Erythroid-specific transcription

Current Opinion in Hematology

Volumn 5, Issue 2, 1998, Pages 145-150

  Bieker, James J ^a  

^a MOUNT SINAI SCHOOL OF MEDICINE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

BETA GLOBIN; DNA; TRANSCRIPTION FACTOR; TRANSCRIPTION FACTOR GATA 1;

CHROMATIN STRUCTURE; ERYTHROID CELL; GENE SWITCHING; PRIORITY JOURNAL; PROTEIN DNA INTERACTION; PROTEIN PROTEIN INTERACTION; REVIEW; TRANSCRIPTION REGULATION;

EID: 0031946863     PISSN: 10656251     EISSN: None     Source Type: Journal    
DOI: 10.1097/00062752-199803000-00010     Document Type: Review

References (62)

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38. +/+ fetal livers, as judged by both steady-state RNA analysis and single-cell primary transcript (in situ) RNA analysis. Hypersensitive site analysis indicated that the β-globin promoter was resistant to DNAse I in the absence of EKLF and HS3 partially so; HS1, HS2, HS4, and the α-globin promoter were unaffected. Consistent with its temporally extended expression, the γ-globin promoter remained accessible to nuclease. These results are discussed in terms of current models of globin locus gene competition, gene silencing, and chromatin structure. (Also see reference 38.)
39. +/+ fetal livers. The data are discussed within the context of EKLF's key role in facilitating the probability of β-over γ-globin expression.
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41. Bieker JJ, Ouyang L, Chen X: Transcriptional factors for specific globin genes. Ann N Y Acad Sci 1997, 85:in press. EKLF was shown to be phosphorylated at serine and threonine in erythroid cells. Its transactivation capability was critically dependent on the status of a protein kinase CKII site within its interaction domain. EKLF interacted with CKII in vitro, and its activity in vivo was augmented by cotransfection with CKII.
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44. Li Q, Clegg C, Peterson K, et al.: Binary transgenic mouse model for studying the trans control of globin gene switching: evidence that GATA-1 is an in vivo repressor of human e gene expression. Proc Natl Acad Sci U S A 1997, 94:2444-2448. The human β-locus-containing transgenic mouse was crossed with mice that overexpress GATA-1. Levels of β- and γ-globin were normal, and the γ-to β-switch was unaffected by excess GATA-1 expression. However, ε-globin levels had a fivefold to sixfold lower level of expression, suggesting a role for GATA-1 in repression of the ε-globin gene.
45. Onodera K, Takahashi S, Nishimura S, et al.: GATA-1 transcription is controlled by distinct regulatory mechanisms during primitive and definitive erythropoiesis. Proc Natl Acad Sci U S A 1997, 94:4487-4492. Fusions between portions of the GATA-1 promoter and a LacZ reporter were tested in transgenic mice. An upstream region was sufficient to generate reporter expression in primitive erythroid cells, but recapitulation of expression in definitive cells required an additional element within the first GATA-1 intron.
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