Source:http://linkedlifedata.com/resource/pubmed/id/20596607
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
2010-7-2
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pubmed:abstractText |
Human immunodeficiency virus type 1 (HIV-1) latency remains a major problem for the eradication of viruses in infected individuals undergoing highly active anti-retroviral therapy. By inhibiting HIV-1 gene expression and virus production, histone deacetylase (HDAC) may contribute to the quiescence of HIV-1 within resting CD4+ T cells. A novel HDAC inhibitor, Scriptaid, has been found to have robust activity and lower toxicity compared to trichostatin A (TSA). We therefore investigated Scriptaid for its capability to reverse HIV-1 latency by inducing HIV-1 activation in the Jurkat T cell line containing latent HIV proviruses. We found that Scriptaid can activate HIV-1 gene expression in these latent infected cells by 2-15-fold over background levels, as analyzed by flow cytometry. Chromatin immunoprecipitation (ChIP) assays further revealed that the Scriptaid increased the acetylation level of histones H3 and H4 at the nucleosome 1 site of the HIV-1 long terminal repeat compared to mock treatment. In addition, Scriptaid can synergize with prostratin or tumor necrosis factor-alpha to activate the HIV-1 promoter, with relatively lower toxicity compared to TSA. These studies suggest the potential of Scriptaid in anti-latency therapies.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Histone Deacetylase Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Histones,
http://linkedlifedata.com/resource/pubmed/chemical/Hydroxylamines,
http://linkedlifedata.com/resource/pubmed/chemical/Phorbol Esters,
http://linkedlifedata.com/resource/pubmed/chemical/Quinolines,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha,
http://linkedlifedata.com/resource/pubmed/chemical/prostratin,
http://linkedlifedata.com/resource/pubmed/chemical/scriptaid
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
1791-244X
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
26
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
265-72
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pubmed:meshHeading |
pubmed-meshheading:20596607-Acetylation,
pubmed-meshheading:20596607-Drug Synergism,
pubmed-meshheading:20596607-Epigenesis, Genetic,
pubmed-meshheading:20596607-HIV Long Terminal Repeat,
pubmed-meshheading:20596607-HIV-1,
pubmed-meshheading:20596607-Histone Deacetylase Inhibitors,
pubmed-meshheading:20596607-Histones,
pubmed-meshheading:20596607-Humans,
pubmed-meshheading:20596607-Hydroxylamines,
pubmed-meshheading:20596607-Jurkat Cells,
pubmed-meshheading:20596607-Phorbol Esters,
pubmed-meshheading:20596607-Promoter Regions, Genetic,
pubmed-meshheading:20596607-Quinolines,
pubmed-meshheading:20596607-Tumor Necrosis Factor-alpha,
pubmed-meshheading:20596607-Virus Latency
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pubmed:year |
2010
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pubmed:articleTitle |
Histone deacetylase inhibitor Scriptaid reactivates latent HIV-1 promoter by inducing histone modification in in vitro latency cell lines.
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pubmed:affiliation |
State Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Sciences, Fudan University, Shanghai 200433, P.R. China.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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