| Project/Area Number |
26830035
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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 |
Nerve anatomy/Neuropathology
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| Research Institution | Hiroshima University |
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Principal Investigator |
Ohsawa Ryosuke 広島大学, 原爆放射線医科学研究所, 助教 (20719356)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 筋萎縮性側索硬化症 / 神経変性疾患 / ALS / Optineurin / オートファジー |
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| Outline of Final Research Achievements |
In this study I investigated physiological roles of Optineurin, the causative gene for amyotrophic lateral sclerosis. Upon induction of mitochondrial damage, Optineurin is recruited to the surface of damaged mitochondria in the presence of Parkin, a gene shown to be mutated in Parkinson's disease. Furthermore, optineurin is degraded through mitophagy, suggestiong that optineurin serves as an autophagic receptor during mitophagy. In addition, it is suggested that TBK1 cooperates with Optineurin to promote mitophagy.
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