Curriculum Vitaes

Hayashi Kensuke

  (林 謙介)

Profile Information

Affiliation
Professor, Faculty of Science and Technology, Department of Materials and Life Sciences, Sophia University
Degree
理学博士(東京大学)

Contact information
kensuk-hsophia.ac.jp
Researcher number
50218567
J-GLOBAL ID
200901093609757481
researchmap Member ID
1000161071

1983-1988 Faculty of Science, University of Tokyo. Study on the development of chicken digestive tract.
1988-1993 National Institute of Neuroscience, NCNP. Study on the development of chicken skeletal muscles.
1993-1998 Gunma University School of Medicine. Study on actin binding proteins in neurons.
1998-2004 Institute for Molecular and Cellular Regulation, Gunma University. Study on the cell polarity and cell migration of neurons.
2004- present Faculty of Science and Technology, Sophia University. Study on the microtubule formation in neurons.


Papers

 49
  • Akari Nakamura, Mami Ikeda, Seina Kusayanagi, Kensuke Hayashi
    IBRO Neuroscience Reports, 13 264-273, Dec, 2022  Peer-reviewedLast authorCorresponding author
  • Kaho Miyata, Kensuke Hayashi
    Developmental Neuroscience, 44 1-11, Sep, 2022  Peer-reviewedLast authorCorresponding author
    Neuronal migration and axon elongation in the developing brain are essential events for neural network formation. Leading processes of migrating neurons and elongating axons have growth cones at their tips. Cytoskeletal machinery for advance of growth cones of the two processes has been thought the same. In this study, we compared axonal-elongating growth cones and leading-process growth cones in the same conditions that manipulated filopodia, lamellipodia, and drebrin, the latter mediates actin filament-microtubule interaction. Cerebral cortex (CX) neurons and medial ganglionic eminence (MGE) neurons from embryonic mice were cultured on less-adhesive cover glasses. Inhibition of filopodia formation by triple knockdown of mammalian-enabled, Ena-VASP-like, and vasodilator-stimulated phosphoprotein or double knockdown of Daam1 and fascin affected axon formation of CX neurons but did not affect the morphology of leading process of MGE neurons. On the other hand, treatment with CK666, to inhibit lamellipodia formation, did not affect axons but destroyed the leading-process growth cones. When drebrin was knocked down, the morphology of CX neurons remained unchanged, but the leading processes of MGE neurons became shorter. In vivo assay of radial migration of CX neurons revealed that drebrin knockdown inhibited migration, while it did not affect axon elongation. These results showed that the filopodia-microtubule system is the main driving machinery in elongating growth cones, while the lamellipodia-drebrin-microtubule system is the main system in leading-process growth cones of migrating neurons.
  • Koyo Ide, Mika Muko, Kensuke Hayashi
    Histochemistry and Cell Biology, 156 273-281, Jun 10, 2021  Peer-reviewedLast authorCorresponding author
  • Suzuki Y, Otake A, Ueno S, Hayashi K, Ishii H, Miyoshi N, Kuroiwa K, Tachikawa M, Fujimaki Y, Nishiyama K, Manabe K, Yamazaki R, Asai A
    ACS Med. Chem. Lett., 11(6) 1287-1291, 2020  Peer-reviewed
    As a part of our continuous structure-activity relationship (SAR) studies on 1-(quinazolin-4-yl)-1-(4-methoxyphenyl)ethan-1-ols, the synthesis of derivatives and their cytotoxicity against the human lung cancer cell line A549 were explored. This led to the discovery of 1-(2-(furan-3-yl)quinazolin-4-yl)-1-(4-methoxyphenyl)ethan-1-ol (PVHD303) with potent antiproliferative activity. PVHD303 disturbed microtubule formation at the centrosomes and inhibited the growth of tumors dose-dependently in the HCT116 human colon cancer xenograft model in vivo.
  • Mimori Yamada, Kensuke Hayashi
    Cytoskeleton, 76 339-345, 2019  Peer-reviewedLast authorCorresponding author

Misc.

 12

Research Projects

 23