ArticleNature2011
TRIM5 is an innate immune sensor for the retrovirus capsid lattice.
Article in Nature, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 417 papers, 2 of them syntheses that pooled it.
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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.
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Who cites it
417 citing papers in PubMed, 2 syntheses or guidelines pooled it, 656 citations in OpenAlex.
- To TRIM the Immunity: From Innate to Adaptive Immunity.Frontiers in immunology · 2020Pooled it
- Identification of 64 Novel Genetic Loci Provides an Expanded View on the Genetic Architecture of Coronary Artery Disease.Circulation research · 2018Pooled it
- MxB N-Terminus Adopts a Stable α-Helix to Engage the HIV-1 Capsid Trimer Interface.bioRxiv : the preprint server for biology · 2026Article
- Compound delivery of eVLPs enhances prime editing for targeted genome engineering and high-throughput screening.Cell genomics · 2026Article
- Hiding in Plain Sight: HIV-1 Membraneless Organelles as Nuclear Hubs-Host Hijacking, Replication, Immune Evasion, and Drug-Access Implications.Pathogens (Basel, Switzerland) · 2026Review
- Independent proviral and antiviral host factors recognize the same capsid protein in divergent human herpesviruses.PLoS pathogens · 2026Article
- Hijacking the Host: Post-Translational Modifications as Molecular Switches in HIV Persistence and Immune Evasion.Journal of medical virology · 2026Review
- Alternative splicing broadens antiviral diversity at the human OAS2 locus.The EMBO journal · 2026Article
- TRIM5 integrates hypoglycemic stress and influenza infection.Nature communications · 2026Article
- Restraint of Powassan virus replication by TRIM5α facilitates viral avoidance of antiviral immunity.bioRxiv : the preprint server for biology · 2026Article
- BeyondFrontiers in genetics · 2026Review
- Updates on the role of TRIM proteins in AIDS: molecular mechanisms and potential for interventions.Frontiers in immunology · 2026Review
- TRIM proteins as emerging regulators of immune pathways: potential therapeutic targets in immune-related disorders.Frontiers in immunology · 2026Review
- SAMD9L inhibits flavivirus translation independently of its capacity to trigger innate immune response.PLoS pathogens · 2025Article
- Alternative polyadenylation upon CPSF6 knock-out enhances HIV-1 infection in primary T cells.PLoS pathogens · 2025Article
- Seneca Valley virus 3C protease targets TRIM32 for cleavage to antagonize its antiviral effects.Journal of virology · 2025Article
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- TRIM14 restricts tembusu virus infection through degrading viral NS1 protein and activating type I interferon signaling.PLoS pathogens · 2025Article
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357 more citing papers are in PubMed but not listed here.
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Authors and funding
17 authors at 5 institutions in 3 countries.
Funding
Abstract
TRIM5 is a RING domain-E3 ubiquitin ligase that restricts infection by human immunodeficiency virus (HIV)-1 and other retroviruses immediately following virus invasion of the target cell cytoplasm. Antiviral potency correlates with TRIM5 avidity for the retrovirion capsid lattice and several reports indicate that TRIM5 has a role in signal transduction, but the precise mechanism of restriction is unknown. Here we demonstrate that TRIM5 promotes innate immune signalling and that this activity is amplified by retroviral infection and interaction with the capsid lattice. Acting with the heterodimeric, ubiquitin-conjugating enzyme UBC13-UEV1A (also known as UBE2N-UBE2V1), TRIM5 catalyses the synthesis of unattached K63-linked ubiquitin chains that activate the TAK1 (also known as MAP3K7) kinase complex and stimulate AP-1 and NFκB signalling. Interaction with the HIV-1 capsid lattice greatly enhances the UBC13-UEV1A-dependent E3 activity of TRIM5 and challenge with retroviruses induces the transcription of AP-1 and NF-κB-dependent factors with a magnitude that tracks with TRIM5 avidity for the invading capsid. Finally, TAK1 and UBC13-UEV1A contribute to capsid-specific restriction by TRIM5. Thus, the retroviral restriction factor TRIM5 has two additional activities that are linked to restriction: it constitutively promotes innate immune signalling and it acts as a pattern recognition receptor specific for the retrovirus capsid lattice.
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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.