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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
4
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pubmed:dateCreated |
2001-3-12
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pubmed:abstractText |
Apicidin [cyclo(N-O-methyl-L-tryptophanyl-L-isoleucinyl-D-pipecolinyl-l-2-amino-8-oxodecanoyl)], a novel histone deacetylase inhibitor, has been identified as an antiprotozoal and antiproliferative agent. In this study, we show apicidin induces transcriptional activation of p21(WAF1/CIP1) (p21) in human prostate carcinoma cells. Apicidin induces expression of p21 protein and mRNA and activation of p21 promoter-luciferase reporter constructs. Apicidin causes an accumulation of acetylated histones H3 and H4 in total cellular chromatin. Chromatin immunoprecipitation shows p21 promoter DNA is associated with hyperacetylated histones H3 and H4 after treatment with apicidin. Therefore, the data here demonstrate that apicidin activates p21 transcription associated with the acetylation of histones H3 and H4.
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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/Antineoplastic Agents,
http://linkedlifedata.com/resource/pubmed/chemical/CDKN1A protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Chromatin,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclin-Dependent Kinase Inhibitor...,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclins,
http://linkedlifedata.com/resource/pubmed/chemical/Histone Deacetylase Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Histone Deacetylases,
http://linkedlifedata.com/resource/pubmed/chemical/Histones,
http://linkedlifedata.com/resource/pubmed/chemical/Luciferases,
http://linkedlifedata.com/resource/pubmed/chemical/Peptides, Cyclic,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Fusion Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/apicidin
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0006-291X
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pubmed:author |
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pubmed:copyrightInfo |
Copyright 2001 Academic Press.
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pubmed:issnType |
Print
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pubmed:day |
9
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pubmed:volume |
281
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
866-71
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:11237739-Acetylation,
pubmed-meshheading:11237739-Antineoplastic Agents,
pubmed-meshheading:11237739-Blotting, Northern,
pubmed-meshheading:11237739-Chromatin,
pubmed-meshheading:11237739-Cyclin-Dependent Kinase Inhibitor p21,
pubmed-meshheading:11237739-Cyclins,
pubmed-meshheading:11237739-Dose-Response Relationship, Drug,
pubmed-meshheading:11237739-Histone Deacetylase Inhibitors,
pubmed-meshheading:11237739-Histone Deacetylases,
pubmed-meshheading:11237739-Histones,
pubmed-meshheading:11237739-Humans,
pubmed-meshheading:11237739-Luciferases,
pubmed-meshheading:11237739-Peptides, Cyclic,
pubmed-meshheading:11237739-Promoter Regions, Genetic,
pubmed-meshheading:11237739-RNA, Messenger,
pubmed-meshheading:11237739-Recombinant Fusion Proteins,
pubmed-meshheading:11237739-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:11237739-Time Factors,
pubmed-meshheading:11237739-Transcriptional Activation,
pubmed-meshheading:11237739-Tumor Cells, Cultured
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pubmed:year |
2001
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pubmed:articleTitle |
Transcriptional activation of p21(WAF1/CIP1) by apicidin, a novel histone deacetylase inhibitor.
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pubmed:affiliation |
Medicine Branch, National Cancer Institute, Bethesda, Maryland 20892, USA. jskim@mail.nih.gov
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pubmed:publicationType |
Journal Article
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