Parkin restrictions for damaged mitochondria
نویسندگان
چکیده
منابع مشابه
Parkin restrictions for damaged mitochondria
Cdc14 in good repair C dc14 is an essential regulator of the yeast cell cycle, but its vertebrate homologues appear to be surprisingly dispensable, Mocciaro et al. report. They are required for effi cient DNA repair, however. Yeast Cdc14 is a phosphatase that counteracts the cyclin-dependent kinases to control many aspects of the cell cycle including mitotic exit. Vertebrates have at least two ...
متن کاملDamaged mitochondria get a Parkin ticket
Loss-of-function mutations in PARK2, the gene encoding the ubiquitin ligase Parkin, are the most common cause of autosomal recessive Parkinson’s disease. But just seven short years ago, the cellular function of Parkin was completely unknown; even the enzyme’s subcellular localization was uncertain. That all changed, however, when Richard Youle and colleagues demonstrated that Parkin is specifi ...
متن کاملPINK1 stabilized by mitochondrial depolarization recruits Parkin to damaged mitochondria and activates latent Parkin for mitophagy
Parkinson's disease (PD) is a prevalent neurodegenerative disorder. Recent identification of genes linked to familial forms of PD such as Parkin and PINK1 (PTEN-induced putative kinase 1) has revealed that ubiquitylation and mitochondrial integrity are key factors in disease pathogenesis. However, the exact mechanism underlying the functional interplay between Parkin-catalyzed ubiquitylation an...
متن کاملA Polyubiquitin Chain Reaction: Parkin Recruitment to Damaged Mitochondria
Mutations in the E3 ubiquitin ligase Parkin or the mitochondrial kinase PINK1 cause autosomal recessive forms of Parkinson’s disease [1, 2]. Genetic and cell biological studies have implicated PINK1 and Parkin as critical elements in mitophagy, a mitochondrial quality control pathway that involves the ubiquitin-proteasome system (UPS) and the autophagy-lysosomal system [1, 2]. Under basal condi...
متن کاملPINK1 autophosphorylation upon membrane potential dissipation is essential for Parkin recruitment to damaged mitochondria
Dysfunction of PINK1, a mitochondrial Ser/Thr kinase, causes familial Parkinson's disease (PD). Recent studies have revealed that PINK1 is rapidly degraded in healthy mitochondria but accumulates on the membrane potential (ΔΨm)-deficient mitochondria, where it recruits another familial PD gene product, Parkin, to ubiquitylate the damaged mitochondria. Despite extensive study, the mechanism unde...
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ژورنال
عنوان ژورنال: Journal of Cell Biology
سال: 2010
ISSN: 1540-8140,0021-9525
DOI: 10.1083/jcb.1894iti2