Mitochondrial antiviral-signaling protein: Difference between revisions

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== Function ==
== Function ==


[[Double-stranded RNA virus]]es are recognized in a cell type-dependent manner by the transmembrane receptor [[TLR3]] or by the cytoplasmic RNA helicases [[MDA5]] and [[RIG-I|RIGI]].  These interactions initiate signaling pathways that differ in their initial steps but converge in the activation of the protein kinases [[IKKA]] (CHUK) and [[IKK2|IKKB]] (IKBKB; MIM 603258), which activate [[NFKB]], or [[TANK-binding kinase 1|TBK1]] and [[IKBKE]] (IKBKE), which activate IRF3. Activated IRF3 and NFKB induce transcription of [[interferon beta|IFNβ]] (IFNB1). For the TLR3 pathway, the intermediary molecule before the pathways converge is the cytoplasmic protein [[TRIF]] (TICAM1). For RIGI, the intermediary protein is mitochondria-bound MAVS.<ref name="entrez" /><ref name="pmid16239922">{{cite journal |vauthors=Sen GC, Sarkar SN | title = Hitching RIG to action | journal = Nat. Immunol. | volume = 6 | issue = 11 | pages = 1074–6 | year = 2005 | pmid = 16239922 | doi = 10.1038/ni1105-1074 }}</ref>
[[Double-stranded RNA virus]]es are recognized in a cell type-dependent manner by the transmembrane receptor [[TLR3]] or by the cytoplasmic RNA helicases [[MDA5]] and [[RIG-I]].  These interactions initiate signalling pathways that differ in their initial steps but converge in the activation of the protein kinases [[IKKA]] (CHUK) and [[IKK2|IKKB]] (IKBKB; MIM 603258), which activate [[NFKB|NF-κB]], or [[TANK-binding kinase 1|TBK1]] and [[IKBKE]], which activate IRF3. Activated IRF3 and NF-κB induce transcription of [[interferon beta|IFNβ]] (IFNB1). For the TLR3 pathway, the intermediary molecule before the pathways converge is the cytoplasmic protein [[TRIF]] (TICAM1). For RIG-I, the intermediary protein is mitochondria-bound MAVS.<ref name="entrez" /><ref name="pmid16239922">{{cite journal |vauthors=Sen GC, Sarkar SN | title = Hitching RIG to action | journal = Nat. Immunol. | volume = 6 | issue = 11 | pages = 1074–6 | year = 2005 | pmid = 16239922 | doi = 10.1038/ni1105-1074 }}</ref>


==References==
==References==
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*{{cite journal |vauthors=Hirata Y, Broquet AH, Menchén L, Kagnoff MF | title = Activation of innate immune defense mechanisms by signaling through RIG-I/IPS-1 in intestinal epithelial cells. | journal = J. Immunol. | volume = 179 | issue = 8 | pages = 5425–32 | year = 2007 | pmid = 17911629 | doi = 10.4049/jimmunol.179.8.5425 }}
*{{cite journal |vauthors=Hirata Y, Broquet AH, Menchén L, Kagnoff MF | title = Activation of innate immune defense mechanisms by signaling through RIG-I/IPS-1 in intestinal epithelial cells. | journal = J. Immunol. | volume = 179 | issue = 8 | pages = 5425–32 | year = 2007 | pmid = 17911629 | doi = 10.4049/jimmunol.179.8.5425 }}
*{{cite journal |vauthors=Zeng W, Xu M, Liu S, Sun L, Chen ZJ | title =Key Role of Ubc5 and Lysine-63 Polyubiquitination in Viral Activation of IRF3. | journal = Mol Cell | volume =  36| issue = 3 | pages = 315–25 | year = 2009 | pmid = 19854139  | doi = 10.1016/j.molcel.2009.09.037 | pmc=2779157}}
*{{cite journal |vauthors=Zeng W, Xu M, Liu S, Sun L, Chen ZJ | title =Key Role of Ubc5 and Lysine-63 Polyubiquitination in Viral Activation of IRF3. | journal = Mol Cell | volume =  36| issue = 3 | pages = 315–25 | year = 2009 | pmid = 19854139  | doi = 10.1016/j.molcel.2009.09.037 | pmc=2779157}}
*{{cite journal |vauthors=Liu S, Chen J, Cai X, Wu J, Chen X, Wu Y, Sun L, Chen ZJ | title =MAVS Recruits Multiple Ubiquitin E3 Ligases to Activate Antiviral Signaling Cascades. | journal = Elife | volume = 2 | issue = e00785 | year = 2013 | pmid = 23951545  | doi = 10.7554/eLife.00785 | pmc=3743401}}
*{{cite journal |vauthors=Liu S, Chen J, Cai X, Wu J, Chen X, Wu Y, Sun L, Chen ZJ | title =MAVS Recruits Multiple Ubiquitin E3 Ligases to Activate Antiviral Signaling Cascades. | journal = eLife | volume = 2 | issue = e00785 | year = 2013 | pmid = 23951545  | doi = 10.7554/eLife.00785 | pmc=3743401}}
*{{cite journal |vauthors=Liu S, Cai X, Wu J, Cong Q, Chen X, Li T, Du F, Ren J, Wu Y, Grishin N, Chen ZJ | title =Phosphorylation of innate immune adaptor proteins MAVS, STING, and TRIF induces IRF3 activation. | journal = Science | volume = 347 | issue = 6227 | year = 2015 | pmid = 25636800  | doi = 10.1126/science.aaa2630 | page=aaa2630}}
*{{cite journal |vauthors=Liu S, Cai X, Wu J, Cong Q, Chen X, Li T, Du F, Ren J, Wu Y, Grishin N, Chen ZJ | title =Phosphorylation of innate immune adaptor proteins MAVS, STING, and TRIF induces IRF3 activation. | journal = Science | volume = 347 | issue = 6227 | year = 2015 | pmid = 25636800  | doi = 10.1126/science.aaa2630 | page=aaa2630}}
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Latest revision as of 07:22, 10 January 2019

