| Project/Area Number |
23700437
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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 | Tohoku University |
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Principal Investigator |
TORII Satoru 東北大学, 大学院・生命科学研究科, 助教 (10444001)
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| Project Period (FY) |
2011 – 2012
|
| Project Status |
Completed (Fiscal Year 2012)
|
| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 細胞内情報伝達 / アポトーシス / 神経変性疾患 |
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| Research Abstract |
As a result of the analysis about regulatory mechanism of IPAS- induced cell death, we have shown that IPAS was bound to pro-survival Bcl-2 family proteins, such as Bcl-xL. Furthermore, IPAS was bound to PINK1 and Parkin in a mitochondria uncoupler, CCCP-dependent manner, leading to ubiquitination and degradation of IPAS. To elucidate the physiological function of IPAS in neuronal cell death in vivo, we performed the production of IPAS knockout mouse. We have already obtained IPAS chimera mice.
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