ArticleJournal of virology2018
TRIM21 Promotes Innate Immune Response to RNA Viral Infection through Lys27-Linked Polyubiquitination of MAVS.
Article in Journal of virology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers, 1 of them a synthesis that pooled it.
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Who cites it
111 citing papers in PubMed, 1 synthesis or guideline pooled it, 148 citations in OpenAlex.
- To TRIM the Immunity: From Innate to Adaptive Immunity.Frontiers in immunology · 2020Pooled it
- ATG13 promotes K63-linked polyubiquitination of MAVS via ASB1 to restrict influenza A virus replication.Emerging microbes & infections · 2026Article
- TRIM21 blocks DDX3X-driven stress granule formation during Mycobacterium tuberculosis infection via a non-canonical E3 ligase mechanism.PLoS pathogens · 2026Article
- Unraveling the Multifaceted Role of TRIM21 in Virus-Triggered Innate Immunity and Diseases.Biomolecules · 2026Review
- The ADAP-TRIM21-ZEB2 axis regulates CD8iScience · 2026Article
- Review
- TRIM47 catalyzes MAVS SUMOylation to safeguard chronic viral infections and tissue inflammation.Cell communication and signaling : CCS · 2026Article
- Exploiting Ubiquitination: African Swine Fever Virus-Mediated Recruitment of Host E3 Ligases During Viral Infection and Immune Regulation.Pathogens (Basel, Switzerland) · 2026Review
- SARS-CoV-2 ORF3a suppresses host antiviral interferon responses by promoting STUB1-mediated PTEN proteasomal degradation.Journal of virology · 2026Article
- O-GlcNAcylation licenses RNF166 to degrade the M protein of porcine coronaviruses.PLoS pathogens · 2026Article
- Targeting IRF1-TRIM21 axis enhances anti-tumor immunity by promoting ubiquitin-mediated degradation of FGL1 in non-small cell lung cancer.Communications biology · 2026Article
- TRIM21 is a molecular rheostat for influenza A virus replication.bioRxiv : the preprint server for biology · 2026Article
- Nervous necrosis virus capsid protein functions as a SUMO E3 ligase to activate MAVS-dependent NF-κB signaling.Cellular and molecular life sciences : CMLS · 2026Article
- RND3 restricts encephalomyocarditis virus replication by promoting IKKε ubiquitination and type I interferon production.Microbiology spectrum · 2026Article
- GIPC2 suppresses colorectal cancer progression via regulation by UBA1-mediated ubiquitination.Gastroenterology report · 2026Article
- TRIM21 as a Context-Dependent Regulator in Hepatocellular Carcinoma: Integrating Etiological Landscapes (HBV/NASH) with Core Tumor Progression Mechanisms.Journal of hepatocellular carcinoma · 2026Review
- Exosome Proteomics of SOD1Annals of clinical and translational neurology · 2026Article
- TRIM21 and OTUD6A orchestrate AKT K27-linked atypical ubiquitination to modulate cancer chemoresistance.Nature structural & molecular biology · 2026Article
- OLFML3 negatively regulates RIG-I signaling in RNA virus infection.Frontiers in immunology · 2026Article
- Post-translational control of MAVS signaling: linking mitochondrial antiviral immunity to metabolic and cellular stress contexts.Frontiers in physiology · 2026Review
51 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human innate immunity responds to viral infection by activating the production of interferons (IFNs) and proinflammatory cytokines. The mitochondrial adaptor molecule MAVS plays a critical role in innate immune response to viral infection. In this study, we show that TRIM21 (tripartite motif-containing protein 21) interacts with MAVS to positively regulate innate immunity. Under viral infection, TRIM21 is upregulated through the IFN/JAK/STAT signaling pathway. Knockdown of TRIM21 dramatically impairs innate immune response to viral infection. Moreover, TRIM21 interacts with MAVS and catalyzes its K27-linked polyubiquitination, thereby promoting the recruitment of TBK1 to MAVS. Specifically, the PRY-SPRY domain of TRIM21 is the key domain for its interaction with MAVS, while the RING domain of TRIM21 facilitates the polyubiquitination chains of MAVS. In addition, the MAVS-mediated innate immune response is enhanced by both the PRY-SPRY and RING domains of TRIM21. Mutation analyses of all the lysine residues of MAVS further revealed that Lys325 of MAVS is catalyzed by TRIM21 for the K27-linked polyubiquitination. Overall, this study reveals a novel mechanism by which TRIM21 promotes the K27-linked polyubiquitination of MAVS to positively regulate innate immune response, thereby inhibiting viral 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.