ArticleiScience2024
CBP/p300 lysine acetyltransferases inhibit HIV-1 expression in latently infected T cells.
Article in iScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Hijacking the Host: Post-Translational Modifications as Molecular Switches in HIV Persistence and Immune Evasion.Journal of medical virology · 2026Review
- Epigenetic regulation of HIV-1 transcription: insights into latency mechanisms and therapeutic strategies.Frontiers in cellular and infection microbiology · 2026Review
- Inhibition of Histone Deacetylases Induces Cancer Cell Apoptosis Through the PERK Pathway of ER Stress Response.Journal of cellular and molecular medicine · 2025Article
- PRMT3 reverses HIV-1 latency by increasing chromatin accessibility to form a TEAD4-P-TEFb-containing transcriptional hub.Nature communications · 2025Article
- RYBP promotes HIV-1 latency through promoting H2AK119ub and decreasing H3K4me3.Cell communication and signaling : CCS · 2025Article
- Promotion of HIV clearance by sensitization of HIV reservoirs to cell death.Frontiers in immunology · 2025Article
Corrections and comments
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Authors and funding
2 authors.
Funding
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Abstract
HIV-1 latency is regulated by chromatin modifying enzymes, and histone deacetylase inhibitors (HDACi) cause reactivation of provirus expression. Surprisingly, we observed that inhibitors of the CBP/p300 acetyltransferases also cause reversal of latency in T cells. CBP/p300 inhibitors synergize with various latency reversing agents to cause HIV-1 reactivation. In contrast, inhibition of CBP/p300 impaired reversal of latency by the HDACi SAHA, indicating that CBP/p300 must contribute to acetylation on the HIV-1 LTR associated with HDACi-mediated latency reversal. CBP/p300 inhibition caused loss of H3K27ac and H3K4me3 from the LTR, but did not affect association of the inhibitor protein BRD4. Furthermore, inhibition of the additional lysine acetyltransferases PCAF/GCN5 or KAT6A/KAT6B also caused reversal of latency, suggesting that protein acetylation has an inhibitory effect on HIV-1 expression. Collectively, these observations indicate that transcription from the HIV-1 LTR is controlled both positively and negatively by protein acetylation, likely including both histone and non-histone regulatory targets.
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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 Socratic graph.