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http://purl.uniprot.org/citations/20434986http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/20434986http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/20434986http://www.w3.org/2000/01/rdf-schema#comment"Stringent control of the NF-kappaB and type I interferon signaling pathways is critical to effective host immune responses, yet the molecular mechanisms that negatively regulate these pathways are poorly understood. Here, we show that NLRC5, a member of the highly conserved NOD-like protein family, can inhibit the IKK complex and RIG-I/MDA5 function. NLRC5 inhibited NF-kappaB-dependent responses by interacting with IKKalpha and IKKbeta and blocking their phosphorylation. It also interacted with RIG-I and MDA5, but not with MAVS, to inhibit RLR-mediated type I interferon responses. Consistent with these observations, NLRC5-specific siRNA knockdown not only enhanced the activation of NF-kappaB and its responsive genes, TNF-alpha and IL-6, but also promoted type I interferon signaling and antiviral immunity. Our findings identify NLRC5 as a negative regulator that blocks two central components of the NF-kappaB and type I interferon signaling pathways and suggest an important role for NLRC5 in homeostatic control of innate immunity."xsd:string
http://purl.uniprot.org/citations/20434986http://purl.org/dc/terms/identifier"doi:10.1016/j.cell.2010.03.040"xsd:string
http://purl.uniprot.org/citations/20434986http://purl.org/dc/terms/identifier"doi:10.1016/j.cell.2010.03.040"xsd:string
http://purl.uniprot.org/citations/20434986http://purl.uniprot.org/core/author"Ji J."xsd:string
http://purl.uniprot.org/citations/20434986http://purl.uniprot.org/core/author"Ji J."xsd:string
http://purl.uniprot.org/citations/20434986http://purl.uniprot.org/core/author"Chen Z.J."xsd:string
http://purl.uniprot.org/citations/20434986http://purl.uniprot.org/core/author"Chen Z.J."xsd:string
http://purl.uniprot.org/citations/20434986http://purl.uniprot.org/core/author"Hong J."xsd:string
http://purl.uniprot.org/citations/20434986http://purl.uniprot.org/core/author"Hong J."xsd:string
http://purl.uniprot.org/citations/20434986http://purl.uniprot.org/core/author"Shen P."xsd:string
http://purl.uniprot.org/citations/20434986http://purl.uniprot.org/core/author"Shen P."xsd:string
http://purl.uniprot.org/citations/20434986http://purl.uniprot.org/core/author"Zhu L."xsd:string
http://purl.uniprot.org/citations/20434986http://purl.uniprot.org/core/author"Zhu L."xsd:string
http://purl.uniprot.org/citations/20434986http://purl.uniprot.org/core/author"Zheng S."xsd:string
http://purl.uniprot.org/citations/20434986http://purl.uniprot.org/core/author"Zheng S."xsd:string
http://purl.uniprot.org/citations/20434986http://purl.uniprot.org/core/author"Cui J."xsd:string
http://purl.uniprot.org/citations/20434986http://purl.uniprot.org/core/author"Cui J."xsd:string
http://purl.uniprot.org/citations/20434986http://purl.uniprot.org/core/author"Wang H.Y."xsd:string
http://purl.uniprot.org/citations/20434986http://purl.uniprot.org/core/author"Wang H.Y."xsd:string
http://purl.uniprot.org/citations/20434986http://purl.uniprot.org/core/author"Wang R.F."xsd:string
http://purl.uniprot.org/citations/20434986http://purl.uniprot.org/core/author"Wang R.F."xsd:string
http://purl.uniprot.org/citations/20434986http://purl.uniprot.org/core/author"Xia X."xsd:string
http://purl.uniprot.org/citations/20434986http://purl.uniprot.org/core/author"Xia X."xsd:string