Elucidation of the mechanism of mitochondrial maintenance by Parkinson's disease gene products

2017 Fiscal Year Final Research Report

• Project/Area Number: 26461280
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Neurology
• Research Institution: Juntendo University
• Principal Investigator: SHIBA Kahori 順天堂大学, 医学(系)研究科(研究院), 准教授 (30468582)
• Co-Investigator(Renkei-kenkyūsha): IMAI Yuzuru 順天堂大学, 医学研究科, 先任准教授 (30321730) ; INOSHITA Tsuyoshi 順天堂大学, 医学研究科, 助教 (20601206)
• Research Collaborator: HATTORI Nobutaka 順天堂大学, 医学部, 教授 (80218510) ; AKAMATSU Wado 順天堂大学, 医学研究科, 特任教授 (60338184)
• Project Period (FY): 2014-04-01 – 2018-03-31
• Keywords: Parkin / PINK1 / パーキンソン病 / マイトファジー

Outline of Final Research Achievements

The Parkinson’s disease gene products PINK1 and Parkin are involved in the maintenance of mitochondrial functions. It has been demonstrated that PINK1 activates Parkin through its phosphorylation, which leads to selective removal of damaged mitochondria.
This study uncovered that PINK1 and Parkin have a role to amplify the phospho-ubiquitin chains on the damaged mitochondria as their degradation signal. Moreover, the amplification system of the phospho-ubiquitin signal was compromised in dopaminergic neurons derived for patient’s iPS cells, which strongly suggests that the dysfunction of this system is involved in PD pathogenesis.

Free Research Field

神経学