rdf:type |
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lifeskim:mentions |
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pubmed:issue |
7
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pubmed:dateCreated |
2001-5-23
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pubmed:abstractText |
The mouse kappa opioid receptor (KOR) gene is constitutively expressed in mouse embryonal carcinoma P19 stem cells and suppressed by retinoic acid (RA) in cells undergoing neuronal differentiation. A negative regulatory element is located within intron 1 of the KOR gene, which contains an Ikaros (Ik)-binding site (GGGAAgGGGAT). This sequence is an Ik-1 respondive, functionally negative element as demonstrated in the context of both natural KOR and heterologous promoters. The two underlined G residues of the second half-site are critical for Ik-1 binding and Ik-mediated repression of the KOR gene. RA induces Ik-1 expression within 1 day of treatment and suppresses KOR expression between 2 and 3 days. Overexpression of Ik-1 in P19 suppresses endogenous KOR gene expression, accompanied by increased binding of Ik-1 to the Ik-binding site and chromatin histone deacetylation on KOR promoters. It is proposed that in an RA-induced P19 differentiation model, RA elevates Ik-1 expression, which recruits histone deacetylase to intron 1 of the KOR gene and silences KOR gene promoters.
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pubmed:grant |
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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/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Histones,
http://linkedlifedata.com/resource/pubmed/chemical/Ikaros Transcription Factor,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Opioid, kappa,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/Tretinoin,
http://linkedlifedata.com/resource/pubmed/chemical/Zfpn1a1 protein, mouse
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0021-9258
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
16
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pubmed:volume |
276
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
4597-603
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:11092879-Acetylation,
pubmed-meshheading:11092879-Animals,
pubmed-meshheading:11092879-DNA-Binding Proteins,
pubmed-meshheading:11092879-Gene Expression Regulation, Developmental,
pubmed-meshheading:11092879-Gene Silencing,
pubmed-meshheading:11092879-Histones,
pubmed-meshheading:11092879-Ikaros Transcription Factor,
pubmed-meshheading:11092879-Introns,
pubmed-meshheading:11092879-Mice,
pubmed-meshheading:11092879-Promoter Regions, Genetic,
pubmed-meshheading:11092879-RNA, Messenger,
pubmed-meshheading:11092879-Receptors, Opioid, kappa,
pubmed-meshheading:11092879-Regulatory Sequences, Nucleic Acid,
pubmed-meshheading:11092879-Transcription Factors,
pubmed-meshheading:11092879-Tretinoin,
pubmed-meshheading:11092879-Tumor Cells, Cultured
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pubmed:year |
2001
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pubmed:articleTitle |
An intronic Ikaros-binding element mediates retinoic acid suppression of the kappa opioid receptor gene, accompanied by histone deacetylation on the promoters.
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pubmed:affiliation |
Department of Pharmacology, University of Minnesota Medical School, Minneapolis, MN 55455-0217, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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