S Oyadomari

Summary

Affiliation: New York University
Country: USA

Publications

  1. ncbi Roles of CHOP/GADD153 in endoplasmic reticulum stress
    S Oyadomari
    Department of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University, Kumamoto 860 8556, Japan
    Cell Death Differ 11:381-9. 2004
  2. ncbi Induction of CHOP and apoptosis by nitric oxide in p53-deficient microglial cells
    K Kawahara
    Department of Molecular Genetics, Kumamoto University School of Medicine, Honjo, Japan
    FEBS Lett 506:135-9. 2001
  3. ncbi Co-induction of argininosuccinate synthetase, cationic amino acid transporter-2, and nitric oxide synthase in activated murine microglial cells
    K 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
  4. ncbi Coinduction of endothelial nitric oxide synthase and arginine recycling enzymes in aorta of diabetic rats
    S Oyadomari
    Department of Molecular Genetics, Kumamoto University School of Medicine, Kumamoto 860 0811, Japan
    Nitric Oxide 5:252-60. 2001
  5. ncbi hsp70-DnaJ chaperone pair prevents nitric oxide- and CHOP-induced apoptosis by inhibiting translocation of Bax to mitochondria
    T Gotoh
    Department of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University, Honjo, Kumamoto, Japan
    Cell Death Differ 11:390-402. 2004
  6. ncbi Ischemia-induced neuronal cell death is mediated by the endoplasmic reticulum stress pathway involving CHOP
    S Tajiri
    Department of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan
    Cell Death Differ 11:403-15. 2004
  7. ncbi CCAAT/enhancer-binding protein beta is required for activation of genes for ornithine cycle enzymes by glucocorticoids and glucagon in primary-cultured hepatocytes
    T Kimura
    Department of Molecular Genetics, Kumamoto University School of Medicine, Japan
    FEBS Lett 494:105-11. 2001
  8. ncbi Nitric oxide inhibits the proliferation of murine microglial MG5 cells by a mechanism involving p21 but independent of p53 and cyclic guanosine monophosphate
    K 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
  9. pmc Nitric oxide-induced apoptosis in pancreatic beta cells is mediated by the endoplasmic reticulum stress pathway
    S 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
  10. doi Endoplasmic reticulum stress-induced apoptosis contributes to articular cartilage degeneration via C/EBP homologous protein
    Y Uehara
    Department of Orthopaedic Surgery, Faculty of Life Sciences, Kumamoto University, 1 1 1 Honjo, Chuo Ku, Kumamoto 860 8556, Japan Electronic address
    Osteoarthritis Cartilage 22:1007-17. 2014

Detail Information

Publications10

  1. ncbi Roles of CHOP/GADD153 in endoplasmic reticulum stress
    S 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...
  2. ncbi Induction of CHOP and apoptosis by nitric oxide in p53-deficient microglial cells
    K 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...
  3. ncbi Co-induction of argininosuccinate synthetase, cationic amino acid transporter-2, and nitric oxide synthase in activated murine microglial cells
    K 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...
  4. ncbi Coinduction of endothelial nitric oxide synthase and arginine recycling enzymes in aorta of diabetic rats
    S 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...
  5. ncbi hsp70-DnaJ chaperone pair prevents nitric oxide- and CHOP-induced apoptosis by inhibiting translocation of Bax to mitochondria
    T Gotoh
    Department of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University, Honjo, Kumamoto, Japan
    Cell Death Differ 11:390-402. 2004
    ....
  6. ncbi Ischemia-induced neuronal cell death is mediated by the endoplasmic reticulum stress pathway involving CHOP
    S 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...
  7. ncbi CCAAT/enhancer-binding protein beta is required for activation of genes for ornithine cycle enzymes by glucocorticoids and glucagon in primary-cultured hepatocytes
    T 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...
  8. ncbi Nitric oxide inhibits the proliferation of murine microglial MG5 cells by a mechanism involving p21 but independent of p53 and cyclic guanosine monophosphate
    K 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...
  9. pmc Nitric oxide-induced apoptosis in pancreatic beta cells is mediated by the endoplasmic reticulum stress pathway
    S 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...
  10. doi Endoplasmic reticulum stress-induced apoptosis contributes to articular cartilage degeneration via C/EBP homologous protein
    Y Uehara
    Department of Orthopaedic Surgery, Faculty of Life Sciences, Kumamoto University, 1 1 1 Honjo, Chuo Ku, Kumamoto 860 8556, Japan Electronic address
    Osteoarthritis Cartilage 22:1007-17. 2014
    ..In osteoarthritis (OA) cartilage, Chop expression and apoptosis increase as degeneration progresses. We investigated the role of Chop in murine chondrocyte apoptosis and in the progression of cartilage degeneration...