A self-enabling TGFβ response coupled to stress signaling: Smad engages stress response factor ATF3 for Id1 repression in epithelial cells

Yibin Kang, Chang Rung Chen, Joan Massagué

Research output: Contribution to journalArticlepeer-review

404 Scopus citations

Abstract

Genome-wide transcriptional profiling of human epithelial cells revealed that repression of Id inhibitors of differentiation (Id1, Id2, and Id3) is a general feature of the TGFβ cytostatic program. Opposite responses of Id1 to TGFβ and the related factor BMP are dictated by the specific ability of the TGFβ mediator, Smad3, to activate expression of stress response factor ATF3 and then recruit this factor to the Id1 promoter. Thus, a Smad3-mediated primary gene response, ATF3 induction, enables Smad3 to participate in an ATF3-mediated, secondary gene response. As a common target of TGFβ/Smad signals and stress signals via p38 kinase, ATF3 additionally serves to channel synergy between these pathways in the response of epithelial cells to stress and injury.

Original languageEnglish (US)
Pages (from-to)915-926
Number of pages12
JournalMolecular Cell
Volume11
Issue number4
DOIs
StatePublished - Apr 1 2003
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Cell Biology

Fingerprint Dive into the research topics of 'A self-enabling TGFβ response coupled to stress signaling: Smad engages stress response factor ATF3 for Id1 repression in epithelial cells'. Together they form a unique fingerprint.

Cite this