Interaction of the Ski oncoprotein with Smad3 regulates TGF-β signaling

被引：232

作者：

Sun, Y

Liu, XD

Eaton, EN

Lane, WS

Lodish, HF

Weinberg, RA ^{[1
]}

机构：

[1] Whitehead Inst Biomed Res, Cambridge Ctr 9, Cambridge, MA 02142 USA

[2] MIT, Dept Biol, Cambridge, MA 02139 USA

[3] Harvard Univ, Harvard Microchem Facil, Cambridge, MA 02138 USA

来源：

MOLECULAR CELL | 1999年 / 4卷 / 04期

关键词：

D O I：

10.1016/S1097-2765(00)80201-4

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：

TGF-beta treatment of cells induces a variety of physiologic responses, including growth inhibition, differentiation, and induction of apoptosis. TGF-beta induces phosphorylation and nuclear translocation of Smad3. We describe here the association of Smad3 with the nuclear protooncogene protein Ski in response to the activation of TGF-beta signaling. Association with Ski represses transcriptional activation by Smad3, and overexpression of Ski renders cells resistant to the growth-inhibitory effects of TGF-beta. The transcriptional repression as well as the growth resistance to TGF-beta by overexpression of Ski can be overcome by overexpression of Smad3. These results demonstrate that Ski is a novel component of the TGF-beta signaling pathway and shed light on the mechanism of action of the Ski oncoprotein.

引用

页码：499 / 509

页数：11

共 48 条

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