IFN-beta
This page covers MAVS (mitochondrial antiviral signalling protein, also called VISA, IPS-1 and Cardif), the adapter that links viral RNA sensing to IFN-beta induction. It is required for innate immune defence against viruses and for virus-triggered IFN-beta signalling. Browse Assay Genie's current range of IFN-beta research reagents below, or read on for the biology behind the target.
MAVS is an adapter protein that sits between cytosolic RNA sensors and the transcriptional programme that produces IFN-beta. It acts downstream of DHX33, RIGI and IFIH1 (MDA5), which detect intracellular double-stranded RNA made during viral replication. From there it coordinates pathways that activate NF-kappa-B, IRF3 and IRF7, leading to the induction of antiviral cytokines such as IFN-beta and RANTES (CCL5). It may also activate the same pathways after TLR3 detects extracellular dsRNA.
The protein is found on the outer mitochondrial membrane and on peroxisomes, and the two pools have distinct roles. Peroxisomal MAVS drives rapid, interferon-independent expression of defence factors that give short-term protection. Mitochondrial MAVS activates an interferon-dependent pathway with delayed kinetics, which amplifies and stabilises the antiviral response. The two act in sequence to create an antiviral cellular state.
The MAVS gene belongs to the HGNC group of caspase recruitment domain containing genes, and has orthologs named Mavs in mouse and rat. The aliases VISA, IPS-1, Cardif and KIAA1271 all refer to the same gene product. Beyond interferon induction, MAVS may protect cells from apoptosis and is involved in NLRP3 inflammasome activation by recruiting NLRP3 to mitochondria. Together these roles make it a central node in antiviral and inflammatory signalling.
MAVS is an adapter required for innate immune defence against viruses, acting downstream of the intracellular dsRNA sensors DHX33, RIGI and IFIH1.
The protein is necessary in virus-triggered IFN-beta signalling and is required to activate the transcription factors that regulate IFN-beta expression.
MAVS mediates recruitment of NLRP3 to mitochondria, linking antiviral signalling to NLRP3 inflammasome activation.
Peroxisomal and mitochondrial MAVS act sequentially, giving rapid interferon-independent and delayed interferon-dependent antiviral responses.
MAVS is an intermediary adapter needed for virus-triggered IFN-beta signalling. Acting downstream of RIGI, IFIH1 and DHX33, it is required to activate NF-kappa-B, IRF3 and IRF7, the transcription factors that regulate IFN-beta expression and contribute to antiviral innate immunity.
The HGNC symbol is MAVS, for mitochondrial antiviral signalling protein. Aliases include VISA, KIAA1271, IPS-1 and Cardif. These names refer to the same gene and protein, so literature searches may need to cover several of them.
Mouse and rat both have a Mavs ortholog. The human protein localises to the outer mitochondrial membrane and to peroxisomes, where the two pools act sequentially in antiviral defence. Check the datasheet of any product for its validated reactivity.
RNA sensors, interferon regulatory factors, chemokines and inflammasome components that work alongside MAVS in antiviral signalling.
Gene and protein annotations from HGNC, NCBI Gene and UniProt Q7Z434; product specifications from Assay Genie datasheets.