ArticleJournal of molecular biology2011
Varying modulation of HIV-1 LTR activity by Baf complexes.
Article in Journal of molecular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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The trial behind it
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
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- Multiple Inhibitory Factors Act in the Late Phase of HIV-1 Replication: a Systematic Review of the Literature.Microbiology and molecular biology reviews : MMBR · 2018Pooled it
- Activation of HIV transcription with short-course vorinostat in HIV-infected patients on suppressive antiretroviral therapy.PLoS pathogens · 2014Trial
- Impact of chromatin on HIV-1 latency: a multi-dimensional perspective.Epigenetics & chromatin · 2025Review
- Targeting cyclin-dependent kinase 9 in cancer therapy.Acta pharmacologica Sinica · 2022Review
- DNA Damage Triggers the Nuclear Accumulation of RASSF6 Tumor Suppressor Protein via CDK9 and BAF53 To Regulate p53 Target Gene Transcription.Molecular and cellular biology · 2022Article
- The CREB Regulated Transcription Coactivator 2 Suppresses HIV-1 Transcription by Preventing RNA Pol II from Binding to HIV-1 LTR.Virologica Sinica · 2021Article
- Epigenetic Mechanisms of HIV-1 Persistence.Vaccines · 2021Review
- Balance between Retroviral Latency and Transcription: Based on HIV Model.Pathogens (Basel, Switzerland) · 2020Review
- Targeting HIV-1 proviral transcription.Current opinion in virology · 2019Review
- Longitudinal variation in human immunodeficiency virus long terminal repeat methylation in individuals on suppressive antiretroviral therapy.Clinical epigenetics · 2019Article
- Small Molecule Targeting of Specific BAF (mSWI/SNF) Complexes for HIV Latency Reversal.Cell chemical biology · 2018Article
- Article
- The Short Isoform of BRD4 Promotes HIV-1 Latency by Engaging Repressive SWI/SNF Chromatin-Remodeling Complexes.Molecular cell · 2017Article
- The effects of cocaine on HIV transcription.Journal of neurovirology · 2016Review
- Functional roles of HIV-1 Tat protein in the nucleus.Cellular and molecular life sciences : CMLS · 2016Review
- Mechanisms of HIV Transcriptional Regulation by Drugs of Abuse.Current HIV research · 2016Review
- FACT Proteins, SUPT16H and SSRP1, Are Transcriptional Suppressors of HIV-1 and HTLV-1 That Facilitate Viral Latency.The Journal of biological chemistry · 2015Article
- Therapeutic doses of irradiation activate viral transcription and induce apoptosis in HIV-1 infected cells.Virology · 2015Article
- Role of Bruton's tyrosine kinase inhibitors in HIV-1-infected cells.Journal of neurovirology · 2015Article
- Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
The human immunodeficiency virus type 1 (HIV-1) long terminal repeat is present on both ends of the integrated viral genome and contains regulatory elements needed for transcriptional initiation and elongation. Post-integration, a highly ordered chromatin structure consisting of at least five nucleosomes, is found at the 5' long terminal repeat, the location and modification state of which control the state of active viral replication as well as silencing of the latent HIV-1 provirus. In this context, the chromatin remodeling field rapidly emerges as having a critical role in the control of viral gene expression. In the current study, we focused on unique Baf subunits that are common to the most highly recognized of chromatin remodeling proteins, the SWI/SNF (switching-defective-sucrose non-fermenting) complexes. We find that at least two Baf proteins, Baf53 and Baf170, are highly regulated in HIV-1-infected cells. Previously, studies have shown that the depletion of Baf53 in uninfected cells leads to the expansion of chromosomal territories and the decompaction of the chromatin. Baf53, in the presence of HIV-1 infection, co-elutes off of a chromatographic column as a different-sized complex when compared to uninfected cells and appears to be predominantly phosphorylated. The innate function of Baf53-containing complexes appears to be transcriptionally suppressive, in that knocking down Baf53 increases viral gene expression from cells both transiently and chronically infected with HIV-1. Additionally, cdk9/cyclin T in the presence of Tat is able to phosphorylate Baf53 in vitro, implying that this posttranslationally modified form relieves the suppressive effect and allows for viral transcription to proceed.
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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.