p53 Brings a New Twist to the Smad Signaling Network

被引：22

作者：

Atfi, Azeddine ^{[1
]}

Baron, Roland ^{[2
,3
,4
]}

机构：

[1] Hop St Antoine, INSERM, U893, F-75571 Paris, France

[2] Harvard Univ, Sch Dent Med, Dept Oral Med Infect & Immunol, Boston, MA 02115 USA

[3] Harvard Univ, Sch Med, Boston, MA 02115 USA

[4] Massachusetts Gen Hosp, Endocrine Unit, Boston, MA 02115 USA

来源：

SCIENCE SIGNALING | 2008年 / 1卷 / 26期

关键词：

D O I：

10.1126/scisignal.126pe33

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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.

引用

页数：4

共 25 条

[1] Signal transduction by the TGF-β superfamily [J].