| Literature DB >> 10549282 |
Y Sun1, X Liu, E N Eaton, W S Lane, H F Lodish, R A Weinberg.
Abstract
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.Entities:
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Year: 1999 PMID: 10549282 DOI: 10.1016/s1097-2765(00)80201-4
Source DB: PubMed Journal: Mol Cell ISSN: 1097-2765 Impact factor: 17.970