Labile repressors are involved in the transcriptional control of PDGF-responsive genes

Oncogene Res. 1989;4(3):177-84.

Abstract

Platelet-derived growth factor (PDGF) stimulates the transcription of a number of genes in BALB/c-3T3 fibroblasts. Some of these genes (notably the c-myc and c-fo proto-oncogenes) are induced also by phorbol-based tumor promoters which activate protein kinase C. It appears that the response of these genes to PDGF is actually channeled through the activation of protein kinase C. However, other PDGF-inducible genes such as JE, KC, and JB do not respond to tumor promoter. Data suggest that a labile repressor protein blocks the transcriptional response of these genes to tumor promoter. This labile repressor is specific for elements in the JE, KC, and JB genes for it has no effect on the activation of the SV40 early promoter, which is a known target for phorbol ester-inducible transativation.

MeSH terms

  • Animals
  • Cells, Cultured
  • Cycloheximide / pharmacology
  • Exons
  • Gene Expression Regulation / drug effects
  • Mice
  • Mice, Inbred BALB C
  • Platelet-Derived Growth Factor / pharmacology*
  • Promoter Regions, Genetic
  • Proto-Oncogenes / drug effects*
  • Repressor Proteins / metabolism*
  • Simian virus 40 / genetics
  • Tetradecanoylphorbol Acetate / pharmacology
  • Transcription Factors / metabolism*
  • Transcription, Genetic / drug effects*
  • Transfection

Substances

  • Platelet-Derived Growth Factor
  • Repressor Proteins
  • Transcription Factors
  • Cycloheximide
  • Tetradecanoylphorbol Acetate