Tamotsu Nishida

Summary

Affiliation: Mie University
Country: Japan

Publications

  1. ncbi request reprint Interactions between PIAS proteins and SOX9 result in an increase in the cellular concentrations of SOX9
    Takako Hattori
    Department of Molecular Genetics, University of Texas M D Anderson Cancer Center, Houston, Texas 77030, USA
    J Biol Chem 281:14417-28. 2006
  2. doi request reprint The nucleolar SUMO-specific protease SMT3IP1/SENP3 attenuates Mdm2-mediated p53 ubiquitination and degradation
    Tamotsu Nishida
    Department of Human Functional Genomics, Life Science Research Center, Mie University, 1577 Kurima machiya, Tsu 514 8507, Japan
    Biochem Biophys Res Commun 406:285-91. 2011
  3. doi request reprint SMT3IP1, a nucleolar SUMO-specific protease, deconjugates SUMO-2 from nucleolar and cytoplasmic nucleophosmin
    Tamotsu Nishida
    Department of Human Functional Genomics, Life Science Research Center, Mie University, 1577 Kurima machiya, Tsu 514 8507, Japan
    Biochem Biophys Res Commun 374:382-7. 2008
  4. ncbi request reprint Repression of E1AF transcriptional activity by sumoylation and PIASy
    Tamotsu Nishida
    Department of Human Functional Genomics, Life Science Research Center, Mie University, 1577 Kurima machiya, Tsu 514 8507, Japan
    Biochem Biophys Res Commun 360:226-32. 2007
  5. pmc PIASy controls ubiquitination-dependent proteasomal degradation of Ets-1
    Tamotsu Nishida
    Department of Human Functional Genomics, Life Science Research Center, Mie University, 1577 Kurima machiya, Tsu 514 8507, Japan
    Biochem J 405:481-8. 2007
  6. pmc Molecular genetics of myocardial infarction
    Yoshiji Yamada
    Department of Human Functional Genomics, Life Science Research Center, Mie University, 1577 Kurima machiya, Tsu, Mie, 514 8507, Japan
    Genomic Med 2:7-22. 2008
  7. ncbi request reprint Proinflammatory gene polymorphisms and ischemic stroke
    Yoshiji Yamada
    Department of Human Functional Genomics, Life Science Research Center, Mie University, Tsu, Mie, Japan
    Curr Pharm Des 14:3590-600. 2008
  8. doi request reprint Association of a polymorphism of BTN2A1 with myocardial infarction in East Asian populations
    Yoshiji Yamada
    Life Science Research Center, Mie University, Tsu, Japan
    Atherosclerosis 215:145-52. 2011
  9. ncbi request reprint PIASy-mediated repression of the Ets-1 is independent of its sumoylation
    Tamotsu Nishida
    School of Life Science, Tokyo University of Pharmacy and Life Science, Hachioji, Japan
    Biochem Biophys Res Commun 345:1536-46. 2006
  10. ncbi request reprint Sumoylation of Mdm2 by protein inhibitor of activated STAT (PIAS) and RanBP2 enzymes
    Yasuhiro Miyauchi
    Division of Molecular Life Science, School of Life Science, Tokyo University of Pharmacy and Life Science, 1432 1 Horinouchi, Hachioji, Tokyo 192 0392, Japan
    J Biol Chem 277:50131-6. 2002

