| Project/Area Number |
21700407
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Neurochemistry/Neuropharmacology
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| Research Institution | Hiroshima University |
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Principal Investigator |
SEKI Takahiro Hiroshima University, 大学院・医歯薬学総合研究科, 助教 (50335650)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2010: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2009: ¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
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| Keywords | 神経・精神疾患の病態と治療 / 脊髄小脳失調症 / プルキンエ細胞 / γPKC / Hsc70 / 脊髄小脳失調症(SCA) / プロテインキナーゼCγ(γPKC) / 小脳プルキンエ細胞 |
|---|
| Research Abstract |
To elucidate the mechanism how mutant γPKC causing spinocerebellar ataxia induces neurodegeneration specific to cerebella Purkinje cells (PCs), we investigated moleclular properties of mutant γPKC in PCs and in non-PC neurons of cerebellar primary cultures. Compared with non-PC neurons, the mobility of mutant mutant γPKC was prominently reduced in PCs. Moreover, we identified heat shock cognate protein 70 (Hsc70) as a preferable binding protein to mutant γPKC in PCs. These results suggest that mutant γPKC preferably binds to Hsc70 and impairs its functions, leading to PC-selective neurodegeneration.
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