ArticleThe Journal of biological chemistry2014
Regulation of mitochondrial antiviral signaling (MAVS) expression and signaling by the mitochondria-associated endoplasmic reticulum membrane (MAM) protein Gp78.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 42 citations in OpenAlex.
- O-GlcNAcylation of AMFR stabilizes TSPAN4 to regulate migrasome formation for viral release.Nature communications · 2026Article
- Post-translational control of MAVS signaling: linking mitochondrial antiviral immunity to metabolic and cellular stress contexts.Frontiers in physiology · 2026Review
- Nanoparticle-Loaded Injectable Hydrogel Alleviates Titanium Particle-Induced Osteolysis by Disrupting GATA6/DDX3X-Mediated Macrophage Inflammation.Biomaterials research · 2026Article
- Role of mitochondria-associated membranes (MAMs) in inflammatory signaling: implications for acute lung injury pathogenesis.Frontiers in cell and developmental biology · 2025Review
- A-Syn(ful) MAM: A Fresh Perspective on a Converging Domain in Parkinson's Disease.International journal of molecular sciences · 2024Review
- The endoplasmic reticulum: Homeostasis and crosstalk in retinal health and disease.Progress in retinal and eye research · 2024Review
- WDR77 inhibits prion-like aggregation of MAVS to limit antiviral innate immune response.Nature communications · 2023Article
- Article
- Mitochondrial Interactome: A Focus on Antiviral Signaling Pathways.Frontiers in cell and developmental biology · 2020Review
- Single-walled carbon nanotubes repress viral-induced defense pathways through oxidative stress.Nanotoxicology · 2019Article
- Review
- Mitochondria: the indispensable players in innate immunity and guardians of the inflammatory response.Journal of cell communication and signaling · 2019Article
- Structural Variability in the RLR-MAVS Pathway and Sensitive Detection of Viral RNAs.Medicinal chemistry (Shariqah (United Arab Emirates)) · 2019Review
- The Differential Expression of Mitochondrial Function-Associated Proteins and Antioxidant Enzymes during Bovine Herpesvirus 1 Infection: A Potential Mechanism for Virus Infection-Induced Oxidative Mitochondrial Dysfunction.Mediators of inflammation · 2019Article
- Sec13 is a positive regulator of VISA-mediated antiviral signaling.Virus genes · 2018Article
- CDK5-Mediated Phosphorylation-Dependent Ubiquitination and Degradation of E3 Ubiquitin Ligases GP78 Accelerates Neuronal Death in Parkinson's Disease.Molecular neurobiology · 2018Article
- Mitochondria-associated membranes (MAMs) and inflammation.Cell death & disease · 2018Review
- The Role of Mitophagy in Innate Immunity.Frontiers in immunology · 2018Review
- iRhom2 is essential for innate immunity to RNA virus by antagonizing ER- and mitochondria-associated degradation of VISA.PLoS pathogens · 2017Article
- The dynamic interacting landscape of MAPL reveals essential functions for SUMOylation in innate immunity.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
In a previous study, we identified the E3 ubiquitin ligase Gp78 by RNAi high-throughput screening as a gene whose depletion restricted enterovirus infection. In the current study, we show that Gp78, which localizes to the ER-mitochondria interface, is a regulator of RIG-I-like receptor (RLR) antiviral signaling. We show that depletion of Gp78 results in a robust decrease of vesicular stomatitis virus (VSV) infection and a corresponding enhancement of type I interferon (IFN) signaling. Mechanistically, we show that Gp78 modulates type I IFN induction by altering both the expression and signaling of the mitochondria-localized RLR adaptor mitochondrial antiviral signaling (MAVS). Expression of mutants of Gp78 that abolish its E3 ubiquitin ligase and its participation in ER-associated degradation (ERAD) lost their ability to degrade MAVS, but surprisingly maintained their ability to repress RLR signaling. In contrast, Gp78 lacking its entire C terminus lost both its ability to degrade MAVS and repress RLR signaling. We show that Gp78 interacts with both the N- and C-terminal domains of MAVS via its C-terminal RING domain, and that this interaction is required to abrogate Gp78-mediated attenuation of MAVS signaling. Our data thus implicate two parallel pathways by which Gp78 regulates MAVS signaling; one pathway requires its E3 ubiquitin ligase and ERAD activity to directly degrade MAVS, whereas the other pathway occurs independently of these activities, but requires the Gp78 RING domain and occurs via a direct association between this region and MAVS.
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Registered trials
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.