S
Seiichi Oyadomari
Researcher at University of Tokushima
Publications - 88
Citations - 12806
Seiichi Oyadomari is an academic researcher from University of Tokushima. The author has contributed to research in topics: Unfolded protein response & Endoplasmic reticulum. The author has an hindex of 36, co-authored 83 publications receiving 11457 citations. Previous affiliations of Seiichi Oyadomari include New York University & Kumamoto University.
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Journal ArticleDOI
Roles of CHOP/GADD153 in endoplasmic reticulum stress.
TL;DR: The current understanding of the roles of C/EBP homologous protein (CHOP) and GADD153 in ER stress-mediated apoptosis and in diseases including diabetes, brain ischemia and neurodegenerative disease are summarized.
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CHOP induces death by promoting protein synthesis and oxidation in the stressed endoplasmic reticulum
Stefan J. Marciniak,Chi Yun,Seiichi Oyadomari,Isabel Novoa,Yuhong Zhang,Rivka Jungreis,Kazuhiro Nagata,Heather P. Harding,David Ron +8 more
TL;DR: This work finds that CHOP directly activates GADD34, which promotes ER client protein biosynthesis by dephosphorylating phospho-Ser 51 of the alpha-subunit of translation initiation factor 2 (eIF2alpha) in stressed cells, and protects cells from ER stress by decreasing client protein load and changing redox conditions within the organelle.
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Obesity-induced gut microbial metabolite promotes liver cancer through senescence secretome
Shin Yoshimoto,Tze Mun Loo,Tze Mun Loo,Koji Atarashi,Hiroaki Kanda,Seidai Sato,Seiichi Oyadomari,Yoichiro Iwakura,Kenshiro Oshima,Hidetoshi Morita,Masahira Hattori,Kenya Honda,Yuichi Ishikawa,Eiji Hara,Naoko Ohtani +14 more
TL;DR: It is shown that senescence-associated secretory phenotype (SASP) has crucial roles in promoting obesity-associated hepatocellular carcinoma (HCC) development in mice, and a similar pathway may contribute to at least certain aspects of obesity- associated HCC development in humans as well.
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Targeted disruption of the Chop gene delays endoplasmic reticulum stress–mediated diabetes
Seiichi Oyadomari,Akio Koizumi,Kiyoshi Takeda,Tomomi Gotoh,Shizuo Akira,Eiichi Araki,Masataka Mori +6 more
TL;DR: It is concluded that ER overload in beta cells causes ER stress and leads to apoptosis via Chop induction and a new therapeutic approach for preventing the onset of diabetes by inhibiting Chop induction or by increasing chaperone capacity in the ER is suggested.
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Nitric oxide-induced apoptosis in pancreatic β cells is mediated by the endoplasmic reticulum stress pathway
Seiichi Oyadomari,Kiyoshi Takeda,Masaki Takiguchi,Tomomi Gotoh,Makoto Matsumoto,Ikuo Wada,Shizuo Akira,Eiichi Araki,Masataka Mori +8 more
TL;DR: It is concluded that ER Ca2+ stores are a new target of NO, and the ER stress pathway is a major mechanism of NO-mediated β cell apoptosis.