Project/Area Number |
10044245
|
Research Category |
Grant-in-Aid for Scientific Research (B).
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Neuroscience in general
|
Research Institution | The University of Tokyo |
Principal Investigator |
MIKOSHIBA Katsuhiko The Institute of Medical Science, The University of Tokyo, Department of Molecular Neurobiology, Professor, 医科学研究所, 教授 (30051840)
|
Co-Investigator(Kenkyū-buntansha) |
OGAWA Masaharu The Institute of Physical and Chemical Research (RIKEN) The team of Development Neurobiology, researcher, 脳科学総合研究センター, チームリーダー(研究職) (50111951)
CURRAN Tom セントジュード研究病院, 教授
|
Project Period (FY) |
1998 – 1999
|
Project Status |
Completed (Fiscal Year 1999)
|
Budget Amount *help |
¥8,800,000 (Direct Cost: ¥8,800,000)
Fiscal Year 1999: ¥4,000,000 (Direct Cost: ¥4,000,000)
Fiscal Year 1998: ¥4,800,000 (Direct Cost: ¥4,800,000)
|
Keywords | reelin / CR-50 antibody / cerebral cortex / cortex / 大脳 / リーラー / CR50モノクローナル抗体 / リーラーマウス / 小脳 / プルキンエ細胞 / 海馬 / ニューロン |
Research Abstract |
Reelin is a key mediator of ordered neuronal alignment in the brain. Here we demonstrate that Reelin molecules assemble each other to forms a huge protein complex both in vitro and in vivo. The Reelin-Reelin interaction is clearly inhibited by the function-blocking anti-Reelin antibody, CR-50, at a concentration known to inhibit Reelin function. This assembly is mediated by electrostatic interaction via the α-helix domains in the CR-50 epitope region. Recombinant CR-50 epitope fragments spontaneously constitute a soluble, string-like homopolymer with a regularly repeated structure composed of more than 40 monomers. These data suggest that Reelin exerts its biological function by composing a large protein assembly driven by the CR-50 epitope region, proposing a novel model of the Reelin signaling in neurodevelopment.
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