ArticleGenes & development1997
Histone acetyltransferases regulate HIV-1 enhancer activity in vitro.
Article in Genes & development, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
87 citing papers in PubMed.
- Differences in HIV burden and immune activation within the gut of HIV-positive patients receiving suppressive antiretroviral therapy.The Journal of infectious diseases · 2010Trial
- Design and implementation of a randomized crossover study of valproic acid and antiretroviral therapy to reduce the HIV reservoir.HIV clinical trialsTrial
- Cell heterogeneity contributes to the variable response of HIV-1 to latency-reversing agents.Science advances · 2026Article
- Breaking into HIV-1's Epigenetic Vault: Cure Strategies to Eliminate the Viral Reservoir.Viruses · 2026Review
- Impact of chromatin on HIV-1 latency: a multi-dimensional perspective.Epigenetics & chromatin · 2025Review
- The HIV-1 Transcriptional Program: From Initiation to Elongation Control.Journal of molecular biology · 2025Review
- ORC1 enhances repressive epigenetic modifications on HIV-1 LTR to promote HIV-1 latency.Journal of virology · 2024Article
- Lentiviral Nef Proteins Differentially Govern the Establishment of Viral Latency.Journal of virology · 2022Article
- Host T Cell Dedifferentiation Effects Drive HIV-1 Latency Stability.Journal of virology · 2022Article
- Article
- Balance between Retroviral Latency and Transcription: Based on HIV Model.Pathogens (Basel, Switzerland) · 2020Review
- The multifaceted nature of HIV latency.The Journal of clinical investigation · 2020Review
- Review
- HUSH, a Link Between Intrinsic Immunity and HIV Latency.Frontiers in microbiology · 2019Review
- Small Molecule Targeting of Specific BAF (mSWI/SNF) Complexes for HIV Latency Reversal.Cell chemical biology · 2018Article
- HIV latency in isolated patient CD4Science translational medicine · 2018Article
- Getting the "Kill" into "Shock and Kill": Strategies to Eliminate Latent HIV.Cell host & microbe · 2018Review
- Repetitive element transcripts are elevated in the brain of C9orf72 ALS/FTLD patients.Human molecular genetics · 2017Article
- Epigenetic Metabolite Acetate Inhibits Class I/II Histone Deacetylases, Promotes Histone Acetylation, and Increases HIV-1 Integration in CD4Journal of virology · 2017Article
- Underlying mechanisms of HIV-1 latency.Virus genes · 2017Review
27 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Specific inhibitors of histone deacetylase, such as trichostatin A (TSA) and trapoxin (TPX), are potent inducers of HIV-1 transcription in latently infected T-cell lines. Activation of the integrated HIV-1 promoter is accompanied by the loss or rearrangement of a positioned nucleosome (nuc-1) near the viral RNA start site. Here we show that TSA strongly induces HIV-1 transcription on chromatin in vitro, concomitant with an enhancer factor-assisted increase in the level of acetylated histone H4. TSA treatment, however, did not detectably alter enhancer factor binding or the positioning of nuc-1 on the majority of the chromatin templates indicating that protein acetylation and chromatin remodeling may be limiting steps that occur only on transcriptionally competent templates, or that remodeling of nuc-1 requires additional factors. To assess the number of active chromatin templates in vitro, transcription was limited to a single round with low levels of the detergent Sarkosyl. Remarkably, HIV-1 transcription on chromatin was found to arise from a small number of active templates that can each support nearly 100 rounds of transcription, and TSA increased the number of active templates in each round. In contrast, transcription on naked DNA was limited to only a few rounds and was not responsive to TSA. We conclude that HIV-1 enhancer complexes greatly facilitate transcription reinitiation on chromatin in vitro, and act at a limiting step to promote the acetylation of histones or other transcription factors required for HIV-1 enhancer activity.
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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.