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• W2250617219 endingPage "6287" @default.
• W2250617219 startingPage "6270" @default.
• W2250617219 abstract "Mutations in Cu/Zn superoxide dismutase (SOD1) cause autosomal dominant amyotrophic lateral sclerosis (ALS), a devastating neurodegenerative disease with no effective treatment. Despite ample evidence indicating involvement of mutation-induced SOD1 protein misfolding and aggregation in ALS pathogenesis, the molecular mechanisms that control cellular management of misfolded, aggregation-prone SOD1 mutant proteins remain unclear. Here, we report that parkin, an E3 ubiquitin-protein ligase which is linked to Parkinson's disease, is a novel regulator of cellular defense against toxicity induced by ALS-associated SOD1 mutant proteins. We find that parkin mediates K63-linked polyubiquitination of SOD1 mutants in cooperation with the UbcH13/Uev1a E2 enzyme and promotes degradation of these misfolded SOD1 proteins by the autophagy-lysosome system. In response to strong proteotoxic stress associated with proteasome impairment, parkin promotes sequestration of misfolded and aggregated SOD1 proteins to form perinuclear aggresomes, regulates positioning of lysosomes around misfolded SOD1 aggresomes, and facilitates aggresome clearance by autophagy. Our findings reveal parkin-mediated cytoprotective mechanisms against misfolded SOD1 toxicity and suggest that enhancing parkin-mediated cytoprotection may provide a novel therapeutic strategy for treating ALS." @default.
• W2250617219 created "2016-06-24" @default.
• W2250617219 creator A5000323703 @default.
• W2250617219 creator A5006144208 @default.
• W2250617219 creator A5027222229 @default.
• W2250617219 creator A5054892264 @default.
• W2250617219 date "2015-11-13" @default.
• W2250617219 modified "2023-10-17" @default.
• W2250617219 title "Parkin Protects Against Misfolded SOD1 Toxicity by Promoting Its Aggresome Formation and Autophagic Clearance" @default.
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• W2250617219 doi "https://doi.org/10.1007/s12035-015-9537-z" @default.
• W2250617219 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4866905" @default.
• W2250617219 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26563499" @default.
• W2250617219 hasPublicationYear "2015" @default.
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• W2250617219 hasAuthorship W2250617219A5000323703 @default.

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