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http://purl.uniprot.org/citations/15767370http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/15767370http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/15767370http://www.w3.org/2000/01/rdf-schema#comment"Toll-like receptors (TLRs) recognize microbial pathogens and trigger innate immune responses. Among TLR family members, TLR7, TLR8, and TLR9 induce interferon (IFN)-alpha in plasmacytoid dendritic cells (pDCs). This induction requires the formation of a complex consisting of the adaptor MyD88, tumor necrosis factor (TNF) receptor-associated factor 6 (TRAF6) and IFN regulatory factor (IRF) 7. Here we show an essential role of IL-1 receptor-associated kinase (IRAK)-1 in TLR7- and TLR9-mediated IRF7 signaling pathway. IRAK-1 directly bound and phosphorylated IRF7 in vitro. The kinase activity of IRAK-1 was necessary for transcriptional activation of IRF7. TLR7- and TLR9-mediated IFN-alpha production was abolished in Irak-1-deficient mice, whereas inflammatory cytokine production was not impaired. Despite normal activation of NF-kappaB and mitogen-activated protein kinases, IRF7 was not activated by a TLR9 ligand in Irak-1-deficient pDCs. These results indicated that IRAK-1 is a specific regulator for TLR7- and TLR9-mediated IFN-alpha induction in pDCs."xsd:string
http://purl.uniprot.org/citations/15767370http://purl.org/dc/terms/identifier"doi:10.1084/jem.20042372"xsd:string
http://purl.uniprot.org/citations/15767370http://purl.org/dc/terms/identifier"doi:10.1084/jem.20042372"xsd:string
http://purl.uniprot.org/citations/15767370http://purl.uniprot.org/core/author"Kato H."xsd:string
http://purl.uniprot.org/citations/15767370http://purl.uniprot.org/core/author"Kato H."xsd:string
http://purl.uniprot.org/citations/15767370http://purl.uniprot.org/core/author"Kawai T."xsd:string
http://purl.uniprot.org/citations/15767370http://purl.uniprot.org/core/author"Kawai T."xsd:string
http://purl.uniprot.org/citations/15767370http://purl.uniprot.org/core/author"Matsuda M."xsd:string
http://purl.uniprot.org/citations/15767370http://purl.uniprot.org/core/author"Matsuda M."xsd:string
http://purl.uniprot.org/citations/15767370http://purl.uniprot.org/core/author"Sato S."xsd:string
http://purl.uniprot.org/citations/15767370http://purl.uniprot.org/core/author"Sato S."xsd:string
http://purl.uniprot.org/citations/15767370http://purl.uniprot.org/core/author"Yamamoto M."xsd:string
http://purl.uniprot.org/citations/15767370http://purl.uniprot.org/core/author"Yamamoto M."xsd:string
http://purl.uniprot.org/citations/15767370http://purl.uniprot.org/core/author"Akira S."xsd:string
http://purl.uniprot.org/citations/15767370http://purl.uniprot.org/core/author"Akira S."xsd:string
http://purl.uniprot.org/citations/15767370http://purl.uniprot.org/core/author"Takeuchi O."xsd:string
http://purl.uniprot.org/citations/15767370http://purl.uniprot.org/core/author"Takeuchi O."xsd:string
http://purl.uniprot.org/citations/15767370http://purl.uniprot.org/core/author"Ishii K.J."xsd:string
http://purl.uniprot.org/citations/15767370http://purl.uniprot.org/core/author"Ishii K.J."xsd:string
http://purl.uniprot.org/citations/15767370http://purl.uniprot.org/core/author"Takeshita F."xsd:string
http://purl.uniprot.org/citations/15767370http://purl.uniprot.org/core/author"Takeshita F."xsd:string
http://purl.uniprot.org/citations/15767370http://purl.uniprot.org/core/author"Uematsu S."xsd:string
http://purl.uniprot.org/citations/15767370http://purl.uniprot.org/core/author"Uematsu S."xsd:string