A combinatorial mechanism for determining the specificity of E2F activation and repression

Oncogene. 2009 Aug 13;28(32):2873-81. doi: 10.1038/onc.2009.153. Epub 2009 Jun 22.

Abstract

Various studies have detailed the role of E2F proteins in both transcription activation and repression. Further study has shown that distinct promoter elements, but comprising the same E2F-recognition motif, confer positive or negative E2F control and that this reflects binding of either activator or repressor E2F proteins, respectively. We now show that the specificity of binding of an activator or repressor E2F protein is determined by adjacent sequences that bind a cooperating transcription factor. We propose that the functional E2F element is a module comprising not only the E2F-binding site but also the adjacent site for the cooperating transcription factor.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Binding Sites / genetics
  • CDC2 Protein Kinase
  • Cell Cycle Proteins / genetics
  • Cell Line
  • Cell Line, Tumor
  • Chromatin Immunoprecipitation
  • Cyclin B / genetics
  • Cyclin-Dependent Kinases
  • E2F Transcription Factors / metabolism*
  • Electrophoretic Mobility Shift Assay
  • Gene Expression Regulation*
  • Humans
  • Mutation
  • Nuclear Proteins / genetics
  • Promoter Regions, Genetic / genetics
  • Protein Binding
  • Protein Biosynthesis
  • Response Elements / genetics*
  • Transcription, Genetic
  • Transfection

Substances

  • CDC6 protein, human
  • Cell Cycle Proteins
  • Cyclin B
  • E2F Transcription Factors
  • Nuclear Proteins
  • CDC2 Protein Kinase
  • CDK1 protein, human
  • Cyclin-Dependent Kinases