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.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
Protein Aliases: CARD adapter inducing interferon beta; CARD adaptor inducing IFN-beta; Cardif; IFN-B promoter stimulator 1; Interferon beta promoter stimulator protein 1; IPS-1; MAVS; Mitochondrial antiviral-signaling protein; Putative NF-kappa-B-activating protein 031N; virus-induced signaling adaptor; Virus-induced-signaling adapter; VISA
Gene Aliases: CARDIF; IPS-1; IPS1; KIAA1271; MAVS; VISA
UniProt ID: (Human) Q7Z434
Entrez Gene ID: (Human) 57506