A common mechanism underlying the E1A repression and the cAMP stimulation of the H ferritin transcription

J Biol Chem. 1997 Aug 15;272(33):20736-41. doi: 10.1074/jbc.272.33.20736.

Abstract

Transcription of the H ferritin gene in vivo is stimulated by cAMP and repressed by the E1A oncoprotein. We report here the identification of the cis-element in the human promoter responsive to both cAMP- and E1A-mediated signals. This promoter region is included between positions -62 to -45 and binds a approximate 120-kDa transcription factor called Bbf. Bbf forms a complex in vivo with the coactivator molecules p300 and CBP. Recombinant E1A protein reduces the formation of these complexes. In vivo overexpression of p300 in HeLa cells reverses the E1A-mediated inhibition of the ferritin promoter transcription driven by Bbf. These data suggest the existence of a common mechanism for the cAMP activation and the E1A-mediated repression of H ferritin transcription.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenovirus E1A Proteins / physiology*
  • Cyclic AMP / physiology*
  • Cyclic AMP Response Element-Binding Protein / physiology
  • Cyclic AMP-Dependent Protein Kinases / physiology
  • Ferritins / genetics*
  • HeLa Cells
  • Humans
  • Promoter Regions, Genetic
  • Transcription Factors / metabolism
  • Transcription, Genetic*

Substances

  • Adenovirus E1A Proteins
  • Cyclic AMP Response Element-Binding Protein
  • Transcription Factors
  • Ferritins
  • Cyclic AMP
  • Cyclic AMP-Dependent Protein Kinases