| Project/Area Number |
26430051
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Nerve anatomy/Neuropathology
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
Torii Satoru 東京医科歯科大学, 難治疾患研究所, プロジェクト講師 (10444001)
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| Co-Investigator(Renkei-kenkyūsha) |
SOGAWA Kazuhiro 東北大学, 生命科学研究科, 教授 (80175421)
YASUMOTO Kenichi 東北大学, 生命科学研究科, 准教授 (90241629)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | IPAS / PINK1 / Parkin / リン酸化 / パーキンソン病 / ＰＩＮＫ１ / Ｐａｒｋｉｎ / 神経変性疾患 / MPTP |
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| Outline of Final Research Achievements |
In this study, we have shown that IPAS is regulated by the PINK1-Parkin pathway. IPAS was phosphorylated by PINK1 in a CCCP-dependent manner, bound to Parkin and eventually degraded. Furthermore, by analysis using tissues from patients of Parkinson’s disease, expression of IPAS was increased in substantia nigra in midbrain of these patients. In addition, MPTP-induced neuronal cell death in substantia nigra was decreased in IPAS knockout mice. These results suggest that IPAS accumulation induces neuronal cell death, leading to onset of Parkinson’s disease when regulation by PINK1 and Parkin is lost due to mutations.
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