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Symbol MAVS contributors: mct/pgu - updated : 30-10-2017
HGNC name mitochondrial antiviral signaling protein
HGNC id 29233
Location 20p13      Physical location : 3.827.448 - 3.856.761
Synonym name
  • virus-induced signaling adapter
  • interferon-beta promoter stimulator protein 1
  • CARD adapter inducing interferon-beta
  • putative NF-kappa-B- activating protein 031N
  • virus-induced signaling adapter variant 1b
  • virus-induced signaling adaptor variant 1a
  • Synonym symbol(s) VISA, KIAA1271, IPS-1, CARDIF, FLJ27482, FLJ41962, DKFZp666M015, MGC3260, FLJ35386, FLJ38051, DKFZp547C224, IPS1
    TYPE functioning gene
    STRUCTURE 29.32 kb     7 Exon(s)
    MAPPING cloned Y linked N status provisional
    TRANSCRIPTS type messenger
    identificationnb exonstypebpproduct
    ProteinkDaAAspecific expressionYearPubmed
    7 - 11760 56 540 - 2005 116125763
    6 - 11596 - 399 - 2005 116125763
    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
    at STAGE
    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