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http://purl.uniprot.org/citations/17974920http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/17974920http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/17974920http://www.w3.org/2000/01/rdf-schema#comment"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."xsd:string
http://purl.uniprot.org/citations/17974920http://purl.org/dc/terms/identifier"doi:10.1101/gad.1593307"xsd:string
http://purl.uniprot.org/citations/17974920http://purl.org/dc/terms/identifier"doi:10.1101/gad.1593307"xsd:string
http://purl.uniprot.org/citations/17974920http://purl.uniprot.org/core/author"Campbell A.D."xsd:string
http://purl.uniprot.org/citations/17974920http://purl.uniprot.org/core/author"Campbell A.D."xsd:string
http://purl.uniprot.org/citations/17974920http://purl.uniprot.org/core/author"Liu Q."xsd:string
http://purl.uniprot.org/citations/17974920http://purl.uniprot.org/core/author"Liu Q."xsd:string
http://purl.uniprot.org/citations/17974920http://purl.uniprot.org/core/author"Shen Y."xsd:string
http://purl.uniprot.org/citations/17974920http://purl.uniprot.org/core/author"Shen Y."xsd:string
http://purl.uniprot.org/citations/17974920http://purl.uniprot.org/core/author"Tanabe O."xsd:string
http://purl.uniprot.org/citations/17974920http://purl.uniprot.org/core/author"Tanabe O."xsd:string
http://purl.uniprot.org/citations/17974920http://purl.uniprot.org/core/author"Yamamoto M."xsd:string
http://purl.uniprot.org/citations/17974920http://purl.uniprot.org/core/author"Yamamoto M."xsd:string
http://purl.uniprot.org/citations/17974920http://purl.uniprot.org/core/author"Kuroha T."xsd:string
http://purl.uniprot.org/citations/17974920http://purl.uniprot.org/core/author"Kuroha T."xsd:string
http://purl.uniprot.org/citations/17974920http://purl.uniprot.org/core/author"Engel J.D."xsd:string
http://purl.uniprot.org/citations/17974920http://purl.uniprot.org/core/author"Engel J.D."xsd:string
http://purl.uniprot.org/citations/17974920http://purl.uniprot.org/core/date"2007"xsd:gYear
http://purl.uniprot.org/citations/17974920http://purl.uniprot.org/core/date"2007"xsd:gYear
http://purl.uniprot.org/citations/17974920http://purl.uniprot.org/core/name"Genes Dev."xsd:string
http://purl.uniprot.org/citations/17974920http://purl.uniprot.org/core/name"Genes Dev."xsd:string
http://purl.uniprot.org/citations/17974920http://purl.uniprot.org/core/pages"2832-2844"xsd:string
http://purl.uniprot.org/citations/17974920http://purl.uniprot.org/core/pages"2832-2844"xsd:string