ArticleNature communications2019
Cellular TRIM33 restrains HIV-1 infection by targeting viral integrase for proteasomal degradation.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
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Who cites it
48 citing papers in PubMed.
- TRIP12 promotes HIV-1 replication and latency reactivation by stabilizing Tat via USP7-mediated deubiquitination.Journal of virology · 2026Article
- UVB-induced genotoxic stress activates the DNA damage response and innate immune pathways in sea urchin coelomocytes.Frontiers in immunology · 2026Article
- Seneca Valley virus 3C protease targets TRIM32 for cleavage to antagonize its antiviral effects.Journal of virology · 2025Article
- Aquarius helicase facilitates HIV-1 integration into R-loop enriched genomic regions.Nature microbiology · 2025Article
- TRIM33 loss reduces androgen receptor transcriptional output and H2BK120 ubiquitination.Communications biology · 2025Article
- Protein-S-nitrosylation of human cytomegalovirus pp65 reduces its ability to undermine cGAS.Journal of virology · 2025Article
- A No-Brainer! The Therapeutic Potential of TRIM Proteins in Viral and Central Nervous System Diseases.Viruses · 2025Review
- Article
- Comprehensive SUMO Proteomic Analyses Identify HIV Latency-Associated Proteins in Microglia.Cells · 2025Article
- Insights into the protein domains of C-VI TRIM subfamily in viral infection.Frontiers in cellular and infection microbiology · 2025Review
- Comprehensive analysis of lncRNAs and mRNAs revealed potential participants in the process of avian reovirus infection.Frontiers in microbiology · 2025Article
- TRIM32 inhibits Venezuelan equine encephalitis virus infection by targeting a late step in viral entry.PLoS pathogens · 2024Article
- Functional 20S Proteasomes in Retroviruses: Evidence in Favor.International journal of molecular sciences · 2024Article
- Involvement of Human Cellular Proteins and Structures in Realization of the HIV Life Cycle: A Comprehensive Review, 2024.Viruses · 2024Review
- Ubiquitination of NS1 Confers Differential Adaptation of Zika Virus in Mammalian Hosts and Mosquito Vectors.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Antiviral factors and their counteraction by HIV-1: many uncovered and more to be discovered.Journal of molecular cell biology · 2024Review
- TRIM32 inhibits Venezuelan Equine Encephalitis Virus Infection by targeting a late step in viral entry.bioRxiv : the preprint server for biology · 2024Article
- The Immune Modulatory Role of TIF1 Proteins.Advances in experimental medicine and biology · 2024Review
- Changes in SUMO-modified proteins in Epstein-Barr virus infection identifies reciprocal regulation of TRIM24/28/33 complexes and the lytic switch BZLF1.PLoS pathogens · 2023Article
- The Involvement of Ubiquitination and SUMOylation in Retroviruses Infection and Latency.Viruses · 2023Review
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Productive HIV-1 replication requires viral integrase (IN), which catalyzes integration of the viral genome into the host cell DNA. IN, however, is short lived and is rapidly degraded by the host ubiquitin-proteasome system. To identify the cellular factors responsible for HIV-1 IN degradation, we performed a targeted RNAi screen using a library of siRNAs against all components of the ubiquitin-conjugation machinery using high-content microscopy. Here we report that the E3 RING ligase TRIM33 is a major determinant of HIV-1 IN stability. CD4-positive cells with TRIM33 knock down show increased HIV-1 replication and proviral DNA formation, while those overexpressing the factor display opposite effects. Knock down of TRIM33 reverts the phenotype of an HIV-1 molecular clone carrying substitution of IN serine 57 to alanine, a mutation known to impair viral DNA integration. Thus, TRIM33 acts as a cellular factor restricting HIV-1 infection by preventing provirus formation.
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