| Project/Area Number |
16K19523
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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 |
Neurology
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| Research Institution | Juntendo University |
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Principal Investigator |
Arano Taku 順天堂大学, 医学(系)研究科(研究院), 博士研究員 (80750091)
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | Parkin / ドーパミン神経 / ミトコンドリア / CHCHD2 / ユビキチン / パーキンソン病 / ショウジョウバエ / PINK1 / Parkinson's disease / Drosophila melanogaster / dopaminergic neuron / ubiquitination |
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| Outline of Final Research Achievements |
The parkin genes responsible for autosomal recessive early-onset Parkinson’s disease, which encodes ubiquitin-ligase, is known to regulate mitochondrial quality control. However, the pathogenesis of selective dopaminergic neuron death caused by Parkin mutations remained unknown. To address this issue, I tried to search dopaminergic neuron-specific or glia-specific ubiquitination substrates of Parkin using the combination of BioUb6-BirA system and Drosophila.
Newly identified autosomal dominant late-onset Parkinson’s disease gene, CHCHD2, encodes a mitochondrial protein with unknown functions. I tried to determine CHCHD2-binding proteins from human cultured cells and isolated a mitochondrial matrix protein p32. The biological significance of CHCHD2-p32 interaction was assessed using Drosophila models.
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