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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
12
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pubmed:dateCreated |
2011-9-28
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pubmed:abstractText |
Chromatin remodeling, especially in relation to the transactivator Tat, is an essential event for human immunodeficiency virus-1 (HIV-1) transcription. Curcumin has been shown to suppress pathways linked to HIV-1 replication. We investigated whether curcumin had the potential to inhibit Tat-induced long terminal repeat region (LTR) transactivation. As we shown, curcumin inhibited Tat-induced LTR transcativation, while knockdown of histone deacetylase 1 (HDAC1) by siRNA potentiated Tat-induced HIV-1 transcativation. Curcumin reversed Tat-induced down-regulation of HDAC1 expression in multinuclear activation of galactosidase indicator (MAGI) cells. Treatment with curcumin reversed Tat-induced dissociation of HDAC1 from LTR; and curcumin caused a decline in the binding of p65/NF?B to LTR promoters stimulated by Tat. Curcumin attenuated Tat-induced p65 phosphorylation and IKK phosphorylation. Curcumin reversed Tat-mediated reduction in AMPK activation and downstream acetyl-CoA carboxylase (ACC) activation. Collectively, our data provide new insights into understanding of the molecular mechanisms of curcumin inhibited Tat-regulated transcription, suggesting that targeting AMPK/HDAC1/NF?B pathway could serve as new anti-HIV-1 agents.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/AMP-Activated Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Acetyl-CoA Carboxylase,
http://linkedlifedata.com/resource/pubmed/chemical/Anti-HIV Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Curcumin,
http://linkedlifedata.com/resource/pubmed/chemical/HDAC1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Histone Deacetylase 1,
http://linkedlifedata.com/resource/pubmed/chemical/Histones,
http://linkedlifedata.com/resource/pubmed/chemical/I-kappa B Kinase,
http://linkedlifedata.com/resource/pubmed/chemical/RELA protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factor RelA,
http://linkedlifedata.com/resource/pubmed/chemical/p300-CBP Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/tat Gene Products, Human...
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
1097-4652
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pubmed:author |
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pubmed:copyrightInfo |
Copyright © 2011 Wiley-Liss, Inc.
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pubmed:issnType |
Electronic
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pubmed:volume |
226
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
3385-91
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pubmed:meshHeading |
pubmed-meshheading:21344388-AMP-Activated Protein Kinases,
pubmed-meshheading:21344388-Acetyl-CoA Carboxylase,
pubmed-meshheading:21344388-Acetylation,
pubmed-meshheading:21344388-Anti-HIV Agents,
pubmed-meshheading:21344388-Binding Sites,
pubmed-meshheading:21344388-Chromatin Assembly and Disassembly,
pubmed-meshheading:21344388-Curcumin,
pubmed-meshheading:21344388-Dose-Response Relationship, Drug,
pubmed-meshheading:21344388-Down-Regulation,
pubmed-meshheading:21344388-Energy Metabolism,
pubmed-meshheading:21344388-Enzyme Activation,
pubmed-meshheading:21344388-HIV Long Terminal Repeat,
pubmed-meshheading:21344388-HIV-1,
pubmed-meshheading:21344388-HeLa Cells,
pubmed-meshheading:21344388-Histone Deacetylase 1,
pubmed-meshheading:21344388-Histones,
pubmed-meshheading:21344388-Humans,
pubmed-meshheading:21344388-I-kappa B Kinase,
pubmed-meshheading:21344388-Phosphorylation,
pubmed-meshheading:21344388-RNA Interference,
pubmed-meshheading:21344388-Signal Transduction,
pubmed-meshheading:21344388-Transcription Factor RelA,
pubmed-meshheading:21344388-Transcriptional Activation,
pubmed-meshheading:21344388-Transfection,
pubmed-meshheading:21344388-p300-CBP Transcription Factors,
pubmed-meshheading:21344388-tat Gene Products, Human Immunodeficiency Virus
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pubmed:year |
2011
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pubmed:articleTitle |
HDAC1/NF?B pathway is involved in curcumin inhibiting of Tat-mediated long terminal repeat transactivation.
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pubmed:affiliation |
College of Life Science & Bioengineering, Beijing University of Technology, Beijing, China. zhanghs@bjut.edu.cn
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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