FEATURES

DESCRIPTION

Also known as MAVS_HUMAN, MAVS, IPS1, KIAA1271, VISA. Required for innate immune defense against viruses (PubMed:16125763, PubMed:16127453, PubMed:16153868, PubMed:16177806, PubMed:19631370, PubMed:20451243, PubMed:23087404, PubMed:20127681, PubMed:21170385). Acts downstream of DHX33, 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 IFNB and RANTES (CCL5) (PubMed:16125763, PubMed:16127453, PubMed:16153868, PubMed:16177806, PubMed:19631370, PubMed:20451243, PubMed:23087404, PubMed:25636800, PubMed:20127681, PubMed:21170385, PubMed:20628368, PubMed:33110251). Peroxisomal and mitochondrial MAVS act sequentially to create an antiviral cellular state (PubMed:20451243). 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 (PubMed:20451243). May activate the same pathways following detection of extracellular dsRNA by TLR3 (PubMed:16153868). May protect cells from apoptosis (PubMed:16125763). Self-associates and polymerizes (via CARD domains) to form 400 nM long three-stranded helical filaments on mitochondria, filament nucleation requires interaction with DDX58/RIG-I whose CARD domains act as a template for filament assembly (PubMed:24569476, PubMed:25018021). Interacts with DDX58/RIG-I, IFIH1/MDA5, TRAF2, TRAF6 and C1QBP (PubMed:16125763, PubMed:16127453, PubMed:17600090, PubMed:33110251). May interact with FADD, RIPK1, CHUK and IKBKB (PubMed:16153868, PubMed:16177806, PubMed:16127453). Interacts (when phosphorylated) with IRF3; following activation and phosphorylation on the pLxIS motif by TBK1, recruits IRF3 (PubMed:25636800, PubMed:27302953, PubMed:33110251). Interacts with NLRX1 (PubMed:18200010). Interaction with NLRX1 requires the CARD domain (PubMed:18200010). Interacts with PSMA7 (PubMed:19734229). Interacts with TRAFD1 (By similarity). Interacts (via C-terminus) with PCBP2 in a complex containing MAVS/IPS1, PCBP2 and ITCH (PubMed:19881509). Interacts with CYLD (PubMed:18636086). Interacts with SRC (PubMed:19419966). Interacts with DHX58/LGP2 and IKBKE (PubMed:16177806, PubMed:17020950, PubMed:28011935). Interacts with STING1 (PubMed:19416887). Interacts with IFIT3 (via N-terminus) (PubMed:21813773). Interacts with TBK1 only in the presence of IFIT3 (PubMed:21813773, PubMed:28011935). Interacts with TTLL12; the interaction prevents MAVS binding to TBK1 and IKBKE (PubMed:28011935). Interacts with MUL1 (PubMed:23399697). Interacts with ANKRD17 (PubMed:23711367). Interacts with NDFIP1 (PubMed:23087404). Interacts with SMURF1; the interaction is mediated by NDFIP1 and leads to MAVS ubiquitination and degradation (PubMed:23087404). Interacts with UBXN1; this interaction inhibits MAVS-mediated antiviral pathway (PubMed:23545497). Interacts (via C-terminus) with GPATCH3; the interaction is markedly increased upon viral infection (PubMed:28414768). Directly interacts (via CARD domain) with ATG5 and ATG12, either as ATG5 and ATG12 monomers or as ATG12-ATG5 conjugates (PubMed:17709747). Interacts with DHX33 (via the helicase C-terminal domain) (By similarity). Interacts with DDX3X (via C-terminus); this interaction occurs rapidly, but transiently after Sendai virus infection (PubMed:20127681, PubMed:21170385, PubMed:27980081). The interaction with DDX3X potentiates MAVS-mediated IFNB induction (PubMed:20127681). Conversely inhibition of this interaction, for instance by HCV core protein, prevents MAVS-mediated IFNB induction (PubMed:21170385). Transiently interacts with TRAF3 early during Sendai virus infection (PubMed:27980081). Interacts with CLPB; the interaction is enhanced by Sendai virus infection (PubMed:31522117). Interacts with TRAF3IP3 (PubMed:31390091). Interacts with TOMM70; the interaction is enhanced by Sendai virus infection (PubMed:20628368).

Also known as MAVS_HUMAN, MAVS, IPS1, KIAA1271, VISA. Required for innate immune defense against viruses (PubMed:16125763, PubMed:16127453, PubMed:16153868, PubMed:16177806, PubMed:19631370, ...

EXTERNAL LINKS

MAVS

Mutations

Mutation(s) distribution

Mutations table