Two distinct signaling pathways activate the host innate immunity against viral infection. One pathway is reliant on members of the Toll-like receptor (TLR) family while the other uses the RNA helicase RIG-I as a receptor for intracellular viral double-stranded RNA as a trigger for the immune response. MAVS is a mitochondrial membrane protein that was identified as a critical component in the IFN beta signaling pathways that recruits IRF-3 to RIG-I, leading to its activation and that of NF-kappa-B. MAVS is also thought to interact with other components of the innate immune pathway such as the TLR adapter protein TRIF, TRAF2 and TRAF6. MAVS also interacts with the IKK-alpha, IKK-beta and IKK-iota kinases through its C-terminal region. Cleavage of this region by the Hepatitis C virus (HCV) protease allows HCV to escape the host immune system. Multiple isoforms of MAVS are known to exist.
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Protein Aliases: CARD adapter inducing interferon beta; CARD adaptor inducing IFN-beta; Cardif; IFN-B promoter stimulator 1; IFN-beta promoter stimulator-1; Interferon beta promoter stimulator protein 1; IPS-1; MAVS; mitochondrial anti-viral signaling protein; Mitochondrial antiviral-signaling protein; Putative NF-kappa-B-activating protein 031N; virus-induced signaling adapter; virus-induced signaling adaptor; Virus-induced-signaling adapter; VISA
Gene Aliases: CARDIF; D430028G21Rik; IPS-1; IPS1; KIAA1271; MAVS; VISA