Phospholipase C-mediated hydrolysis of phosphatidylcholine is a target of transforming growth factor beta 1 inhibitory signals. | Zendy

Marı́a T. Diaz-Meco | Zendy; Isabel Domínguez | Zendy; Laura Sanz | Zendy; M.M. Municio | Zendy; Edurne Berra | Zendy; M E Cornet | Zendy; Antonio Garcı́a de Herreros | Zendy; Terje Johansen | Zendy; Jorge Moscat | Zendy

Open Access

Phospholipase C-mediated hydrolysis of phosphatidylcholine is a target of transforming growth factor beta 1 inhibitory signals.

Author(s) -

Marı́a T. Diaz-Meco,

Isabel Domínguez,

Laura Sanz,

M.M. Municio,

Edurne Berra,

M E Cornet,

Antonio Garcı́a de Herreros,

Terje Johansen,

Jorge Moscat

Publication year - 1992

Publication title -

molecular and cellular biology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.14

H-Index - 327

eISSN - 1067-8824

pISSN - 0270-7306

DOI - 10.1128/mcb.12.1.302

Subject(s) - transforming growth factor , biology , transforming growth factor beta , cell growth , phosphatidylcholine , phospholipase c , phospholipase , signal transduction , microbiology and biotechnology , phospholipase d , beta (programming language) , tgf beta signaling pathway , growth factor , biochemistry , receptor , enzyme , phospholipid , membrane , computer science , programming language

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.

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