http://hdl.handle.net/1765/2488




Transcriptional Activation by hypersensitive site three of the human β-globin Locus Control Region in murine erythroleukemia cells.


Article
volume 1219, issue 2 pp 351-360.
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In this paper we describe a complete deletional analysis of hypersensitive site three (HS3) of the human beta-globin Locus Control Region (LCR). The previously defined core fragment consists of 6 footprinted regions, with multiple binding sites for the erythroid-specific factor GATA-1 and G-rich motifs that can interact with ubiquitous factors such as Sp1 and TEF-2. We show in this paper that the 5' half of this fragment is the most important for activity in murine erythroleukemia (MEL) cells. A fragment containing footprints 1-4 can stimulate transcription of a linked human beta-globin gene to levels of about 40% of that obtained with footprints 1-6. Constructs containing either footprints 1-3 or 3-6 cannot be distinguished from the beta-globin gene alone. We further show that binding sites for the erythroid-specific factor NF-E2 can co-operatively interact with parts of the HS3 core fragment, and that HS3 requires elements upstream from -103 in the human beta-globin promoter for full activity. The importance of these results is discussed in the context of the regulation of the genes in the human beta-globin cluster.



Keywords


Automatically Extracted Terms
  • footprint
  • promoter
  • fragment
  • expression
  • level
  • deletion
  • core fragment
  • result
  • binding
  • expression level
  • nf-e 2
  • globin
  • grosveld
  • activity
  • /3-
  • /3- globin gene
  • / biochimica
  • 1-6
  • sequence
  • oligo


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