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東北電力 女川原発2号機 地元自治体が再稼働をどう判断か注目 (NHK)

26日、原子力規制委員会の審査に合格した宮城県にある女川原子力発電所2号機について国と東北電力は、再稼働に必要な自治体の同意に向けた手続きを進めることになり今後...

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Mitofusin-1 and Mitofusin-2 are ubiquitinated in a PINK1/parkin dependent manner upon induction of mitophagy.

著者 Gegg ME , Cooper JM , Chau KY , Rojo M , Schapira AH , Taanman JW
Hum Mol Genet.2010 Sep 24 ; ():.
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Department of Clinical Neurosciences, Institute of Neurology, University College London, UK.

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Mitochondrial dysfunction and perturbed degradation of proteins have been implicated in Parkinson's disease (PD) pathogenesis. Mutations in the Parkin and PINK1 genes are a cause of familial PD. PINK1 is a putative kinase associated with mitochondria and loss of PINK1 expression leads to mitochondrial dysfunction, which increases with time. Parkin is suggested to be downstream of PINK1 and also mediates the removal of damaged mitochondria by macroautophagy (mitophagy). We investigated whether mitochondrial dysfunction in dopaminergic SH-SY5Y cells following decreased PINK1 expression by RNAi may in part be due to inhibition of mitophagy. Reduced flux through the macroautophagy pathway was found to be coincident with inhibition of ATP synthesis following 12 days of PINK1 silencing. Over expression of parkin in these cells restored both autophagic flux and ATP synthesis. Over expression and RNAi studies also indicated that PINK1 and parkin were required for mitophagy following CCCP induced mitochondrial damage. Ubiquitination of several mitochondrial proteins, including mitofusin 1 and mitofusin 2, were detected within 3 hours of CCCP treatment. These post-translational modifications were reduced following silencing of parkin or PINK1. The ubiquitination of mitochondrial proteins appears to identify mitochondria for degradation and facilitate mitophagy. PINK1 and parkin are thus required for the removal of damaged mitochondria in dopaminergic cells and inhibition of this pathway may lead to the accumulation of defective mitochondria which may contribute to PD pathogenesis.
PMID: 20871098 [PubMed - as supplied by publisher]
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