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rdf:type
lifeskim:mentions
pubmed:dateCreated
2011-9-14
pubmed:abstractText
Protein aggregation is a common hallmark of a number of age-related neurodegenerative diseases, including Alzheimer's, Parkinson's, and polyglutamine-expansion disorders such as Huntington's disease, but how aggregation-prone proteins lead to pathology is not known. Using a genome-wide RNAi screen in a C. elegans-model for polyglutamine aggregation, we previously identified 186 genes that suppress aggregation. Using an RNAi screen for human orthologs of these genes, we here present 26 human genes that suppress aggregation of mutant huntingtin in a human cell line. Among these are genes that have not been previously linked to mutant huntingtin aggregation. They include those encoding eukaryotic translation initiation, elongation and translation factors, and genes that have been previously associated with other neurodegenerative diseases, like the ATP-ase family gene 3-like 2 (AFG3L2) and ubiquitin-like modifier activating enzyme 1 (UBA1). Unravelling the role of these genes will broaden our understanding of the pathogenesis of Huntington's disease.
pubmed:language
eng
pubmed:journal
pubmed:status
PubMed-not-MEDLINE
pubmed:issn
2157-3999
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
3
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
RRN1255
pubmed:year
2011
pubmed:articleTitle
Modifiers of mutant huntingtin aggregation: functional conservation of C. elegans-modifiers of polyglutamine aggregation.
pubmed:affiliation
Department of Genetics, University Medical Centre Groningen, University of Groningen, PO Box 30001, 9700 RB Groningen; Groningen Bioinformatics Centre, Nijenborgh 7, 9747 AG Groningen, The Netherlands and Genomics Coordination Center, Department of Genetics, University Medical Center Groningen and Groningen Bioinformatics Center, University of Groningen, P.O. Box 30001, 9700 RB, Groningen, The Netherlands.
pubmed:publicationType
Journal Article