed ID 23103419
DOI 10.1016/j.nbd.2012.10.016
Web of Science KeyUT 000313758100023
Related Url isVersionOf https://doi.org/10.1016/j.nbd.2012.10.016
Author Masumoto, Toshio| Suzuki, Koichiro| Ohmori, Iori| Michiue, Hiroyuki| Tomizawa, Kazuhito| Fujimura, Atsushi| Nishiki, Tei-ichi| Matsui, Hideki|
Published Date 2012-01
Publication Title Molecular and Cellular Neuroscience
Volume volume49
Issue issue1
Content Type Journal Article
Author Fujimura, Atsushi| Michiue, Hiroyuki| Nishiki, Tei-ichi| Ohmori, Iori| Wei, Fanyan| Matsui, Hideki| Tomizawa, Kazuhito|
Published Date 2011-05-14
Publication Title PLoS ONE
Volume volume6
Issue issue3
Content Type Journal Article
FullText URL 118_205.pdf
Author 道上 宏之| 富澤 一仁| 魏 范研| 松下 正之| 陸 雲飛| 市川 智継| 田宮 隆| 松井 秀樹| 伊達 勲|
Keywords プロテインセラピー 悪性脳腫瘍 p 53 エンドソーム 蛋白導入ドメイン
Publication Title 岡山医学会雑誌
Published Date 2007-01-04
Volume volume118
Issue issue3
Start Page 205
End Page 208
ISSN 00301558
language 日本語
Copyright Holders Copyright© 岡山医学会
File Version publisher
DOI 10.4044/joma1947.118.3_205
NAID 10018454083
Author Hayashi, Keiichiro| Ueshima, Satoshi| Ouchida, Mamoru| Mashimo, Tomoji| Nishiki, Teiichi| Sendo, Toshiaki| Serikawa, Tadao| Matsui, Hideki| Ohmori, Iori|
Published Date 2011-05
Publication Title Epilepsia
Volume volume52
Issue issue5
Content Type Journal Article
JaLCDOI 10.18926/AMO/43824
FullText URL 65_1_1.pdf
Author Han, Xiao-Jian| Tomizawa, Kazuhito| Fujimura, Atsushi| Ohmori, Iori| Nishiki, Tei-ichi| Matsushita, Masayuki| Matsui, Hideki|
Abstract Mitochondria are important cellular organelles in most metabolic processes and have a highly dynamic nature, undergoing frequent fission and fusion. The dynamic balance between fission and fusion plays critical roles in mitochondrial functions. In recent studies, several large GTPases have been identified as key molecular factors in mitochondrial fission and fusion. Moreover, the posttranslational modifications of these large GTPases, including phosphorylation, ubiquitination and SUMOylation, have been shown to be involved in the regulation of mitochondrial dynamics. Neurons are particularly sensitive and vulnerable to any abnormalities in mitochondrial dynamics, due to their large energy demand and long extended processes. Emerging evidences have thus indicated a strong linkage between mitochondria and neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease and Huntington's disease. In this review, we will describe the regulation of mitochondrial dynamics and its role in neurodegenerative diseases.
