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http://purl.uniprot.org/citations/19279216http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/19279216http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/19279216http://www.w3.org/2000/01/rdf-schema#comment"Neurodegenerative disease in humans and mice can be caused by mutations affecting the microtubule motor dynein or its biochemical regulator, dynactin, a multiprotein complex required for dynein function (1-4). A single amino acid change, G59S, in the conserved cytoskeletal-associated protein glycine-rich (CAP-Gly) domain of the p150(glued) subunit of dynactin can cause motor neuron degeneration in humans and mice, which resembles ALS (2, 5-8). The molecular mechanism by which G59S impairs the function of dynein is not understood. Also, the relevance of the CAP-Gly domain for dynein motility has not been demonstrated in vivo. Here, we generate a mutant that is analogous to G59S in budding yeast, and show that this mutation produces a highly specific phenotype related to dynein function. The effect of the point mutation is identical to that of complete loss of the CAP-Gly domain. Our results demonstrate that the CAP-Gly domain has a critical role in the initiation and persistence of dynein-dependent movement of the mitotic spindle and nucleus, but it is otherwise dispensable for dynein-based movement. The need for this function appears to be context-dependent, and we speculate that CAP-Gly activity may only be necessary when dynein needs to overcome high force thresholds to produce movement."xsd:string
http://purl.uniprot.org/citations/19279216http://purl.org/dc/terms/identifier"doi:10.1073/pnas.0810828106"xsd:string
http://purl.uniprot.org/citations/19279216http://purl.org/dc/terms/identifier"doi:10.1073/pnas.0810828106"xsd:string
http://purl.uniprot.org/citations/19279216http://purl.uniprot.org/core/author"Sept D."xsd:string
http://purl.uniprot.org/citations/19279216http://purl.uniprot.org/core/author"Sept D."xsd:string
http://purl.uniprot.org/citations/19279216http://purl.uniprot.org/core/author"Cooper J.A."xsd:string
http://purl.uniprot.org/citations/19279216http://purl.uniprot.org/core/author"Cooper J.A."xsd:string
http://purl.uniprot.org/citations/19279216http://purl.uniprot.org/core/author"Moore J.K."xsd:string
http://purl.uniprot.org/citations/19279216http://purl.uniprot.org/core/author"Moore J.K."xsd:string
http://purl.uniprot.org/citations/19279216http://purl.uniprot.org/core/date"2009"xsd:gYear
http://purl.uniprot.org/citations/19279216http://purl.uniprot.org/core/date"2009"xsd:gYear
http://purl.uniprot.org/citations/19279216http://purl.uniprot.org/core/name"Proc. Natl. Acad. Sci. U.S.A."xsd:string
http://purl.uniprot.org/citations/19279216http://purl.uniprot.org/core/name"Proc. Natl. Acad. Sci. U.S.A."xsd:string
http://purl.uniprot.org/citations/19279216http://purl.uniprot.org/core/pages"5147-5152"xsd:string
http://purl.uniprot.org/citations/19279216http://purl.uniprot.org/core/pages"5147-5152"xsd:string
http://purl.uniprot.org/citations/19279216http://purl.uniprot.org/core/title"Neurodegeneration mutations in dynactin impair dynein-dependent nuclear migration."xsd:string
http://purl.uniprot.org/citations/19279216http://purl.uniprot.org/core/title"Neurodegeneration mutations in dynactin impair dynein-dependent nuclear migration."xsd:string
http://purl.uniprot.org/citations/19279216http://purl.uniprot.org/core/volume"106"xsd:string
http://purl.uniprot.org/citations/19279216http://purl.uniprot.org/core/volume"106"xsd:string
http://purl.uniprot.org/citations/19279216http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/19279216
http://purl.uniprot.org/citations/19279216http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/19279216
http://purl.uniprot.org/citations/19279216http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/19279216
http://purl.uniprot.org/citations/19279216http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/19279216