| http://purl.uniprot.org/citations/22079989 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/22079989 | http://www.w3.org/2000/01/rdf-schema#comment | "TNFR-associated factor (TRAF) 3 is an important adaptor that transmits upstream activation signals to protein kinases that phosphorylate transcription factors to induce the production of type I IFNs, the important effectors in innate antiviral immune response. MIP-T3 interacts specifically with TRAF3, but its function in innate IFN response remains unclear. In this study, we demonstrated a negative regulatory role of MIP-T3 in type I IFN production. Overexpression of MIP-T3 inhibited RIG-I-, MDA5-, VISA-, TBK1-, and IKKε-induced transcriptional activity mediated by IFN-stimulated response elements and IFN-β promoter. MIP-T3 interacted with TRAF3 and perturbed in a dose-dependent manner the formation of functional complexes of TRAF3 with VISA, TBK1, IKKε, and IFN regulatory factor 3. Consistent with this finding, retinoic acid-inducible gene I- and TBK1-induced phosphorylation of IFN regulatory factor 3 was significantly diminished when MIP-T3 was overexpressed. Depletion of MIP-T3 facilitated Sendai virus-induced activation of IFN production and attenuated the replication of vesicular stomatitis virus. In addition, MIP-T3 was found to be dissociated from TRAF3 during the course of Sendai virus infection. Our findings suggest that MIP-T3 functions as a negative regulator of innate IFN response by preventing TRAF3 from forming protein complexes with critical downstream transducers and effectors."xsd:string |
| http://purl.uniprot.org/citations/22079989 | http://purl.org/dc/terms/identifier | "doi:10.4049/jimmunol.1100719"xsd:string |
| http://purl.uniprot.org/citations/22079989 | http://purl.uniprot.org/core/author | "Li J."xsd:string |
| http://purl.uniprot.org/citations/22079989 | http://purl.uniprot.org/core/author | "Ng M.H."xsd:string |
| http://purl.uniprot.org/citations/22079989 | http://purl.uniprot.org/core/author | "Ho T.H."xsd:string |
| http://purl.uniprot.org/citations/22079989 | http://purl.uniprot.org/core/author | "Jin D.Y."xsd:string |
| http://purl.uniprot.org/citations/22079989 | http://purl.uniprot.org/core/author | "Siu K.L."xsd:string |
| http://purl.uniprot.org/citations/22079989 | http://purl.uniprot.org/core/author | "Kok K.H."xsd:string |
| http://purl.uniprot.org/citations/22079989 | http://purl.uniprot.org/core/date | "2011"xsd:gYear |
| http://purl.uniprot.org/citations/22079989 | http://purl.uniprot.org/core/name | "J Immunol"xsd:string |
| http://purl.uniprot.org/citations/22079989 | http://purl.uniprot.org/core/pages | "6473-6482"xsd:string |
| http://purl.uniprot.org/citations/22079989 | http://purl.uniprot.org/core/title | "MIP-T3 is a negative regulator of innate type I IFN response."xsd:string |
| http://purl.uniprot.org/citations/22079989 | http://purl.uniprot.org/core/volume | "187"xsd:string |
| http://purl.uniprot.org/citations/22079989 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/22079989 |
| http://purl.uniprot.org/citations/22079989 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/22079989 |
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