Keywords mitochondria phosphorylation ubiquitination SUMOylation neurodegeneration
Amo Type Review
Published Date 2011-02
Publication Title Acta Medica Okayama
Volume volume65
Issue issue1
Publisher Okayama University Medical School
Start Page 1
End Page 10
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
Copyright Holders CopyrightⒸ 2011 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 21339790
Web of Science KeyUT 000287620500001
Title Alternative A CACNB4 mutation showing altered Ca(v)2.1 function in a patient with Dravet syndrome
FullText URL 121_149.pdf
Author Ohmori, Iori| Ouchida, Mamoru| Mimaki, Nobuyoshi| Nishiki, Teiichi| Tomizawa, Kazuhito| Matsui, Hideki|
Keywords てんかん Dravet 症候群 CACNB4遺伝子 SCN1A 遺伝子
Publication Title 岡山医学会雑誌
Published Date 2009-12-01
Volume volume121
Issue issue3
Start Page 149
End Page 156
ISSN 0030-1558
language 日本語
Copyright Holders 岡山医学会
File Version publisher
DOI 10.4044/joma.121.149
NAID 120002308814
FullText URL Epilepsia_49_3_521.pdf
Author Ohmori, Iori| Ouchida, Mamoru| Kobayashi, Katsuhiro| Jitsumori, Yoshimi| Inoue, Takushi| Shimizu, Kenji| Matsui, Hideki| Ohtsuka, Yoko| Maegaki, Yoshihiro|
Keywords Rasmussen encephalitis SCN1A genetic-environmental interaction
Published Date 2007-11-21
Publication Title Epilepsia
Volume volume49
Issue issue3
Publisher Blackwell
Start Page 521
End Page 526
ISSN 0013-9580
NCID AA00180597
Content Type Journal Article
language 英語
OAI-PMH Set 岡山大学
File Version author
PubMed ID 18031552
DOI 10.1111/j.1528-1167.2007.01411.x
Web of Science KeyUT 000253477800020
Related Url isVersionOf https://doi.org/10.1111/j.1528-1167.2007.01411.x
JaLCDOI 10.18926/AMO/31858
FullText URL fulltext.pdf
Author Ogawa, Tomoyuki| Ono, Shigeki| Ichikawa, Tomotsugu| Arimitsu, Seiji| Onoda, Keisuke| Tokunaga, Koji| Sugiu, Kenji| Tomizawa, Kazuhito| Matsui, Hideki| Date, Isao|
Abstract <p>Many studies have shown that a motif of 11 consecutive arginines (11R) is one of the most effective protein transduction domains (PTD) for introducing proteins into the cell membrane. By conjugating this &#34;11R&#34;, all sorts of proteins can effectively and harmlessly be transferred into any kind of cell. We therefore examined the transduction efficiency of 11R in cerebral arteries and obtained results showing that 11R fused enhanced green fluorescent protein (11R-EGFP) immediately and effectively penetrated all layers of the rat basilar artery (BA), especially the tunica media. This method provides a revolutionary approach to cerebral arteries and ours is the first study to demonstrate the successful transductionof a PTD fused protein into the cerebral arteries. In this review, we present an outline of our studies and other key studies related to cerebral vasospasm and 11R, problems to be overcome, and predictions regarding future use of the 11R protein transduction method for cerebral vasospasm (CV).</p>
Keywords cerebral vasospasm 11 consecutive arginines (11R) enhanced green fluorescent protein (EGFP)
Amo Type Review
Published Date 2009-02
Publication Title Acta Medica Okayama
Volume volume63
Issue issue1
Publisher Okayama University Medical School
Start Page 1
End Page 7
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 19247417
Web of Science KeyUT 000263730300001
Title Alternative Novel protein transduction method for cerebral arteries using 11R
FullText URL 120_129.pdf
Author Ogawa, Tomoyuki| Ono, Shigeki| Ichikawa, Tomotsugu| Arimitsu, Seiji| Onoda, Keisuke| Tokunaga, Koji| Sugiu, Kenji| Tomizawa, Kazuhito| Matsui, Hideki| Date, Isao|
Keywords cerebral vasospasm 11R protein transduction method
Publication Title 岡山医学会雑誌
Published Date 2008-08-01
Volume volume120
Issue issue2
Start Page 129
End Page 133
ISSN 00301558
language 日本語
Copyright Holders 岡山医学会
File Version publisher
DOI 10.4044/joma.120.129
NAID 120002310545
Author Matsui, Hideki|
Published Date 2009-12-01
Publication Title 岡山医学会雑誌
Volume volume121
Issue issue3
Content Type Journal Article
Author Kuramitsu, Makoto| Itano, Toshifumi| Matsui, Hideki| Tokuda, Masaaki| Hatase, Osamu| Murakami, Tetsuhide| Nisida, Isamu| Hayashi, Hideo|
Published Date 1979-04-30
Publication Title 岡山医学会雑誌
Volume volume91
Issue issue3-4
Content Type Journal Article
Author Matsui, Hideki|
Published Date 1982-04-30
Publication Title 岡山医学会雑誌
Volume volume94
Issue issue3-4
Content Type Journal Article
Author 野口 洋文| 松下 正之| Kobayashi, Naoya| Susan Bonner-Weir| 松井 秀樹| 田中 紀章| 田中 紘一| 松本 慎一|
Published Date 2005-09-01
Publication Title 岡山医学会雑誌
Volume volume117
