background:
MAVS (Mitochondrial Antiviral Signaling) mediates the activation of NF-kappaB and IRF3 in response to antiviral infection. Silencing of MAVS expression permits derepression of viral replication, while over expression of MAVS boosts antiviral immunity.
Function:
Required for innate immune defense against viruses. Acts downstream of DDX58 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). May activate the same pathways following detection of extracellular dsRNA by TLR3. May protect cells from apoptosis.
Subunit:
Interacts with DDX58, IFIH1, TRAF2 and TRAF6. May interact with IRF3, FADD, RIPK1, IKBKE, CHUK and IKBKB. Does not interact with TBK1. Interacts with and is cleaved by HCV and hepatitis GB virus B NS3/4A proteases. Interacts with and is cleaved by HHAV protein 3ABC. Interacts with NLRX1. Interaction with NLRX1 requires the CARD domain. Interacts with PSMA7. Interacts with TRAFD1 (By similarity). Interacts (via SLCterminus) with PCBP2 in a complex containing MAVS, PCBP2 and ITCH. Interacts with CYLD. Interacts with SRC.
Subcellular Location:
Mitochondrion outer membrane.
Tissue Specificity:
Present in T-cells, monocytes, epithelial cells and hepatocytes (at protein level). Ubiquitously expressed, with highest levels in heart, skeletal muscle, liver, placenta and peripheral blood leukocytes.
Post-translational modifications:
Ubiquitinated; undergoes 'Lys-48'-linked polyubiquitination catalyzed by ITCH; ITCH-dependent polyubiquitination is mediated by the interaction with PCBP2 and leads to MAVS proteasomal degradation.
Similarity:
Contains 1 CARD domain.
Database links:
UniProtKB/Swiss-Prot: Q7Z434.2
Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
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