Selected-GenAtlas references SOURCE GeneCards NCBI Gene Swiss-Prot Ensembl
HGNC UniGene Nucleotide OMIM UCSC
Home Page
FLASH GENE
Symbol MAVS contributors: mct/pgu - updated : 30-10-2017
HGNC name mitochondrial antiviral signaling protein
HGNC id 29233
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • 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
  • HOMOLOGY
    Homologene
    FAMILY
    CATEGORY regulatory
    SUBCELLULAR LOCALIZATION     intracellular
    intracellular,cytoplasm,organelle,mitochondria,outer
    intracellular,cytoplasm,organelle,membrane
    intracellular,cytoplasm,organelle,peroxisome
    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
  • CELLULAR PROCESS
    PHYSIOLOGICAL PROCESS immunity/defense
    PATHWAY
    metabolism
    signaling signal transduction
    NF-kappa-B signaling pathway (positive regulation of I-kappaB kinase/NF-kappaB cascade)
    a component
    INTERACTION
    DNA binding
    RNA
    small molecule
    protein
  • 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
    REGULATION
    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
    ASSOCIATED DISORDERS
    corresponding disease(s)
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    constitutional     --over  
    induces apoptosis by activation of caspase-3, -8, and -9
    Susceptibility
    Variant & Polymorphism
    Candidate gene
    Marker
    Therapy target
    ANIMAL & CELL MODELS