ArticleNature communications2017
Multiple truncated isoforms of MAVS prevent its spontaneous aggregation in antiviral innate immune signalling.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 82 citations in OpenAlex.
- Mitophagy in pathogenesis and therapeutic implications for infection.Experimental & molecular medicine · 2026Review
- Review
- African swine fever virus pE199L, as a mitophagy receptor, suppresses antiviral innate immunity to promote viral replication.Autophagy · 2026Article
- MAVS oligomerization drives a faster and more efficient antiviral signaling activation at peroxisomes compared to mitochondria.The FEBS journal · 2026Article
- Occludin modulates HIV and ischaemic stroke response via the mitochondrial antiviral signalling pathway.Brain : a journal of neurology · 2026Article
- Human papillomavirus E7 inhibits immune responses in keratinocytes by activating HTRA1‑mediated mitophagy.International journal of molecular medicine · 2026Article
- Old dogs-new tricks: multifaceted functions of MAVS beyond antivirus activity in human health and diseases.Cell & bioscience · 2025Review
- Novel strategies for PEDV to interfere with host antiviral immunity through Caspase-1.Virulence · 2025Article
- STING-ΔN, a novel splice isoform of STING, modulates innate immunity and autophagy in response to DNA virus infection.Cell communication and signaling : CCS · 2025Article
- Induction of the ISR by AB5 subtilase cytotoxin drives type-I IFN expression in pDCs via STING activation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Mitochondrial Antiviral Signaling Protein Activation by Retinoic Acid-Inducible Gene I Agonist Triggers Potent Antiviral Defense in Umbilical Cord Mesenchymal Stromal Cells Without Compromising Mitochondrial Function.International journal of molecular sciences · 2025Article
- Identification and Characterization of a Novel Rat MAVS Variant Modulating NFκB Signaling.Biomolecules · 2025Article
- Cellular RNA interacts with MAVS to promote antiviral signaling.Science (New York, N.Y.) · 2024Article
- MAVS Cys508 palmitoylation promotes its aggregation on the mitochondrial outer membrane and antiviral innate immunity.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- MITOCHONDRIAL ANTIVIRAL PATHWAYS CONTROL ANTI-HIV RESPONSES AND ISCHEMIC STROKE OUTCOMES VIA THE RIG-1 SIGNALING AND INNATE IMMUNITY MECHANISMS.bioRxiv : the preprint server for biology · 2024Article
- Transcription of endogenous retroviruses in senescent cells contributes to the accumulation of double-stranded RNAs that trigger an anti-viral response that reinforces senescence.Cell death & disease · 2024Article
- Article
- Deubiquitylating Enzymes in Cancer and Immunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Review
- Alternative Transcripts Diversify Genome Function for Phenome Relevance to Health and Diseases.Genes · 2023Review
- Overexpression of the mitochondrial anti-viral signaling protein, MAVS, in cancers is associated with cell survival and inflammation.Molecular therapy. Nucleic acids · 2023Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In response to virus infection, RIG-I-like receptors (RLRs) sense virus RNA and induce MAVS to form prion-like aggregates to further propagate antiviral signalling. Although monomeric MAVS recombinant protein can assemble into prion-like filaments spontaneously in vitro, endogenous MAVS in cells is prevented from aggregation until viral infection. The mechanism preventing cellular MAVS from spontaneous aggregation is unclear. Here we show that multiple N-terminal truncated isoforms of MAVS are essential in preventing full-length MAVS from spontaneous aggregation through transmembrane domain-mediated homotypic interaction. Without these shorter isoforms, full-length MAVS is prone to spontaneous aggregation and Nix-mediated mitophagic degradation. In the absence of N-terminally truncated forms, blocking Nix-mediated mitophagy stabilizes full-length MAVS, which aggregates spontaneously and induces the subsequent expression of type I interferon and other proinflammatory cytokines. Our data thus uncover an important mechanism preventing spontaneous aggregation of endogenous MAVS to avoid accidental activation of antiviral innate immune signalling.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.