@article{88476,
  keywords = {Animals, Humans, cell cycle, Promoter Regions, Genetic, Transcription, Genetic, Binding Sites, Transcription Factors, Trans-Activators, DNA-Binding Proteins, Tumor Cells, Cultured, Nuclear Proteins, Cell Cycle Proteins, Gene Silencing, Active Transport, Cell Nucleus, Cercopithecus aethiops, Transforming Growth Factor beta, COS Cells, Retinoblastoma-Like Protein p107, Proto-Oncogene Proteins c-myc, Smad3 Protein, E2F4 Transcription Factor, E2F5 Transcription Factor, Receptors, Transforming Growth Factor beta, Transcription Factor DP1},
  author = {Chang-Rung Chen and Yibin Kang and Peter Siegel and Joan Massagu{\'e}},
  title = {E2F4/5 and p107 as Smad cofactors linking the TGFbeta receptor to c-myc repression.},
  abstract = {<p>Smad3 is a direct mediator of transcriptional activation by the TGFbeta receptor. Its target genes in epithelial cells include cyclin-dependent kinase inhibitors that generate a cytostatic reponse. We defined how, in the same context, Smad3 can also mediate transcriptional repression of the growth-promoting gene c-myc. A complex containing Smad3, the transcription factors E2F4/5 and DP1, and the corepressor p107 preexists in the cytoplasm. In response to TGFbeta, this complex moves into the nucleus and associates with Smad4, recognizing a composite Smad-E2F site on c-myc for repression. Previously known as the ultimate recipients of cdk regulatory signals, E2F4/5 and p107 act here as transducers of TGFbeta receptor signals upstream of cdk. Smad proteins therefore mediate transcriptional activation or repression depending on their associated partners.</p>
},
  year = {2002},
  journal = {Cell},
  volume = {110},
  pages = {19-32},
  month = {07/2002},
  issn = {0092-8674},
  language = {eng},
}