Aliases for MAVS Gene
- Mitochondrial Antiviral Signaling Protein 2 3 5
- Interferon Beta Promoter Stimulator Protein 1 3 4
- Putative NF-Kappa-B-Activating Protein 031N 3 4
- CARD Adapter Inducing Interferon Beta 3 4
- Virus-Induced Signaling Adaptor 2 3
- Virus-Induced-Signaling Adapter 3 4
- CARD Adaptor Inducing IFN-Beta 2 3
- IFN-B Promoter Stimulator 1 2 3
External Ids for MAVS Gene
Previous GeneCards Identifiers for MAVS Gene
This gene encodes an intermediary protein necessary in the virus-triggered beta interferon signaling pathways. It is required for activation of transcription factors which regulate expression of beta interferon and contributes to antiviral immunity. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Sep 2011]
GeneCards Summary for MAVS Gene
MAVS (Mitochondrial Antiviral Signaling Protein) is a Protein Coding gene. Diseases associated with MAVS include Chikungunya and Retinitis Pigmentosa-40. Among its related pathways are Innate Immune System and Toll-like Receptor Signaling Pathway. GO annotations related to this gene include protein kinase binding and CARD domain binding.
UniProtKB/Swiss-Prot for MAVS Gene
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.