ArticleRetrovirology2013
The ability of TNPO3-depleted cells to inhibit HIV-1 infection requires CPSF6.
Article in Retrovirology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
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Who cites it
74 citing papers in PubMed, 94 citations in OpenAlex.
- Alternative polyadenylation upon CPSF6 knock-out enhances HIV-1 infection in primary T cells.PLoS pathogens · 2025Article
- CPSF6 promotes HIV-1 preintegration complex function.Journal of virology · 2025Article
- Article
- Cyclophilin A Regulates Tripartite Motif 5 Alpha Restriction of HIV-1.International journal of molecular sciences · 2025Review
- Disruption of CPSF6 enhances cellular permissivity to HIV-1 infection through alternative polyadenylation.Research square · 2024Article
- Dominantly inherited muscle disorders: understanding their complexity and exploring therapeutic approaches.Disease models & mechanisms · 2024Review
- HIV-1-induced translocation of CPSF6 to biomolecular condensates.Trends in microbiology · 2024Review
- Spatiotemporal binding of cyclophilin A and CPSF6 to capsid regulates HIV-1 nuclear entry and integration.bioRxiv : the preprint server for biology · 2024Article
- Biochemical Detection of Capsid in the Nucleus During HIV-1 Infection.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Capsid-host interactions for HIV-1 ingress.Microbiology and molecular biology reviews : MMBR · 2023Review
- TRIM5α Restriction of HIV-1-N74D Viruses in Lymphocytes Is Caused by a Loss of Cyclophilin A Protection.Viruses · 2022Article
- GS-CA1 and lenacapavir stabilize the HIV-1 core and modulate the core interaction with cellular factors.iScience · 2022Article
- Transcriptomic Evidence of the Immune Response Activation in Individuals With Limb Girdle Muscular Dystrophy Dominant 2 (LGMDD2) Contributes to Resistance to HIV-1 Infection.Frontiers in cell and developmental biology · 2022Article
- Nuclear Import of HIV-1.Viruses · 2021Review
- Disassembling the Nature of Capsid: Biochemical, Genetic, and Imaging Approaches to Assess HIV-1 Capsid Functions.Viruses · 2021Review
- CRISPR/Cas9-Induced Mutagenesis Corroborates the Role of Transportin-SR2 in HIV-1 Nuclear Import.Microbiology spectrum · 2021Article
- HIV-1 capsid variability: viral exploitation and evasion of capsid-binding molecules.Retrovirology · 2021Review
- Cleavage and Polyadenylation Specificity Factor 6 Is Required for Efficient HIV-1 Latency Reversal.mBio · 2021Article
- The Role of Capsid in the Early Steps of HIV-1 Infection: New Insights into the Core of the Matter.Viruses · 2021Review
- Role of Transportin-SR2 in HIV-1 Nuclear Import.Viruses · 2021Review
14 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundExpression of the cellular karyopherin TNPO3/transportin-SR2/Tnp3 is necessary for HIV-1 infection. Depletion of TNPO3 expression in mammalian cells inhibits HIV-1 infection after reverse transcription but prior to integration.
resultsThis work explores the role of cleavage and polyadenylation specificity factor subunit 6 (CPSF6) in the ability of TNPO3-depleted cells to inhibit HIV-1 infection. Our findings showed that depletion of TNPO3 expression inhibits HIV-1 infection, while the simultaneous depletion of TNPO3 and CPSF6 expression rescues HIV-1 infection. Several experiments to understand the rescue of infectivity by CPSF6 were performed. Our experiments revealed that the HIV-1 capsid binding ability of the endogenously expressed CPSF6 from TNPO3-depleted cells does not change when compared to CPSF6 from wild type cells. In agreement with our previous results, depletion of TNPO3 did not change the nuclear localization of CPSF6. Studies on the formation of 2-LRT circles during HIV-1 infection revealed that TNPO3-depleted cells are impaired in the integration process or exhibit a defect in the formation of 2-LTR circles. To understand whether the cytosolic fraction of CPSF6 is responsible for the inhibition of HIV-1 in TNPO3-depleted cells, we tested the ability of a cytosolic full-length CPSF6 to block HIV-1 infection. These results demonstrated that overexpression of a cytosolic full-length CPSF6 blocks HIV-1 infection at the nuclear import step. Fate of the capsid assays revealed that cytosolic expression of CPSF6 enhances stability of the HIV-1 core during infection.
conclusionsThese results suggested that inhibition of HIV-1 by TNPO3-depleted cells requires CPSF6.
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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.