Anti-MAVS

In 1X PBS, pH 7.4, with 0.09% sodium azide. Double-stranded RNA viruses are recognized in a cell type-dependent manner by the transmembrane receptor TLR3 or by the cytoplasmic RNA helicases MDA5 and RIGI. These interactions initiate signaling pathways that differ in their initial steps but converge in the activation of the protein kinases IKKA and IKKB which activate NFKB, or TBK1 and IKKE (IKBKE, MIM 605048), which activate IRF3. Activated IRF3 and NFKB induce transcription of IFNB. For the TLR3 pathway, the intermediary molecule before the pathways converge is the cytoplasmic protein TRIF. For RIGI, the intermediary protein is mitochondria-bound IPS1. Protein function: Required for innate immune defense against viruses. Acts downstream of DDX58/RIG-I and IFIH1/MDA5, which detect intracellular dsRNA produced during viral replication, to coordinate pathways leading to the activation of NF-kappa-B, IRF3 and IRF7, and to the subsequent induction of antiviral cytokines such as IFN-beta and RANTES (CCL5). Peroxisomal and mitochondrial MAVS act sequentially to create an antiviral cellular state. Upon viral infection, peroxisomal MAVS induces the rapid interferon- independent expression of defense factors that provide short-term protection, whereas mitochondrial MAVS activates an interferon- dependent signaling pathway with delayed kinetics, which amplifies and stabilizes the antiviral response. May activate the same pathways following detection of extracellular dsRNA by TLR3. May protect cells from apoptosis. [The UniProt Consortium]