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http://purl.uniprot.org/citations/16306937http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/16306937http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/16306937http://www.w3.org/2000/01/rdf-schema#comment"Toll-like receptors (TLRs) are activated by pathogen-associated molecular patterns to induce innate immune responses and production of pro-inflammatory cytokines, interferons and anti-inflammatory cytokines. TLRs activate downstream effectors through adaptors that contain Toll/interleukin-1 receptor (TIR) domains, but the mechanisms accounting for diversification of TLR effector functions are unclear. To dissect biochemically TLR signalling, we established a system for isolating signalling complexes assembled by dimerized adaptors. Using MyD88 as a prototypical adaptor, we identified TNF receptor-associated factor 3 (TRAF3) as a new component of TIR signalling complexes that is recruited along with TRAF6. Using myeloid cells from TRAF3- and TRAF6-deficient mice, we show that TRAF3 is essential for the induction of type I interferons (IFN) and the anti-inflammatory cytokine interleukin-10 (IL-10), but is dispensable for expression of pro-inflammatory cytokines. In fact, TRAF3-deficient cells overproduce pro-inflammatory cytokines owing to defective IL-10 production. Despite their structural similarity, the functions of TRAF3 and TRAF6 are largely distinct. TRAF3 is also recruited to the adaptor TRIF (Toll/IL-1 receptor domain-containing adaptor-inducing IFN-beta) and is required for marshalling the protein kinase TBK1 (also called NAK) into TIR signalling complexes, thereby explaining its unique role in activation of the IFN response."xsd:string
http://purl.uniprot.org/citations/16306937http://purl.org/dc/terms/identifier"doi:10.1038/nature04369"xsd:string
http://purl.uniprot.org/citations/16306937http://purl.org/dc/terms/identifier"doi:10.1038/nature04369"xsd:string
http://purl.uniprot.org/citations/16306937http://purl.uniprot.org/core/author"Blagoev B."xsd:string
http://purl.uniprot.org/citations/16306937http://purl.uniprot.org/core/author"Blagoev B."xsd:string
http://purl.uniprot.org/citations/16306937http://purl.uniprot.org/core/author"Kratchmarova I."xsd:string
http://purl.uniprot.org/citations/16306937http://purl.uniprot.org/core/author"Kratchmarova I."xsd:string
http://purl.uniprot.org/citations/16306937http://purl.uniprot.org/core/author"Mann M."xsd:string
http://purl.uniprot.org/citations/16306937http://purl.uniprot.org/core/author"Mann M."xsd:string
http://purl.uniprot.org/citations/16306937http://purl.uniprot.org/core/author"Karin M."xsd:string
http://purl.uniprot.org/citations/16306937http://purl.uniprot.org/core/author"Karin M."xsd:string
http://purl.uniprot.org/citations/16306937http://purl.uniprot.org/core/author"Raz E."xsd:string
http://purl.uniprot.org/citations/16306937http://purl.uniprot.org/core/author"Raz E."xsd:string
http://purl.uniprot.org/citations/16306937http://purl.uniprot.org/core/author"Hsu L.C."xsd:string
http://purl.uniprot.org/citations/16306937http://purl.uniprot.org/core/author"Hsu L.C."xsd:string
http://purl.uniprot.org/citations/16306937http://purl.uniprot.org/core/author"Kamps M.P."xsd:string
http://purl.uniprot.org/citations/16306937http://purl.uniprot.org/core/author"Kamps M.P."xsd:string
http://purl.uniprot.org/citations/16306937http://purl.uniprot.org/core/author"Wang G.G."xsd:string
http://purl.uniprot.org/citations/16306937http://purl.uniprot.org/core/author"Wang G.G."xsd:string
http://purl.uniprot.org/citations/16306937http://purl.uniprot.org/core/author"Wagner H."xsd:string
http://purl.uniprot.org/citations/16306937http://purl.uniprot.org/core/author"Wagner H."xsd:string
http://purl.uniprot.org/citations/16306937http://purl.uniprot.org/core/author"Hacker H."xsd:string
http://purl.uniprot.org/citations/16306937http://purl.uniprot.org/core/author"Hacker H."xsd:string