ArticlePLoS pathogens2015
TRIM32 Senses and Restricts Influenza A Virus by Ubiquitination of PB1 Polymerase.
Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers.
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Who cites it
112 citing papers in PubMed, 156 citations in OpenAlex.
- Oncogenic viral infection triggers LAMP2A SUMOylation and chaperone-mediated autophagy to promote tumorigenesis.Nature microbiology · 2026Article
- Ubiquitin-Dependent Regulation of Influenza A Virus Polymerase and vRNP Function: Mechanisms and Therapeutic Opportunities.Microorganisms · 2026Review
- KCMF1-mediated influenza A virus PB1 ubiquitination at K653 regulates viral replication.Journal of virology · 2026Article
- TRIM28 and TRIM32: multifaceted regulators of innate immunity and antiviral defence.Immunologic research · 2026Review
- Inhibition of coronaviral exoribonuclease activity by TRIM-mediated SUMOylation.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Ribosomal protein L35 negatively regulates FMDV replication by recruiting AMFR to promote the ubiquitination and degradation of VP2.Journal of virology · 2025Article
- Genetic strategies for avian influenza resilience in poultry: from host-pathogen interaction studies to precision breeding.Functional & integrative genomics · 2025Review
- TRIM45 restricts influenza virus infection through modulating the chaperone-mediated autophagic degradation of viral PB2 protein.PLoS pathogens · 2025Article
- Role of the Chaperone Protein 14-3-3η in Regulation of the Infection Dynamics of the Influenza A (H1N1) Virus.Viruses · 2025Article
- Heat shock protein A1L restricts influenza A virus by ubiquitination of NA.Journal of virology · 2025Article
- Seneca Valley virus 3C protease targets TRIM32 for cleavage to antagonize its antiviral effects.Journal of virology · 2025Article
- The Trim32-DPEP2 axis is an inflammatory switch in macrophages during intestinal inflammation.Cell death and differentiation · 2025Article
- IncRNA IPAN antagonizes RIG-I/TRIM25-mediated degradation of influenza A virus PB1 to promote viral replication.Biosafety and health · 2025Article
- Article
- MARCH8 promotes the proteasomal degradation of foot-and-mouth disease virus VP1, VP2, and VP3 to negatively regulate viral replication.Veterinary research · 2025Article
- Glucosidase alpha neutral C promotes influenza virus replication by inhibiting proteosome-dependent degradation of hemagglutinin.Signal transduction and targeted therapy · 2025Article
- Restriction of influenza A virus replication by host DCAF7-CRL4B axis.Journal of virology · 2025Article
- Phosphorylation Modifications and Their Role in Viral Pneumonia: Mechanisms and Therapeutic Implications.Infection and drug resistance · 2025Review
- RING finger protein 5 is a key anti-FMDV host factor through inhibition of virion assembly.PLoS pathogens · 2025Article
- TRIM32 inhibits Venezuelan equine encephalitis virus infection by targeting a late step in viral entry.PLoS pathogens · 2024Article
52 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 3 countries.
Funding
Abstract
Polymerase basic protein 1 (PB1) is the catalytic core of the influenza A virus (IAV) RNA polymerase complex essential for viral transcription and replication. Understanding the intrinsic mechanisms which block PB1 function could stimulate development of new anti-influenza therapeutics. Affinity purification coupled with mass spectrometry (AP-MS) was used to identify host factors interacting with PB1. Among PB1 interactors, the E3 ubiquitin ligase TRIM32 interacts with PB1 proteins derived from multiple IAV strains. TRIM32 senses IAV infection by interacting with PB1 and translocates with PB1 to the nucleus following influenza infection. Ectopic TRIM32 expression attenuates IAV infection. Conversely, RNAi depletion and knockout of TRIM32 increase susceptibility of tracheal and lung epithelial cells to IAV infection. Reconstitution of trim32-/- mouse embryonic fibroblasts with TRIM32, but not a catalytically inactive mutant, restores viral restriction. Furthermore, TRIM32 directly ubiquitinates PB1, leading to PB1 protein degradation and subsequent reduction of polymerase activity. Thus, TRIM32 is an intrinsic IAV restriction factor which senses and targets the PB1 polymerase for ubiquitination and protein degradation. TRIM32 represents a model of intrinsic immunity, in which a host protein directly senses and counters viral infection in a species specific fashion by directly limiting viral replication.
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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.