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http://purl.uniprot.org/citations/27794068http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/27794068http://www.w3.org/2000/01/rdf-schema#comment"TLR2 associates with TLR1 and recognizes microbial lipoproteins. Pam3CSK4, a triacylated lipoprotein, is anchored to the extracellular domain of TLR1 and TLR2 and induces pro-inflammatory signals. Here we show that C4b binding protein (C4BP), which is a complement pathway inhibitor, is a TLR2-associated molecule. Immunoprecipitation assay using anti-TLR2 mAb shows that C4BP binds to TLR2. In C4BP-deficient mice, Pam3CSK4-induced IL-6 levels were increased compared with wild type mice. In C4BP-expressing cells, Pam3CSK4-induced IL-8 production was reduced depending on the C4BP expression levels. These results reveal the important role of C4BP in negative regulation of TLR1/2-dependent pro-inflammatory cytokine production. Furthermore, using a fluorescent conjugated Pam3CSK4, we show that C4BP blocks the binding of Pam3CSK4 to TLR1/2. Finally, we show that exogenous C4BP also inhibits Pam3CSK4-induced signaling leading to IL-8 production. Our results indicate C4BP binding to TLR2 and consequent neutralization of its activity otherwise inducing pro-inflammatory cytokine production. C4BP is a negative regulator of TLR1/2 activity."xsd:string
http://purl.uniprot.org/citations/27794068http://purl.org/dc/terms/identifier"doi:10.1177/1753425916672312"xsd:string
http://purl.uniprot.org/citations/27794068http://purl.uniprot.org/core/author"Kobayashi T."xsd:string
http://purl.uniprot.org/citations/27794068http://purl.uniprot.org/core/author"Morita N."xsd:string
http://purl.uniprot.org/citations/27794068http://purl.uniprot.org/core/author"Shibata T."xsd:string
http://purl.uniprot.org/citations/27794068http://purl.uniprot.org/core/author"Takahashi K."xsd:string
http://purl.uniprot.org/citations/27794068http://purl.uniprot.org/core/author"Miyake K."xsd:string
http://purl.uniprot.org/citations/27794068http://purl.uniprot.org/core/author"Takagi H."xsd:string
http://purl.uniprot.org/citations/27794068http://purl.uniprot.org/core/author"Kusumoto Y."xsd:string
http://purl.uniprot.org/citations/27794068http://purl.uniprot.org/core/author"Nonaka M.I."xsd:string
http://purl.uniprot.org/citations/27794068http://purl.uniprot.org/core/author"Ichimonji I."xsd:string
http://purl.uniprot.org/citations/27794068http://purl.uniprot.org/core/author"Yamai I."xsd:string
http://purl.uniprot.org/citations/27794068http://purl.uniprot.org/core/author"Takamura S.A."xsd:string
http://purl.uniprot.org/citations/27794068http://purl.uniprot.org/core/date"2017"xsd:gYear
http://purl.uniprot.org/citations/27794068http://purl.uniprot.org/core/name"Innate Immun"xsd:string
http://purl.uniprot.org/citations/27794068http://purl.uniprot.org/core/pages"11-19"xsd:string
http://purl.uniprot.org/citations/27794068http://purl.uniprot.org/core/title"C4b binding protein negatively regulates TLR1/2 response."xsd:string
http://purl.uniprot.org/citations/27794068http://purl.uniprot.org/core/volume"23"xsd:string
http://purl.uniprot.org/citations/27794068http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/27794068
http://purl.uniprot.org/citations/27794068http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/27794068
http://purl.uniprot.org/uniprot/#_E9PUZ8-mappedCitation-27794068http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27794068
http://purl.uniprot.org/uniprot/#_F6QLW4-mappedCitation-27794068http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27794068
http://purl.uniprot.org/uniprot/#_P08607-mappedCitation-27794068http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27794068
http://purl.uniprot.org/uniprot/#_Q3UW06-mappedCitation-27794068http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27794068