RDF/XMLNTriplesTurtleShow queryShare
SubjectPredicateObject
http://purl.uniprot.org/citations/18818105http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/18818105http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/18818105http://www.w3.org/2000/01/rdf-schema#comment"Viral infection triggers activation of transcription factors such as NF-kappaB and IRF3, which collaborate to induce type I interferons (IFNs) and elicit innate antiviral response. Here, we identified MITA as a critical mediator of virus-triggered type I IFN signaling by expression cloning. Overexpression of MITA activated IRF3, whereas knockdown of MITA inhibited virus-triggered activation of IRF3, expression of type I IFNs, and cellular antiviral response. MITA was found to localize to the outer membrane of mitochondria and to be associated with VISA, a mitochondrial protein that acts as an adaptor in virus-triggered signaling. MITA also interacted with IRF3 and recruited the kinase TBK1 to the VISA-associated complex. MITA was phosphorylated by TBK1, which is required for MITA-mediated activation of IRF3. Our results suggest that MITA is a critical mediator of virus-triggered IRF3 activation and IFN expression and further demonstrate the importance of certain mitochondrial proteins in innate antiviral immunity."xsd:string
http://purl.uniprot.org/citations/18818105http://purl.org/dc/terms/identifier"doi:10.1016/j.immuni.2008.09.003"xsd:string
http://purl.uniprot.org/citations/18818105http://purl.org/dc/terms/identifier"doi:10.1016/j.immuni.2008.09.003"xsd:string
http://purl.uniprot.org/citations/18818105http://purl.uniprot.org/core/author"He X."xsd:string
http://purl.uniprot.org/citations/18818105http://purl.uniprot.org/core/author"He X."xsd:string
http://purl.uniprot.org/citations/18818105http://purl.uniprot.org/core/author"Li S."xsd:string
http://purl.uniprot.org/citations/18818105http://purl.uniprot.org/core/author"Li S."xsd:string
http://purl.uniprot.org/citations/18818105http://purl.uniprot.org/core/author"Li Y."xsd:string
http://purl.uniprot.org/citations/18818105http://purl.uniprot.org/core/author"Li Y."xsd:string
http://purl.uniprot.org/citations/18818105http://purl.uniprot.org/core/author"Lei C."xsd:string
http://purl.uniprot.org/citations/18818105http://purl.uniprot.org/core/author"Lei C."xsd:string
http://purl.uniprot.org/citations/18818105http://purl.uniprot.org/core/author"Tien P."xsd:string
http://purl.uniprot.org/citations/18818105http://purl.uniprot.org/core/author"Tien P."xsd:string
http://purl.uniprot.org/citations/18818105http://purl.uniprot.org/core/author"Zhang L."xsd:string
http://purl.uniprot.org/citations/18818105http://purl.uniprot.org/core/author"Zhang L."xsd:string
http://purl.uniprot.org/citations/18818105http://purl.uniprot.org/core/author"Yang Y."xsd:string
http://purl.uniprot.org/citations/18818105http://purl.uniprot.org/core/author"Yang Y."xsd:string
http://purl.uniprot.org/citations/18818105http://purl.uniprot.org/core/author"Zhong B."xsd:string
http://purl.uniprot.org/citations/18818105http://purl.uniprot.org/core/author"Zhong B."xsd:string
http://purl.uniprot.org/citations/18818105http://purl.uniprot.org/core/author"Wang Y.-Y."xsd:string
http://purl.uniprot.org/citations/18818105http://purl.uniprot.org/core/author"Wang Y.-Y."xsd:string
http://purl.uniprot.org/citations/18818105http://purl.uniprot.org/core/author"Shu H.-B."xsd:string
http://purl.uniprot.org/citations/18818105http://purl.uniprot.org/core/author"Shu H.-B."xsd:string