Issue issue2
Content Type Journal Article
Author 魏 范研| 長嶋 一昭| 大島 登志男| 佐伯 恭範| 陸 雲飛| 松下 正之| 山田 祐一郎| 御子柴 克彦| 清野 裕| 松井 秀樹| 富澤 一仁|
Published Date 2007-05-01
Publication Title 岡山医学会雑誌
Volume volume119
Issue issue1
Content Type Journal Article
Author 松井 秀樹|
Published Date 1982-03-31
Publication Title
Content Type Thesis or Dissertation
Title Alternative The 10th Congress on Neutron Capture Therapy
FullText URL 126_73.pdf
Author Matsui, Hideki|
Publication Title 岡山医学会雑誌
Published Date 2014-04-01
Volume volume126
Issue issue1
Start Page 73
End Page 74
ISSN 0030-1558
Related Url http://www.okayama-u.ac.jp/user/oma/
language 日本語
Copyright Holders Copyright (c) 2014 岡山医学会
File Version publisher
DOI 10.4044/joma.126.73
JaLCDOI 10.18926/AMO/32907
FullText URL fulltext.pdf
Author Fujisawa, Toru| Moriwaki, Akiyoshi| Matsushita, Masayuki| Tomizawa, Kazuhito| Matsui, Hideki|
Abstract Oxytocin (OT) is one of the neuropituitary hormones and is synthesized in the neurons of the paraventricular nucleus (PVN) and supraoptic nucleus (SON). Previous studies have shown that the mRNAs encoding OT are delivered from the soma to both dendrites and axons of the neurons in the PVN and SON. However, it has not been elucidated whether a translational regulation mechanism to enable local synthesis of the hormone exists in the axons of the neurons of PVN and SON. Elongation factor 2 (EF2) is essential for polypeptide synthesis during protein translation. Moreover, phosphorylation of EF2 by EF2 kinase enhances the translation of certain mRNA species. In the present study, in order to shed light on the mechanisms involved in the translational regulation of OT synthesis, we investigated the localization of phosphorylated EF2. Phospho-EF2 was localized in the soma of the neurons in PVN and SON, and in the swellings of the median eminence where axonal tracts of the neurons in the PVN and SON exist. The phosphorylated form was also observed in the rat hypophysis. Moreover, phospho-EF2 and OT were colocalized in a part of the neurons in the PVN and SON. These results suggest that OT may be partially translated in the axons of neurons in the PVN and SON, and then secreted from the pituitary.
Keywords oxytocin PVN SON elongation factor 2 local translation
Amo Type Original Article
Published Date 2007-06
Publication Title Acta Medica Okayama
Volume volume61
Issue issue3
Publisher Okayama University Medical School
Start Page 161
End Page 166
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 17593952
Web of Science KeyUT 000247574700005
JaLCDOI 10.18926/AMO/32905
FullText URL fulltext.pdf
Author Wu, Hai-Yan| Tomizawa, Kazuhito| Matsui, Hideki|
Abstract Intracellular calcium is a powerful secondary messenger that affects a number of calcium sensors, including calpain, a Ca2+-dependent cysteine protease, and calcineurin, a Ca2+/calmodulin-dependent protein phosphatase. Maintenance of low basal levels of intracellular calcium allows for the tightly regulated physiological activation of these proteins, which is crucial to a wide variety of cellular processes, such as fertilization, proliferation, development, learning, and memory. Deregulation of calpain and calcineurin has been implicated in the pathogenesis of several disorders, including hypertension, heart disease, diabetes, cerebral ischemia, and Alzheimer's disease. Recent studies have demonstrated an interplay between calpain and calcineurin, in which calpain can directly regulate calcineurin activity through proteolysis in glutamate-stimulated neurons in culture and in vivo. The calpain-mediated proteolytic cleavage of calcineurin increases phosphatase activity, which promotes caspase-mediated neuronal cell death. Thus, the activation of the calpain-calcineurin pathway could contribute to calcium-dependent disorders, especially those associated with Alzheimer's disease and myocardial hypertrophy. Here, we focus briefly on recent advances in revealing the structural and functional properties of these 2 calcium-activated proteins, as well as on the interplay between the 2, in an effort to understand how calpain-calcineurin signaling may relate to the pathogenesis of calcium- dependent disorders.
Keywords calpain calcineurin calcium proteolysis neurodegeneration
Amo Type Review
Published Date 2007-06
Publication Title Acta Medica Okayama
Volume volume61
Issue issue3
Publisher Okayama University Medical School
Start Page 123
End Page 137
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 17593948
Web of Science KeyUT 000247574700001