2015 Fiscal Year Final Research Report
Identification of molecular mechanism underlying ALS pathogenesis by Optineurin mutation
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 |
Research Field |
Nerve anatomy/Neuropathology
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Research Institution | Hiroshima University |
Principal Investigator |
Ohsawa Ryosuke 広島大学, 原爆放射線医科学研究所, 助教 (20719356)
|
Project Period (FY) |
2014-04-01 – 2016-03-31
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Keywords | 筋萎縮性側索硬化症 / 神経変性疾患 |
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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Free Research Field |
分子生物学
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