| pubmed-article:17974920 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17974920 | lifeskim:mentions | umls-concept:C1333663 | lld:lifeskim |
| pubmed-article:17974920 | lifeskim:mentions | umls-concept:C1335073 | lld:lifeskim |
| pubmed-article:17974920 | lifeskim:mentions | umls-concept:C0040649 | lld:lifeskim |
| pubmed-article:17974920 | lifeskim:mentions | umls-concept:C1417830 | lld:lifeskim |
| pubmed-article:17974920 | lifeskim:mentions | umls-concept:C1420808 | lld:lifeskim |
| pubmed-article:17974920 | lifeskim:mentions | umls-concept:C1427067 | lld:lifeskim |
| pubmed-article:17974920 | pubmed:issue | 21 | lld:pubmed |
| pubmed-article:17974920 | pubmed:dateCreated | 2007-11-2 | lld:pubmed |
| pubmed-article:17974920 | pubmed:abstractText | When the orphan nuclear receptors TR2 and TR4, the DNA-binding subunits of the DRED repressor complex, are forcibly expressed in erythroid cells of transgenic mice, embryos exhibit a transient mid-gestational anemia as a consequence of a reduction in the number of primitive erythroid cells. GATA-1 mRNA is specifically diminished in the erythroid cells of these TR2/TR4 transgenic embryos as it is in human CD34(+) progenitor cells transfected with forcibly expressed TR2/TR4. In contrast, in loss-of-function studies analyzing either Tr2- or Tr4-germline-null mutant mice or human CD34(+) progenitor cells transfected with force-expressed TR2 and TR4 short hairpin RNAs (shRNAs), GATA-1 mRNA is induced. An evolutionarily conserved direct repeat (DR) element, a canonical binding site for nuclear receptors, was identified in the GATA1 hematopoietic enhancer (G1HE), and TR2/TR4 binds to that site in vitro and in vivo. Mutation of that DR element led to elevated Gata1 promoter activity, and reduced promoter responsiveness to cotransfected TR2/TR4. Thus, TR2/TR4 directly represses Gata1/GATA1 transcription in murine and human erythroid progenitor cells through an evolutionarily conserved binding site within a well-characterized, tissue-specific Gata1 enhancer, thereby providing a mechanism by which Gata1 can be directly silenced during terminal erythroid maturation. | lld:pubmed |
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| pubmed-article:17974920 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:17974920 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:17974920 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17974920 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:17974920 | pubmed:issn | 0890-9369 | lld:pubmed |
| pubmed-article:17974920 | pubmed:author | pubmed-author:YamamotoMasay... | lld:pubmed |
| pubmed-article:17974920 | pubmed:author | pubmed-author:CampbellAndre... | lld:pubmed |
| pubmed-article:17974920 | pubmed:author | pubmed-author:KurohaTakashi... | lld:pubmed |
| pubmed-article:17974920 | pubmed:author | pubmed-author:TanabeOsamuO | lld:pubmed |
| pubmed-article:17974920 | pubmed:author | pubmed-author:EngelJames... | lld:pubmed |
| pubmed-article:17974920 | pubmed:author | pubmed-author:ShenYannanY | lld:pubmed |
| pubmed-article:17974920 | pubmed:author | pubmed-author:LiuQinghuiQ | lld:pubmed |
| pubmed-article:17974920 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17974920 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:17974920 | pubmed:volume | 21 | lld:pubmed |
| pubmed-article:17974920 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17974920 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17974920 | pubmed:pagination | 2832-44 | lld:pubmed |
| pubmed-article:17974920 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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