PT  - JOURNAL ARTICLE
AU  - Atfi, Azeddine
AU  - Baron, Roland
TI  - p53 Brings a New Twist to the Smad Signaling Network
AID  - 10.1126/scisignal.126pe33
DP  - 2008 Jul 01
TA  - Science Signaling
PG  - pe33--pe33
VI  - 1
IP  - 26
4099  - http://stke.sciencemag.org/content/1/26/pe33.short
4100  - http://stke.sciencemag.org/content/1/26/pe33.full
SO  - Sci. Signal.2008 Jul 01; 1
AB  - Transforming growth factor beta (TGF-β) signaling regulates a plethora of cellular responses, including specification of developmental fate during embryogenesis, cell proliferation, differentiation, and apoptosis. Components of this pathway are often mutated in cancers and other human disorders. TGF-β signaling involves activation of transcriptional regulators of the Smad family. The tumor suppressor p53 is an essential partner of Smads, affecting TGF-β signaling at various points in the pathway. Inactivation of p53 may contribute to the aberrant behavior of cancer cells that escape the cytostatic action of TGF-β despite the apparent integrity of the TGF-β receptor or Smads. Thus, the discovery that p53 and TGF-β cooperate in cell-fate decisions and cellular homeostatic mechanisms has important pathophysiological implications.