ArticlePloS one2012
Selective histonedeacetylase inhibitor M344 intervenes in HIV-1 latency through increasing histone acetylation and activation of NF-kappaB.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 40 citations in OpenAlex.
- Development of a High-Throughput Platform for Quantitation of Histone Modifications on a New QTOF Instrument.Molecular & cellular proteomics : MCP · 2025Article
- Mechanisms and efficacy of small molecule latency-promoting agents to inhibit HIV reactivation ex vivo.JCI insight · 2024Article
- Scopoletin Reactivates Latent HIV-1 by Inducing NF-κB Expression without Global T Cell Activation.International journal of molecular sciences · 2023Article
- Structure of a HIV-1 IN-Allosteric inhibitor complex at 2.93 Å resolution: Routes to inhibitor optimization.PLoS pathogens · 2023Article
- A Two-Color Haploid Genetic Screen Identifies Novel Host Factors Involved in HIV-1 Latency.mBio · 2021Article
- Article
- Allosteric HIV Integrase Inhibitors Promote Formation of Inactive Branched Polymers via Homomeric Carboxy-Terminal Domain Interactions.Structure (London, England : 1993) · 2021Article
- BET inhibitors RVX-208 and PFI-1 reactivate HIV-1 from latency.Scientific reports · 2017Article
- The bromodomain and extraterminal domain inhibitor bromosporine synergistically reactivates latent HIV-1 in latently infected cells.Oncotarget · 2017Article
- Reactivation of HIV-1 from Latency by an Ingenol Derivative from Euphorbia Kansui.Scientific reports · 2017Article
- Advancements in Developing Strategies for Sterilizing and Functional HIV Cures.BioMed research international · 2017Review
- The BET inhibitor OTX015 reactivates latent HIV-1 through P-TEFb.Scientific reports · 2016Article
- Small Molecule Inhibitors of BAF; A Promising Family of Compounds in HIV-1 Latency Reversal.EBioMedicine · 2016Article
- Epigenetic control of HIV-1 post integration latency: implications for therapy.Clinical epigenetics · 2015Review
- Designed transcription activator-like effector proteins efficiently induced the expression of latent HIV-1 in latently infected cells.AIDS research and human retroviruses · 2015Article
- Review
- Dilazep synergistically reactivates latent HIV-1 in latently infected cells.Molecular biology reports · 2014Article
- Specific reactivation of latent HIV-1 with designer zinc-finger transcription factors targeting the HIV-1 5'-LTR promoter.Gene therapy · 2014Article
- Altering cell death pathways as an approach to cure HIV infection.Cell death & disease · 2013Review
- HIV-1 transcription and latency: an update.Retrovirology · 2013Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHistone deacetylase (HDAC) inhibitors present an exciting new approach to activate HIV production from latently infected cells to potentially enhance elimination of these cells and achieve a cure. M344, a novel HDAC inhibitor, shows robust activity in a variety of cancer cells and relatively low toxicity compared to trichostatin A (TSA). However, little is known about the effects and action mechanism of M344 in inducing HIV expression in latently infected cells. METHODOLOGY/PRINCIPAL
findingsUsing the Jurkat T cell model of HIV latency, we demonstrate that M344 effectively reactivates HIV-1 gene expression in latently infected cells. Moreover, M344-mediated activation of the latent HIV LTR can be strongly inhibited by a NF-κB inhibitor aspirin. We further show that M344 acts by increasing the acetylation of histone H3 and histone H4 at the nucleosome 1 (nuc-1) site of the HIV-1 long terminal repeat (LTR) and by inducing NF-κB p65 nuclear translocation and direct RelA DNA binding at the nuc-1 region of the HIV-1 LTR. We also found that M344 synergized with prostratin to activate the HIV-1 LTR promoter in latently infected cells. CONCLUSIONS/SIGNIFICANCE: These results suggest the potential of M344 in anti-latency therapies and an important role for histone modifications and NF-κB transcription factors in regulating HIV-1 LTR gene expression.
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