게이코 야마모토, Keiko Tanaka-Yamamoto

Principal Researcher

OFFICE

L7215, +82-2-958-7223

LAB

L7215, +82-2-958-7223

EDUCATION

Ph.D. Graduate School of Veterinary Medicine, Hokkaido University (1996)
B.S. Faculty of Veterinary Medicine, Hokkaido University (1993)

RESEARCH CAREER & ACTIVITIES
  • Principal Researcher, Center for Functional Connectomics, Brain Science Institute, Korea Institute of Science and Technology (KIST) (2012-Present)
  • Research Scientist, Center for Functional Connectomics, Brain Science Institute, Korea Institute of Science and Technology (KIST) (2010-2012)
  • PRESTO Researcher, JST, Department of Biophysics and Biochemistry, Graduate School of Science, University of Tokyo (2008-2010)
  • Postdoctoral Research Fellow, Department of Neurobiology, Duke University Medical Center (2001-2008)
  • Postdoctoral Research Fellow, The 4th Department, Osaka Bioscience Institute (1998-2001)
  • Research Fellow of the Japan Society for the Promotion of Science, Department of Physiology, University of Occupational and Environmental Health (1996-1998)
RESEARCH INTERESTS
  • Regulation of synaptic plasticity
  • Roles of cerebellum integrating motor and cognitive functions
HIGHLIGHT
  • Kim T., Yamamoto Y. *, Tanaka-Yamamoto K. * (2017) Timely regulated sorting from early to late endosomes is required to maintain cerebellar long-term depression. Nat. Commun. 8(1):401.
  • Lee D., Yamamoto Y., Kim E., Tanaka-Yamamoto K. (2015) Functional and Physical Interaction of Diacylglycerol Kinase ζ with Protein Kinase Cα Is Required for Cerebellar Long-Term Depression. J. Neurosci. 35:15453–15465.
  • Kim Y, Kim T, Rhee JK, Lee D, Tanaka-Yamamoto K*, Yamamoto Y*. (2015) Selective transgene expression in cerebellar Purkinje cells and granule cells using adeno-associated viruses together with specific promoters. Brain Res. 1620:1-16.
  • Yamamoto, Y., Lee D., Kim, Y., Lee, B., Seo, C., Kawasaki, H., Kuroda, S., Tanaka-Yamamoto, K. (2012) Raf kinase inhibitory protein is required for cerebellar long-term synaptic depression by mediating PKC-dependent MAPK activation. J. Neurosci. 32; 14254-14264.