| Literature DB >> 1309592 |
M T Diaz-Meco1, I Dominguez, L Sanz, M M Municio, E Berra, M E Cornet, A Garcia de Herreros, T Johansen, J Moscat.
Abstract
Cell growth and tumor transformation can be restrained in certain cell systems by the action of transforming growth factor beta (TGF-beta). It has been established that the mechanism whereby TGF-beta 1 inhibits cell growth does not interfere with the triggering of early mitogenic signal transduction mechanisms. Phospholipase C-catalyzed hydrolysis of phosphatidylcholine (PC) is a relatively late step in the cascade activated by growth factors. Therefore, conceivably activation of phospholipase C-catalyzed hydrolysis of PC could be the target of TGF-beta 1 action. In the study reported here, we demonstrate that TGF-beta 1 inhibits the coupling of ras p21 to the activation of PC hydrolysis, which appears to be critical for the antiproliferative effects of TGF-beta 1.Entities:
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Year: 1992 PMID: 1309592 PMCID: PMC364110 DOI: 10.1128/mcb.12.1.302-308.1992
Source DB: PubMed Journal: Mol Cell Biol ISSN: 0270-7306 Impact factor: 4.272