ArticleThe EMBO journal2019
TRAF3IP3 mediates the recruitment of TRAF3 to MAVS for antiviral innate immunity.
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 37 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
37 citing papers in PubMed, 50 citations in OpenAlex.
- Dysregulation of astrocytic DNAJC6 contributes to sporadic Parkinson's disease pathogenesis.The Journal of clinical investigation · 2026Article
- Nociceptor neurons shape antiviral immunity.Journal of neuroinflammation · 2026Review
- Annexin A2 negatively regulates IFN-β production through targeting the RLR signaling pathway.Journal of virology · 2026Article
- CRM1-dependent nuclear export of TRIM28 promotes MAVS K48-linked ubiquitination and suppresses RIG-I-mediated antiviral response.Frontiers in immunology · 2026Article
- Old dogs-new tricks: multifaceted functions of MAVS beyond antivirus activity in human health and diseases.Cell & bioscience · 2025Review
- Article
- TRAF3IP3 Induces ER Stress-Mediated Apoptosis with Protective Autophagy to Inhibit Lung Adenocarcinoma Proliferation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Analysis of Hepatic Lentiviral Vector Transduction: Implications for Preclinical Studies and Clinical Gene Therapy Protocols.Viruses · 2025Article
- Article
- TRAF3IP3 Blocks Mitophagy to Exacerbate Myocardial Injury Induced by Ischemia-Reperfusion.Cardiovascular toxicology · 2024Article
- Analysis of hepatic lentiviral vector transduction; implications for preclinical studies and clinical gene therapy protocols.bioRxiv : the preprint server for biology · 2024Article
- Stratifying ICIs-responsive tumor microenvironment in HCC: from parsing out immune-hypoxic crosstalk to clinically applicable MRI-radiomics models.British journal of cancer · 2024Article
- Dual modifying of MAVS at lysine 7 by SIRT3-catalyzed deacetylation and SIRT5-catalyzed desuccinylation orchestrates antiviral innate immunity.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- SNORA5A regulates tumor-associated macrophage M1/M2 phenotypes via TRAF3IP3 in breast cancer.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2024Article
- WDR77 inhibits prion-like aggregation of MAVS to limit antiviral innate immune response.Nature communications · 2023Article
- Resolvins and cysteinyl-containing pro-resolving mediators activate resolution of infectious inflammation and tissue regeneration.Prostaglandins & other lipid mediators · 2023Review
- TRAF3 activates STING-mediated suppression of EV-A71 and target of viral evasion.Signal transduction and targeted therapy · 2023Article
- The Endoplasmic Reticulum ATP13A1 is Essential for MAVS-Mediated Antiviral Innate Immunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- DDX5/METTL3-METTL14/YTHDF2 Axis Regulates Replication of Influenza A Virus.Microbiology spectrum · 2022Article
- Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
RIG-I-MAVS antiviral signaling represents an important pathway to stimulate interferon production and confer innate immunity to the host. Upon binding to viral RNA and Riplet-mediated polyubiquitination, RIG-I promotes prion-like aggregation and activation of MAVS. MAVS subsequently induces interferon production by activating two signaling pathways mediated by TBK1-IRF3 and IKK-NF-κB respectively. However, the mechanism underlying the activation of MAVS downstream pathways remains elusive. Here, we demonstrated that activation of TBK1-IRF3 by MAVS-Region III depends on its multimerization state and identified TRAF3IP3 as a critical regulator for the downstream signaling. In response to virus infection, TRAF3IP3 is accumulated on mitochondria and thereby facilitates the recruitment of TRAF3 to MAVS for TBK1-IRF3 activation. Traf3ip3-deficient mice demonstrated a severely compromised potential to induce interferon production and were vulnerable to RNA virus infection. Our findings uncover that TRAF3IP3 is an important regulator for RIG-I-MAVS signaling, which bridges MAVS and TRAF3 for an effective antiviral innate immune response.
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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.