title: p53 brings a new twist to the Smad signaling network.
abstract: Transforming growth factor beta (TGF-beta) 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-beta signaling involves activation of transcriptional regulators of the Smad family. The tumor suppressor p53 is an essential partner of Smads, affecting TGF-beta 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-beta despite the apparent integrity of the TGF-beta receptor or Smads. Thus, the discovery that p53 and TGF-beta cooperate in cell-fate decisions and cellular homeostatic mechanisms has important pathophysiological implications.
authors.affiliation: INSERM U893, Hôpital St-Antoine, 184 Rue du Faubourg St-Antoine, 75571 Paris, France. azeddine.atfi@inserm.fr
authors.forename: Azeddine
authors.initials: A
authors.lastname: Atfi
authors.forename: Roland
authors.initials: R
authors.lastname: Baron
mesh_terms: D000818:Animals; D017209:Apoptosis; D002454:Cell Differentiation; D006801:Humans; D009154:Mutation; D009369:Neoplasms / Q000378:metabolism / Q000473:pathology; D015398:Signal Transduction; D051785:Smad Proteins / Q000235:genetics / Q000502:physiology*; D016212:Transforming Growth Factor beta / Q000235:genetics / Q000502:physiology*
chemical_list: D051785:Smad Proteins; D016212:Transforming Growth Factor beta