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Identifiers
Aliases
External IDsGeneCards: [1]
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

n/a

n/a

RefSeq (protein)

n/a

n/a

Location (UCSC)n/an/a
PubMed searchn/an/a
Wikidata
View/Edit Human

Mitochondrial antiviral-signaling protein (MAVS) is a protein that in humans is encoded by the MAVS gene.[1][2][3] The protein is also known by the names VISA (virus-induced signaling adapter), IPS-1 and Cardif. Aggregated MAVS forms protease resistant prion-like aggregates that activate IRF3 dimerization.[4]

Function

Double-stranded RNA viruses are recognized in a cell type-dependent manner by the transmembrane receptor TLR3 or by the cytoplasmic RNA helicases MDA5 and RIG-I. These interactions initiate signalling pathways that differ in their initial steps but converge in the activation of the protein kinases IKKA (CHUK) and IKKB (IKBKB; MIM 603258), which activate NF-κB, or TBK1 and IKBKE, which activate IRF3. Activated IRF3 and NF-κB induce transcription of IFNβ (IFNB1). For the TLR3 pathway, the intermediary molecule before the pathways converge is the cytoplasmic protein TRIF (TICAM1). For RIG-I, the intermediary protein is mitochondria-bound MAVS.[3][5]

References

  1. Seth RB, Sun L, Ea CK, Chen ZJ (Sep 2005). "Identification and characterization of MAVS, a mitochondrial antiviral signaling protein that activates NF-kappaB and IRF 3". Cell. 122 (5): 669–82. doi:10.1016/j.cell.2005.08.012. PMID 16125763.
  2. Xu LG, Wang YY, Han KJ, Li LY, Zhai Z, Shu HB (Sep 2005). "VISA is an adapter protein required for virus-triggered IFN-beta signaling". Mol Cell. 19 (6): 727–40. doi:10.1016/j.molcel.2005.08.014. PMID 16153868.
  3. 3.0 3.1 "Entrez Gene: VISA virus-induced signaling adapter".
  4. Hou F, Sun L, Zheng H, Skaug B, Jiang QX, Chen ZJ (Aug 5, 2011). "MAVS forms functional prion-like aggregates to activate and propagate antiviral innate immune response". Cell. 146 (3): 448–61. doi:10.1016/j.cell.2011.06.041. PMC 3179916. PMID 21782231.
  5. Sen GC, Sarkar SN (2005). "Hitching RIG to action". Nat. Immunol. 6 (11): 1074–6. doi:10.1038/ni1105-1074. PMID 16239922.

Further reading

This article incorporates text from the United States National Library of Medicine, which is in the public domain.