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http://purl.uniprot.org/citations/19525941http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/19525941http://www.w3.org/2000/01/rdf-schema#comment"Selected vulnerability of neurons in Huntington's disease suggests that alterations occur in a cellular process that is particularly critical for neuronal function. Supporting this idea, pathogenic Htt (polyQ-Htt) inhibits fast axonal transport (FAT) in various cellular and animal models of Huntington's disease (mouse and squid), but the molecular basis of this effect remains unknown. We found that polyQ-Htt inhibited FAT through a mechanism involving activation of axonal cJun N-terminal kinase (JNK). Accordingly, we observed increased activation of JNK in vivo in cellular and mouse models of Huntington's disease. Additional experiments indicated that the effects of polyQ-Htt on FAT were mediated by neuron-specific JNK3 and not by ubiquitously expressed JNK1, providing a molecular basis for neuron-specific pathology in Huntington's disease. Mass spectrometry identified a residue in the kinesin-1 motor domain that was phosphorylated by JNK3 and this modification reduced kinesin-1 binding to microtubules. These data identify JNK3 as a critical mediator of polyQ-Htt toxicity and provide a molecular basis for polyQ-Htt-induced inhibition of FAT."xsd:string
http://purl.uniprot.org/citations/19525941http://purl.org/dc/terms/identifier"doi:10.1038/nn.2346"xsd:string
http://purl.uniprot.org/citations/19525941http://purl.uniprot.org/core/author"Han D."xsd:string
http://purl.uniprot.org/citations/19525941http://purl.uniprot.org/core/author"Huang C.F."xsd:string
http://purl.uniprot.org/citations/19525941http://purl.uniprot.org/core/author"Yoshioka K."xsd:string
http://purl.uniprot.org/citations/19525941http://purl.uniprot.org/core/author"Pigino G."xsd:string
http://purl.uniprot.org/citations/19525941http://purl.uniprot.org/core/author"Liu K."xsd:string
http://purl.uniprot.org/citations/19525941http://purl.uniprot.org/core/author"Kaminska A."xsd:string
http://purl.uniprot.org/citations/19525941http://purl.uniprot.org/core/author"Banker G."xsd:string
http://purl.uniprot.org/citations/19525941http://purl.uniprot.org/core/author"Brady S.T."xsd:string
http://purl.uniprot.org/citations/19525941http://purl.uniprot.org/core/author"Bjorkblom B."xsd:string
http://purl.uniprot.org/citations/19525941http://purl.uniprot.org/core/author"Coffey E.T."xsd:string
http://purl.uniprot.org/citations/19525941http://purl.uniprot.org/core/author"Bagnato C."xsd:string
http://purl.uniprot.org/citations/19525941http://purl.uniprot.org/core/author"Morfini G.A."xsd:string
http://purl.uniprot.org/citations/19525941http://purl.uniprot.org/core/author"Pollema S.L."xsd:string
http://purl.uniprot.org/citations/19525941http://purl.uniprot.org/core/author"You Y.M."xsd:string
http://purl.uniprot.org/citations/19525941http://purl.uniprot.org/core/date"2009"xsd:gYear
http://purl.uniprot.org/citations/19525941http://purl.uniprot.org/core/name"Nat Neurosci"xsd:string
http://purl.uniprot.org/citations/19525941http://purl.uniprot.org/core/pages"864-871"xsd:string
http://purl.uniprot.org/citations/19525941http://purl.uniprot.org/core/title"Pathogenic huntingtin inhibits fast axonal transport by activating JNK3 and phosphorylating kinesin."xsd:string
http://purl.uniprot.org/citations/19525941http://purl.uniprot.org/core/volume"12"xsd:string
http://purl.uniprot.org/citations/19525941http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/19525941
http://purl.uniprot.org/citations/19525941http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/19525941
http://purl.uniprot.org/uniprot/#_A0A0G2JG69-mappedCitation-19525941http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/19525941