| Project/Area Number |
23700450
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Neurochemistry/Neuropharmacology
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| Research Institution | Hiroshima University |
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Principal Investigator |
SEKI Takahiro 広島大学, 大学院・医歯薬保健学研究院, 助教 (50335650)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2011: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | シャペロン介在性オートファジー / 脊髄小脳失調症 |
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| Research Abstract |
Chaperone-mediated autophagy (CMA) isone of the proteolytic pathways. Since there is no simple method to monitor CMA activity, the roles of CMA in physiological functions and pathogenesis of diseases have remained unknown. In the present study, I have established a novel method to monitor CMA activity in a single cell level. To utilize this method, I revealed that mutant γPKC which causes spinocerebellar ataxia type 14(SCA14) impairs CMA activity in primary cultured neural cells. In addition, I elucidated that the amounts of proteins related to CMA are altered in the brain of SCA3, another type of SCA, model mice. These findings suggest that CMA might be related to the pathogenesis of two different types of SCAs.
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