Collaborators

Detail Information

Publications12

  1. ncbi request reprint Interactions between PIAS proteins and SOX9 result in an increase in the cellular concentrations of SOX9
    Takako Hattori
    Department of Molecular Genetics, University of Texas M D Anderson Cancer Center, Houston, Texas 77030, USA
    J Biol Chem 281:14417-28. 2006
    ..Our results suggest that, by controlling the cellular concentrations of SOX9, PIAS proteins and sumoylation may be part of a major regulatory system of SOX9 functions...
  2. doi request reprint The nucleolar SUMO-specific protease SMT3IP1/SENP3 attenuates Mdm2-mediated p53 ubiquitination and degradation
    Tamotsu Nishida
    Department of Human Functional Genomics, Life Science Research Center, Mie University, 1577 Kurima machiya, Tsu 514 8507, Japan
    Biochem Biophys Res Commun 406:285-91. 2011
    ..Interestingly, the desumoylation activity of SMT3IP1 was not necessary for p53 stabilization. These results suggest that SMT3IP1 is a new regulator of the p53-Mdm2 pathway...
  3. doi request reprint SMT3IP1, a nucleolar SUMO-specific protease, deconjugates SUMO-2 from nucleolar and cytoplasmic nucleophosmin
    Tamotsu Nishida
    Department of Human Functional Genomics, Life Science Research Center, Mie University, 1577 Kurima machiya, Tsu 514 8507, Japan
    Biochem Biophys Res Commun 374:382-7. 2008
    ..Our findings suggest that SMT3IP1-mediated desumoylation might control NPM physiological functions at both the nucleolus and other subcellular compartments...
  4. ncbi request reprint Repression of E1AF transcriptional activity by sumoylation and PIASy
    Tamotsu Nishida
    Department of Human Functional Genomics, Life Science Research Center, Mie University, 1577 Kurima machiya, Tsu 514 8507, Japan
    Biochem Biophys Res Commun 360:226-32. 2007
    ..Taken together, our results indicate that PIASy negatively regulates E1AF-mediated transcription by both E1AF sumoylation in a dependent and independent fashion...
  5. pmc PIASy controls ubiquitination-dependent proteasomal degradation of Ets-1
    Tamotsu Nishida
    Department of Human Functional Genomics, Life Science Research Center, Mie University, 1577 Kurima machiya, Tsu 514 8507, Japan
    Biochem J 405:481-8. 2007
    ..Our results suggested that PIASy controls Ets-1 function, at least in part, by inhibiting Ets-1 protein turnover via the ubiquitin-proteasome system...
  6. pmc Molecular genetics of myocardial infarction
    Yoshiji Yamada
    Department of Human Functional Genomics, Life Science Research Center, Mie University, 1577 Kurima machiya, Tsu, Mie, 514 8507, Japan
    Genomic Med 2:7-22. 2008
    ..3 by genome-wide scans. Such studies may provide insight into the function of implicated genes as well as into the role of genetic factors in the development of CHD and MI...
  7. ncbi request reprint Proinflammatory gene polymorphisms and ischemic stroke
    Yoshiji Yamada
    Department of Human Functional Genomics, Life Science Research Center, Mie University, Tsu, Mie, Japan
    Curr Pharm Des 14:3590-600. 2008
    ..Such studies may provide insight into the function of implicated genes as well as into the role of genetic factors in the development of ischemic stroke...
  8. doi request reprint Association of a polymorphism of BTN2A1 with myocardial infarction in East Asian populations
    Yoshiji Yamada
    Life Science Research Center, Mie University, Tsu, Japan
    Atherosclerosis 215:145-52. 2011
    ..We have performed a genome-wide association study (GWAS) to identify genetic variants that confer susceptibility to myocardial infarction (MI) in Japanese and Korean populations...
  9. ncbi request reprint PIASy-mediated repression of the Ets-1 is independent of its sumoylation
    Tamotsu Nishida
    School of Life Science, Tokyo University of Pharmacy and Life Science, Hachioji, Japan
    Biochem Biophys Res Commun 345:1536-46. 2006
    ..PIASy represses the Ets-1-dependent transcription, and its repression is independent of the sumoylation status of Ets-1, but it is dependent on the sumoylation of other factors...
  10. ncbi request reprint Sumoylation of Mdm2 by protein inhibitor of activated STAT (PIAS) and RanBP2 enzymes
    Yasuhiro Miyauchi
    Division of Molecular Life Science, School of Life Science, Tokyo University of Pharmacy and Life Science, 1432 1 Horinouchi, Hachioji, Tokyo 192 0392, Japan
    J Biol Chem 277:50131-6. 2002
    ....
  11. ncbi request reprint Nedd8-modification of Cul1 is promoted by Roc1 as a Nedd8-E3 ligase and regulates its stability
    Mitsuru Morimoto
    Division of Molecular Biology, School of Life Science, Tokyo University of Pharmacy and Life Science, 1432 1 Horinouchi, Hachioji, Tokyo 192 0392, Japan
    Biochem Biophys Res Commun 301:392-8. 2003
    ..Thus, neddylation of Cul1 might regulate SCF function negatively via degradation of Cul1/Roc1 complex...
  12. ncbi request reprint PIAS1 and PIASxalpha function as SUMO-E3 ligases toward androgen receptor and repress androgen receptor-dependent transcription
    Tamotsu Nishida
    Division of Molecular Biology, School of Life Science, Tokyo University of Pharmacy and Life Science, 1432 1 Horinouchi, Hachioji, Japan
    J Biol Chem 277:41311-7. 2002
    ..Thus, PIAS1 and PIASxalpha modulate the AR-dependent transactivation, which, at least in part, can be attributed to their SUMO-E3 activity toward AR...