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http://purl.uniprot.org/citations/28306505http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/28306505http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/28306505http://www.w3.org/2000/01/rdf-schema#comment"Protein aggregation is associated with age-related neurodegenerative disorders, such as Alzheimer's and polyglutamine diseases. As a causal relationship between protein aggregation and neurodegeneration remains elusive, understanding the cellular mechanisms regulating protein aggregation will help develop future treatments. To identify such mechanisms, we conducted a forward genetic screen in a C. elegans model of polyglutamine aggregation and identified the protein MOAG-2/LIR-3 as a driver of protein aggregation. In the absence of polyglutamine, MOAG-2/LIR-3 regulates the RNA polymerase III-associated transcription of small non-coding RNAs. This regulation is lost in the presence of polyglutamine, which mislocalizes MOAG-2/LIR-3 from the nucleus to the cytosol. We then show biochemically that MOAG-2/LIR-3 can also catalyze the aggregation of polyglutamine-expanded huntingtin. These results suggest that polyglutamine can induce an aggregation-promoting activity of MOAG-2/LIR-3 in the cytosol. The concept that certain aggregation-prone proteins can convert other endogenous proteins into drivers of aggregation and toxicity adds to the understanding of how cellular homeostasis can be deteriorated in protein misfolding diseases."xsd:string
http://purl.uniprot.org/citations/28306505http://purl.org/dc/terms/identifier"doi:10.1016/j.molcel.2017.02.022"xsd:string
http://purl.uniprot.org/citations/28306505http://purl.org/dc/terms/identifier"doi:10.1016/j.molcel.2017.02.022"xsd:string
http://purl.uniprot.org/citations/28306505http://purl.uniprot.org/core/author"Wang H.H."xsd:string
http://purl.uniprot.org/citations/28306505http://purl.uniprot.org/core/author"Wang H.H."xsd:string
http://purl.uniprot.org/citations/28306505http://purl.uniprot.org/core/author"Wanker E.E."xsd:string
http://purl.uniprot.org/citations/28306505http://purl.uniprot.org/core/author"Wanker E.E."xsd:string
http://purl.uniprot.org/citations/28306505http://purl.uniprot.org/core/author"Nollen E.A."xsd:string
http://purl.uniprot.org/citations/28306505http://purl.uniprot.org/core/author"Nollen E.A."xsd:string
http://purl.uniprot.org/citations/28306505http://purl.uniprot.org/core/author"Calkhoven C.F."xsd:string
http://purl.uniprot.org/citations/28306505http://purl.uniprot.org/core/author"Calkhoven C.F."xsd:string
http://purl.uniprot.org/citations/28306505http://purl.uniprot.org/core/author"Reinke V."xsd:string
http://purl.uniprot.org/citations/28306505http://purl.uniprot.org/core/author"Reinke V."xsd:string
http://purl.uniprot.org/citations/28306505http://purl.uniprot.org/core/author"Mata-Cabana A."xsd:string
http://purl.uniprot.org/citations/28306505http://purl.uniprot.org/core/author"Mata-Cabana A."xsd:string
http://purl.uniprot.org/citations/28306505http://purl.uniprot.org/core/author"de Jong T."xsd:string
http://purl.uniprot.org/citations/28306505http://purl.uniprot.org/core/author"de Jong T."xsd:string
http://purl.uniprot.org/citations/28306505http://purl.uniprot.org/core/author"Kudron M."xsd:string
http://purl.uniprot.org/citations/28306505http://purl.uniprot.org/core/author"Kudron M."xsd:string
http://purl.uniprot.org/citations/28306505http://purl.uniprot.org/core/author"Aprile F.A."xsd:string
http://purl.uniprot.org/citations/28306505http://purl.uniprot.org/core/author"Aprile F.A."xsd:string
http://purl.uniprot.org/citations/28306505http://purl.uniprot.org/core/author"Guryev V."xsd:string
http://purl.uniprot.org/citations/28306505http://purl.uniprot.org/core/author"Guryev V."xsd:string