Research Topics
Genomes and Genes | S OyadomariSummaryAffiliation: New York University Country: USA Publications
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Detail Information
Publications
Roles of CHOP/GADD153 in endoplasmic reticulum stressS Oyadomari
Department of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University, Kumamoto 860 8556, Japan
Cell Death Differ 11:381-9. 2004..Here, we summarize the current understanding of the roles of CHOP/GADD153 in ER stress-mediated apoptosis and in diseases including diabetes, brain ischemia and neurodegenerative disease...
Co-induction of argininosuccinate synthetase, cationic amino acid transporter-2, and nitric oxide synthase in activated murine microglial cellsK Kawahara
Department of Biofunctional Chemistry, Faculty of Pharmaceutical Sciences, Kumamoto University, 5-1 Ohe-Honmachi, 862-0973, Kumamoto, Japan
Brain Res Mol Brain Res 90:165-73. 2001..These results strongly suggest that both arginine transport by CAT-2 and citrulline-arginine recycling are important for high-output production of NO in activated microglial cells...
Induction of CHOP and apoptosis by nitric oxide in p53-deficient microglial cellsK Kawahara
Department of Molecular Genetics, Kumamoto University School of Medicine, Honjo, Japan
FEBS Lett 506:135-9. 2001..These results suggest that NO-induced apoptosis in MG5 cells occurs through the ER stress pathway involving CHOP, but is independent of p53...
Coinduction of endothelial nitric oxide synthase and arginine recycling enzymes in aorta of diabetic ratsS Oyadomari
Department of Molecular Genetics, Kumamoto University School of Medicine, Kumamoto 860 0811, Japan
Nitric Oxide 5:252-60. 2001..The results also suggest that TGF-beta1 works antiatherogenically at early stages of diabetes by increasing NO production, whereas prolonged elevation of TGF-beta1 functions atherogenically by inhibiting endothelial cell growth...
CCAAT/enhancer-binding protein beta is required for activation of genes for ornithine cycle enzymes by glucocorticoids and glucagon in primary-cultured hepatocytesT Kimura
Department of Molecular Genetics, Kumamoto University School of Medicine, Japan
FEBS Lett 494:105-11. 2001..Therefore, C/EBPbeta is required for hormonal induction of the genes for ornithine cycle enzymes in primary-cultured hepatocytes, while the deficiency of C/EBPbeta is compensated for in vivo...
Nitric oxide inhibits the proliferation of murine microglial MG5 cells by a mechanism involving p21 but independent of p53 and cyclic guanosine monophosphateK Kawahara
Department of Biofunctional Chemistry, Faculty of Pharmaceutical Sciences, Kumamoto University, 5-1 Ohe-Honmachi, Kumamoto 862-0973, Japan
Neurosci Lett 310:89-92. 2001..8-Bromo-cGMP neither induced p21 mRNA nor inhibited [(3)H]thymidine incorporation. These results suggest that NO inhibits the proliferation of MG5 cells by induction of p21, which occurs independent of p53 and cGMP...
Ischemia-induced neuronal cell death is mediated by the endoplasmic reticulum stress pathway involving CHOPS Tajiri
Department of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan
Cell Death Differ 11:403-15. 2004..These results indicate that ischemia-induced neuronal cell death is mediated by the ER stress pathway involving CHOP induction...
hsp70-DnaJ chaperone pair prevents nitric oxide- and CHOP-induced apoptosis by inhibiting translocation of Bax to mitochondriaT Gotoh
Department of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University, Honjo, Kumamoto, Japan
Cell Death Differ 11:390-402. 2004....
Nitric oxide-induced apoptosis in pancreatic beta cells is mediated by the endoplasmic reticulum stress pathwayS Oyadomari
Department of Molecular Genetics, Kumamoto University School of Medicine, Honjo 2 2 1, Kumamoto 860 0811, Japan
Proc Natl Acad Sci U S A 98:10845-50. 2001..We conclude that NO depletes ER Ca(2+), causes ER stress, and leads to apoptosis. Thus, ER Ca(2+) stores are a new target of NO, and the ER stress pathway is a major mechanism of NO-mediated beta cell apoptosis...
