Ets, Ap-1 and GATA factor families regulate the utrophin B promoter: potential regulatory mechanisms for endothelial-specific expression

FEBS Lett. 2003 Mar 13;538(1-3):168-72. doi: 10.1016/s0014-5793(03)00175-3.

Abstract

Duchenne muscular dystrophy is caused by dystrophin deficiency, which can be prevented in the mdx mouse model by over-expression of an autosomal homologue, utrophin. Utrophin has two characterised full-length promoters, A and B. No data are available on the transcriptional regulation of B utrophin, which has been recently localised to the endothelium. Similar to characterised endothelial promoters, Ets and Ap-1 individually trans-activate the human B core promoter. Synergistic activation by GATA-2 and c-jun to the order of 20-fold was observed.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Base Sequence
  • Cell Line
  • Cytoskeletal Proteins / genetics*
  • Electrophoretic Mobility Shift Assay
  • Endothelium / metabolism
  • Gene Expression Regulation / drug effects*
  • Humans
  • Membrane Proteins / genetics*
  • Mice
  • Molecular Sequence Data
  • Promoter Regions, Genetic
  • Sequence Homology, Nucleic Acid
  • Tetradecanoylphorbol Acetate / pharmacology
  • Transcription Factors / physiology*
  • Transcriptional Activation / drug effects
  • Utrophin

Substances

  • Cytoskeletal Proteins
  • Membrane Proteins
  • Transcription Factors
  • Utrn protein, mouse
  • Utrophin
  • Tetradecanoylphorbol Acetate