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http://purl.uniprot.org/citations/12855817http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/12855817http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/12855817http://www.w3.org/2000/01/rdf-schema#comment"Stimulation of Toll-like receptors (TLRs) triggers activation of a common MyD88-dependent signaling pathway as well as a MyD88-independent pathway that is unique to TLR3 and TLR4 signaling pathways leading to interferon (IFN)-beta production. Here we disrupted the gene encoding a Toll/IL-1 receptor (TIR) domain-containing adaptor, TRIF. TRIF-deficient mice were defective in both TLR3- and TLR4-mediated expression of IFN-beta and activation of IRF-3. Furthermore, inflammatory cytokine production in response to the TLR4 ligand, but not to other TLR ligands, was severely impaired in TRIF-deficient macrophages. Mice deficient in both MyD88 and TRIF showed complete loss of nuclear factor kappa B activation in response to TLR4 stimulation. These findings demonstrate that TRIF is essential for TLR3- and TLR4-mediated signaling pathways facilitating mammalian antiviral host defense."xsd:string
http://purl.uniprot.org/citations/12855817http://purl.org/dc/terms/identifier"doi:10.1126/science.1087262"xsd:string
http://purl.uniprot.org/citations/12855817http://purl.org/dc/terms/identifier"doi:10.1126/science.1087262"xsd:string
http://purl.uniprot.org/citations/12855817http://purl.uniprot.org/core/author"Hemmi H."xsd:string
http://purl.uniprot.org/citations/12855817http://purl.uniprot.org/core/author"Hemmi H."xsd:string
http://purl.uniprot.org/citations/12855817http://purl.uniprot.org/core/author"Sato S."xsd:string
http://purl.uniprot.org/citations/12855817http://purl.uniprot.org/core/author"Sato S."xsd:string
http://purl.uniprot.org/citations/12855817http://purl.uniprot.org/core/author"Yamamoto M."xsd:string
http://purl.uniprot.org/citations/12855817http://purl.uniprot.org/core/author"Yamamoto M."xsd:string
http://purl.uniprot.org/citations/12855817http://purl.uniprot.org/core/author"Takeda K."xsd:string
http://purl.uniprot.org/citations/12855817http://purl.uniprot.org/core/author"Takeda K."xsd:string
http://purl.uniprot.org/citations/12855817http://purl.uniprot.org/core/author"Okabe M."xsd:string
http://purl.uniprot.org/citations/12855817http://purl.uniprot.org/core/author"Okabe M."xsd:string
http://purl.uniprot.org/citations/12855817http://purl.uniprot.org/core/author"Akira S."xsd:string
http://purl.uniprot.org/citations/12855817http://purl.uniprot.org/core/author"Akira S."xsd:string
http://purl.uniprot.org/citations/12855817http://purl.uniprot.org/core/author"Sugiyama M."xsd:string
http://purl.uniprot.org/citations/12855817http://purl.uniprot.org/core/author"Sugiyama M."xsd:string
http://purl.uniprot.org/citations/12855817http://purl.uniprot.org/core/author"Hoshino K."xsd:string
http://purl.uniprot.org/citations/12855817http://purl.uniprot.org/core/author"Hoshino K."xsd:string
http://purl.uniprot.org/citations/12855817http://purl.uniprot.org/core/author"Kaisho T."xsd:string
http://purl.uniprot.org/citations/12855817http://purl.uniprot.org/core/author"Kaisho T."xsd:string
http://purl.uniprot.org/citations/12855817http://purl.uniprot.org/core/author"Takeuchi O."xsd:string
http://purl.uniprot.org/citations/12855817http://purl.uniprot.org/core/author"Takeuchi O."xsd:string