c-Ski inhibits the TGF-beta signaling pathway through stabilization of inactive Smad complexes on Smad-binding elements

Oncogene. 2004 Jun 24;23(29):5068-76. doi: 10.1038/sj.onc.1207690.

Abstract

c-Ski inhibits transforming growth factor-beta (TGF-beta) signaling through interaction with Smad proteins. c-Ski represses Smad-mediated transcriptional activation, probably through its action as a transcriptional co-repressor. c-Ski also inhibits TGF-beta-induced downregulation of genes such as c-myc. However, mechanisms for transcriptional regulation of target genes by c-Ski have not been fully determined. In this study, we examined how c-Ski inhibits both TGF-beta-induced transcriptional activation and repression. DNA-affinity precipitation analysis revealed that c-Ski enhances the binding of Smad2 and 4, and to a lesser extent Smad3, to both CAGA and TGF-beta1 inhibitory element probes. A c-Ski mutant, which is unable to interact with Smad4, failed to enhance the binding of Smad complex on these probes and to inhibit the Smad-responsive promoter. These results suggest that stabilization of inactive Smad complexes on DNA is a critical event in c-Ski-mediated inhibition of TGF-beta signaling.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cells, Cultured
  • DNA-Binding Proteins / metabolism*
  • Gene Expression Regulation
  • Humans
  • Mutation
  • Protein Binding
  • Proto-Oncogene Proteins / metabolism*
  • Signal Transduction
  • Smad Proteins
  • Trans-Activators / metabolism*
  • Transfection
  • Transforming Growth Factor beta / metabolism*

Substances

  • DNA-Binding Proteins
  • Proto-Oncogene Proteins
  • Smad Proteins
  • Trans-Activators
  • Transforming Growth Factor beta
  • SKI protein, human