ArticleThe EMBO journal2019
RNF34 functions in immunity and selective mitophagy by targeting MAVS for autophagic degradation.
Article in The EMBO journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.
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Who cites it
85 citing papers in PubMed, 150 citations in OpenAlex.
- ATG13 promotes K63-linked polyubiquitination of MAVS via ASB1 to restrict influenza A virus replication.Emerging microbes & infections · 2026Article
- Review
- Internalized components of membrane attack complexes disrupt proteostasis and acquire alarmin-like properties.Nature communications · 2026Article
- Internalized Components of Membrane Attack Complexes Disrupt Proteostasis and Acquire Alarmin-Like Properties.bioRxiv : the preprint server for biology · 2026Article
- Trifloxystrobin-triggered Drp1 hyperactivation biases mitophagy and imposes long-lasting SVCV susceptibility in teleost.Journal of virology · 2026Article
- Regulation of Innate Immune Signaling by Autophagy.International journal of molecular sciences · 2026Review
- RNF34 restrains endometriosis through SREBP1-dependent metabolic-immune crosstalk.Cellular and molecular life sciences : CMLS · 2026Article
- TRIM21 facilitates inflammasome assembly and contributes to autoinflammatory disease.Nature communications · 2026Article
- SIAH2-EPHB6 axis enhances filopodia formation in hepatocellular carcinoma cells by regulating RHOF.Cell & bioscience · 2026Article
- Duck plague virus LORF2 utilizes RNF34 to inhibit antiviral innate immunity by ubiquitination and degradation of IRF7.PLoS pathogens · 2026Article
- The ubiquitin ligase KLHL6 drives resistance to CD8Nature · 2026Article
- Role of autophagy in antiviral innate immunity.Cellular & molecular biology letters · 2026Review
- Low protein-induced-FGF-21 signaling remodels adipose tissue on reduced markers of senescence during aging.GeroScience · 2026Article
- Old dogs-new tricks: multifaceted functions of MAVS beyond antivirus activity in human health and diseases.Cell & bioscience · 2025Review
- Palmitoylation of TBK1 enhances the type I interferon signaling and strengthens anti-malarial immunity in mice.Nature communications · 2025Article
- From Mitochondria to Immunity: The Emerging Roles of Mitochondria-Derived Vesicles and Small Extracellular Vesicles in Cellular Communication and Disease.Journal of extracellular vesicles · 2025Review
- The RIG-I-like receptor family of immune proteins.Molecular cell · 2025Review
- Molecular regulation of mitophagy signaling in tumor microenvironment and its targeting for cancer therapy.Cytokine & growth factor reviews · 2025Review
- Avian TRIM13 attenuates antiviral innate immunity by targeting MAVS for autophagic degradation.Autophagy · 2025Article
- PCSK9 potentiates innate immune response to RNA viruses by preventing AIP4-mediated polyubiquitination and degradation of VISA/MAVS.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
25 more citing papers are in PubMed but not listed here.
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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 2 institutions in 1 country.
Funding
Abstract
Viral infection triggers the formation of mitochondrial antiviral signaling protein (MAVS) aggregates, which potently promote immune signaling. Autophagy plays an important role in controlling MAVS-mediated antiviral signaling; however, the exact molecular mechanism underlying the targeted autophagic degradation of MAVS remains unclear. Here, we investigated the mechanism by which RNF34 regulates immunity and mitophagy by targeting MAVS. RNF34 binds to MAVS in the mitochondrial compartment after viral infection and negatively regulates RIG-I-like receptor (RLR)-mediated antiviral immunity. Moreover, RNF34 catalyzes the K27-/K29-linked ubiquitination of MAVS at Lys 297, 311, 348, and 362 Arg, which serves as a recognition signal for NDP52-dependent autophagic degradation. Specifically, RNF34 initiates the K63- to K27-linked ubiquitination transition on MAVS primarily at Lys 311, which facilitates the autophagic degradation of MAVS upon RIG-I stimulation. Notably, RNF34 is required for the clearance of damaged mitochondria upon viral infection. Thus, we elucidated the mechanism by which RNF34-mediated autophagic degradation of MAVS regulates the innate immune response, mitochondrial homeostasis, and infection.
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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.