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Search of essential substrates of Parkin in Parkinsonism

Research Project

Project/Area Number 16K19523
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Neurology
Research InstitutionJuntendo University

Principal Investigator

Arano Taku  順天堂大学, 医学(系)研究科(研究院), 博士研究員 (80750091)

Project Period (FY) 2016-04-01 – 2018-03-31
Project Status Completed (Fiscal Year 2017)
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)
KeywordsParkin / 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
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.

Report

(3 results)
  • 2017 Annual Research Report   Final Research Report ( PDF )
  • 2016 Research-status Report

URL: 

Published: 2016-04-21   Modified: 2019-03-29  

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