Katsuhiko MIKOSHIBA, M.D. Ph.D


  Katsuhiko MIKOSHIBA, M.D. Ph.D

Professor, Principal Investigator

Shanghai Institute for Advanced Immunochemical Studies, ShanghaiTech University
Laboratory: Lab of Cell calcium signaling

Email: mikosiba@@shanghaitech.edu.cn


1969   M.D. Keio University School of Medicine

1973   Ph.D. Keio University


1973-1974     Assistant Professor, Dept. of Physiology, Keio Univ. School of Medicine

1974-1982     Lecturer, Dept. of Physiology, Keio Univ. School of Medicine

1976-1977     Research Associate Pasteur Institute, Paris, France (c/o Prof. Jean-Pierre Changeux)

1982-1985     Associate Prof., Department of Physiology, Keio Univ. School of Medicine

1985-1992     Professor, Institute for Protein Research, Osaka University

1986-1991     Professor, National Institute for Basic Biology, Okazaki (Adjunct position)

1992-1997     Chief Scientist, Molecular Neurobiology Laboratory, RIKEN, Tsukuba (Adjunct position)

1992-2007     Professor, The Institute of Medical Science, The University of Tokyo

1998-2009     Team Leader, Group Director, RIKEN Brain Science Institute (BSI) (Adjunct position)

2003-2015      Foreign Professor (Adjunct Professor) at Karolinska Institute (received an honorary doctorate from Karolinska Institute)

2005-present  Member of Science Council of Japan

2007-present  Professor Emeritus of University of Tokyo

2008-2011      Foreign Professor of Seoul National University (Korea) (World Class University Professor, WCU Prof. program)

2009-2019      Senior Team Leader, Lab. for Developmental Neurobiol., BSI, RIKEN

2019-present  Professor, SIAIS (Shanghai Institute for Advanced Immunochemical Studies), ShanghaiTech University



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2. Miyazaki S et al. Block of Ca2+ wave and Ca2+ oscillation by antibody to the inositol 1,4,5-trisphosphate receptor in fertilized hamster eggs. Science 257:251-5. (1992)

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7. Saneyoshi T et al. The Wnt/calcium pathway activates NF-AT and promotes ventral cell fate in Xenopus embryos. Nature 417:295-299. (2002)

8. Higo T et al. Subtype-specific and ER lumenal environment-dependent regulation of inositol 1,4,5-trisphosphate receptor type 1 by ERp44. Cell 120(1):85-98. (2005)

9. Futatsugi A et al. IP3 receptor types 2 and 3 mediate exocrine secretion underlying energy metabolism. Science 309(5744):2232-4. (2005)

10. Ando H et al. IRBIT suppresses IP3 receptor activity by competing with IP3 for the common binding site on the IP3 receptor. Molecular Cell 22(6):795-806. (2006)

11. Higo T et al. Mechanism of ER stress-induced brain damage by IP3 receptor. Neuron 68(5):865-78. (2010)

12. Horikawa K et al. Spontaneous network activity visualized by ultrasensitive Ca2+indicators, yellow Cameleon-Nano. Nature Methods 7:729-732. (2010)

13. Klar J et al. InsP3R2 mutations cause anhidrosis in humans and hypohidrosis in mice. J Clinical Investigation 124(11): 4773-80 (2014)

14. Tsuboi D et al. Disrupted-in-schizophrenia 1 regulates transport of ITPR1 mRNA for synaptic plasticity. Nature Neurosci 18(5): 698-707. (2015)

15. Hisatsune C et al. ERp44 Exerts redox-dependent control of blood pressure at the ER. Molecular Cell 58(6): 1015-27. (2015)

16. Monai H et al. Calcium imaging reveals glial involvement in transcranial direct current stimulation-induced plasticity in mouse brain. Nature Commun doi: 10.1038/ncomms11100 (2016)

17. Bonneau B et al. IRBIT controls apoptosis by interacting with the Bcl-2 homolog, Bcl2l10, and by promoting ER-mitochondria contact. eLife DOI10.7554/eLife19896 (2016)

18. Hamada K, et al. IP3-mediated gating mechanism of the IP3 receptor revealed by mutagenesis and X-ray crystallography. Proc Natl Acad Sci 114(18): 4661-4666. (2017)