M
Masataka Mori
Researcher at Kumamoto University
Publications - 50
Citations - 7930
Masataka Mori is an academic researcher from Kumamoto University. The author has contributed to research in topics: CHOP & Endoplasmic reticulum. The author has an hindex of 34, co-authored 50 publications receiving 7477 citations. Previous affiliations of Masataka Mori include Sojo 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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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.
Journal ArticleDOI
Endoplasmic reticulum stress-mediated apoptosis in pancreatic β-cells
TL;DR: The recent studies revealed that ER stress-mediated apoptosis in β-cells plays an important role in the development of diabetes.
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Nitric oxide-induced apoptosis in RAW 264.7 macrophages is mediated by endoplasmic reticulum stress pathway involving ATF6 and CHOP.
TL;DR: The results indicate that the ER stress pathway involving ATF6 and CHOP plays a key role in NO-mediated apoptosis in macrophages, and peritonealmacrophages from CHOP knockout mice showed resistance to NO-induced apoptosis.