| Project/Area Number |
21590228
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General physiology
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
SAEGUSA Hironao 東京医科歯科大学, 大学院・医歯学総合研究科, 助教 (90261205)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2010: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2009: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | Cav2. 1,カルボキシ末端 / プロテアーゼ / 脊髄小脳変性症6型 / SCA6 / Cav2.1 / カルボキシ末端 |
|---|
| Research Abstract |
Generation of Cav2. 1 carboxyl terminal tail(Cav2. 1CT) is thought to be causally related to spinocerebellar ataxia type 6, a hereditary neurological disease. Cav2. 1CT is generated by cleavage of the full-length Cav2. 1 protein. But the exact mechanism underlying the generation of Cav2. 1CT and the function of this CT fragment remain to be clarified. In the present study, I have tried to clarify the mechanism to generate the Cav2. 1CT from full-length Cav2. 1 protein. Also, I have studied the functional role of the Cav2. 1CT in some in vitro systems. As a result, the following molecules are candidates for the protease responsible for the Cav2. 1CT generation : caspase 6, cathepsin L, and calpain small subunit 1, but further studies are necessary to conclude this. Cav2. 1CT was found to be toxic to cells and it is possible that Cav2. 1CT possess transcription repressing activity
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