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http://purl.uniprot.org/citations/17724133http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/17724133http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/17724133http://www.w3.org/2000/01/rdf-schema#comment"The innate immune system relies on evolutionally conserved Toll-like receptors (TLRs) to recognize diverse microbial molecular structures. Most TLRs depend on a family of adaptor proteins termed MyD88s to transduce their signals. Critical roles of MyD88-1-4 in host defense were demonstrated by defective immune responses in knockout mice. In contrast, the sites of expression and functions of vertebrate MyD88-5 have remained elusive. We show that MyD88-5 is distinct from other MyD88s in that MyD88-5 is preferentially expressed in neurons, colocalizes in part with mitochondria and JNK3, and regulates neuronal death. We prepared MyD88-5/GFP transgenic mice via a bacterial artificial chromosome to preserve its endogenous expression pattern. MyD88-5/GFP was detected chiefly in the brain, where it associated with punctate structures within neurons and copurified in part with mitochondria. In vitro, MyD88-5 co-immunoprecipitated with JNK3 and recruited JNK3 from cytosol to mitochondria. Hippocampal neurons from MyD88-5-deficient mice were protected from death after deprivation of oxygen and glucose. In contrast, MyD88-5-null macrophages behaved like wild-type cells in their response to microbial products. Thus, MyD88-5 appears unique among MyD88s in functioning to mediate stress-induced neuronal toxicity."xsd:string
http://purl.uniprot.org/citations/17724133http://purl.org/dc/terms/identifier"doi:10.1084/jem.20070868"xsd:string
http://purl.uniprot.org/citations/17724133http://purl.org/dc/terms/identifier"doi:10.1084/jem.20070868"xsd:string
http://purl.uniprot.org/citations/17724133http://purl.uniprot.org/core/author"Kim Y."xsd:string
http://purl.uniprot.org/citations/17724133http://purl.uniprot.org/core/author"Kim Y."xsd:string
http://purl.uniprot.org/citations/17724133http://purl.uniprot.org/core/author"Li C."xsd:string
http://purl.uniprot.org/citations/17724133http://purl.uniprot.org/core/author"Li C."xsd:string
http://purl.uniprot.org/citations/17724133http://purl.uniprot.org/core/author"Lee J."xsd:string
http://purl.uniprot.org/citations/17724133http://purl.uniprot.org/core/author"Lee J."xsd:string
http://purl.uniprot.org/citations/17724133http://purl.uniprot.org/core/author"Zhou P."xsd:string
http://purl.uniprot.org/citations/17724133http://purl.uniprot.org/core/author"Zhou P."xsd:string
http://purl.uniprot.org/citations/17724133http://purl.uniprot.org/core/author"Nathan C."xsd:string
http://purl.uniprot.org/citations/17724133http://purl.uniprot.org/core/author"Nathan C."xsd:string
http://purl.uniprot.org/citations/17724133http://purl.uniprot.org/core/author"Qian L."xsd:string
http://purl.uniprot.org/citations/17724133http://purl.uniprot.org/core/author"Qian L."xsd:string
http://purl.uniprot.org/citations/17724133http://purl.uniprot.org/core/author"Chuang J.Z."xsd:string
http://purl.uniprot.org/citations/17724133http://purl.uniprot.org/core/author"Chuang J.Z."xsd:string
http://purl.uniprot.org/citations/17724133http://purl.uniprot.org/core/author"Ding A."xsd:string
http://purl.uniprot.org/citations/17724133http://purl.uniprot.org/core/author"Ding A."xsd:string
http://purl.uniprot.org/citations/17724133http://purl.uniprot.org/core/author"Iadecola C."xsd:string
http://purl.uniprot.org/citations/17724133http://purl.uniprot.org/core/author"Iadecola C."xsd:string
http://purl.uniprot.org/citations/17724133http://purl.uniprot.org/core/date"2007"xsd:gYear
http://purl.uniprot.org/citations/17724133http://purl.uniprot.org/core/date"2007"xsd:gYear