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Symbol MAVS contributors: mct/pgu - updated : 30-10-2017
HGNC name mitochondrial antiviral signaling protein
HGNC id 29233
Type ubiquitous
   expressed in (based on citations)
SystemOrgan level 1Organ level 2Organ level 3Organ level 4LevelPubmedSpeciesStageRna symbol
Digestiveintestinelarge intestinecolon moderately
 mouth   highly
 pancreas exocrine   moderately
Lymphoid/Immunethymus   predominantly
Nervousnerve   highly
Reproductivefemale systemplacenta  moderately
 female systemuteruscervix moderately
Urinarykidney   moderately
SystemTissueTissue level 1Tissue level 2LevelPubmedSpeciesStageRna symbol
cell lineage
cell lines
physiological period pregnancy
Text placenta
  • a N-terminal CARD-like domain
  • a hydrophobic C-terminal transmembrane domain that targets the protein to the mitochondrial membrane
  • a proline-rich region in the middle
  • a TRAF-interaction motif (TIM)
  • C-terminal transmembrane domain was required for its interaction with RNF5
    CATEGORY regulatory
    SUBCELLULAR LOCALIZATION     intracellular
    intracellular,cytoplasm,organelle,endoplasmic reticulum
    basic FUNCTION
  • being essential for NF-kappaB and IRF3 activation by RNA viruses
  • acting as a putative NF-kappaB activator
  • inducing the assembly of the IFN-g enhanceosome
  • activating JNK
  • being a pivotal cellular antiviral protein whose expression level directly determines antiviral immunity
  • being essential for innate immune defense against viruses (essential for the production of IFN1 and inflammatory cytokines in response to RSV infection)
  • like TRAF3, is required for type I interferon production in response to intracellular double-stranded RNA
  • candidate protein in the field of apoptosis regulation
  • had a cytoprotective function
  • IKBKG, like VISA, acts as an adaptor protein that allows DDX58 to activate both the NF-kappaB and IRF signaling )pathways
  • participates in IFN induction by recruitment of downstream partners such as members of the TRAF family, leading to activation of NF-KB, and the IRF3 pathways
  • having a novel function for anoikis induction by caspase-8 activation
  • acts as a critical adapter for assembling a virus-induced complex that signals NF-kappaB and IRF3 activation
  • a prion-like conformational switch of MAVS activates and propagates the antiviral signaling cascade
  • MAVS Y9 phosphorylation contributed to MAVS antiviral function without interfering with its apoptosis property.
  • is required for innate immune responses against RNA viruses
  • is the essential adaptor protein for virus-induced activation of IRF3 and 7 and production of type I IFNs
  • plays a key role in the signal transduction of DHX58-mediated antiviral response
  • MAVS and TMEM173 transduce signals from the cytosolic nucleic acid sensors DDX58 and CGAS, respectively
  • required for the optimal activation of apoptosis-associated specklike protein (PYCARD)-dependent inflammasome
  • an autoinhibitory mechanism modulates MAVS activity in unstimulated cells and, on viral infection, individual regions of MAVS are released following MAVS filament formation to activate antiviral signalling cascades
    PHYSIOLOGICAL PROCESS immunity/defense
    signaling signal transduction
    NF-kappa-B signaling pathway (positive regulation of I-kappaB kinase/NF-kappaB cascade)
    a component
    DNA binding
    small molecule
  • direct and specific interaction between the TRAF domain of TRAF3 and the TIM of MAVS is required for optimal MAVS-mediated antiviral responses
  • PSMA7 is a negative regulator of the MAVS-mediated innate immunity that probably serves to attenuate the establishment of an antiviral state during viral infection
  • binds DAP3 and induces anoikis by caspase activation
  • PCBP2 is a negative regulator in MAVS-mediated signaling
  • PCBP2 interaction with MAVS led to proteasomal degradation of MAVS (is recruited the HECT domain-containing E3 ligase ITCH to polyubiquitinate and degrade MAVS
  • related ubiquitin ligase TRAF5 is a downstream target of MAVS that mediates both IRF3 and NF-kappaB activation
  • RNF5 interacted with MAVS at mitochondria in a viral infection-dependent manner
  • TOMM70A is a mitochondrial import receptor, to interact with MAVS upon RNA virus infection
  • is required for B cell expression of TLR7
  • TSPAN6 functions as a negative regulator of the DDX58 pathway by interacting with MAVS in a ubiquitination-dependent manner
  • interacts with DDX58 and MAVS
  • interaction between the helicase DHX33 and MAVS (interaction between DHX33 and MAVS is mediated by the HELICc region of DHX33 and the C-terminal domain of MAVS)
  • MAVS facilitates the recruitment of NLRP3 to the mitochondria and may enhance its oligomerization and activation by bringing it in close proximity to mitochondrial reactive oxygen species
  • TRIM14 interacts with MAVS
  • DHX15 physically interacted with MAVS and mediated the MAVS-dependent activation of the NFKB1 and MAPK pathways
  • MARCH5 modulates MAVS-mediated antiviral signalling, preventing excessive immune reactions.
  • TAX1BP1 functions as an adaptor molecule for ITCH to target MAVS during RNA virus infection and thus restrict virus-induced apoptosis
  • RIPK3 interacts with MAVS to regulate type I IFN-mediated immunity to Influenza A virus infection
  • ZYX serves as a scaffold for the interactions between DHX58 and MAVS
  • HERPUD1 is a modulator of the ER stress response which is dependent on the participation of MAVS
  • through interacting with TBK1, HERPUD1 amplifies the MAVS signaling and facilitates the phosphorylation and nuclear translocation of IRF3 and NFKB1 to enhance the expression of IFNs, which leads to a broad inhibition of the replication of RNA viruses
  • BST2 is a negative regulator of DHX58-mediated type I IFN signaling by targeting MAVS
  • cell & other
    inhibited by PLK1 (strongly inhibits the ability of MAVS to activate the IRF3 and NF-KB pathways and to induce IFN)
    Other phosphorylated by ABL1
    polyubiquitinated by ITCH and thus degraded
    corresponding disease(s)
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    constitutional     --over  
    induces apoptosis by activation of caspase-3, -8, and -9
    Variant & Polymorphism
    Candidate gene
    Therapy target