PMID: 2510716Aug 15, 1989Paper

Effect of phorbol ester treatment on receptor-mediated versus G-protein-activator-mediated responses in platelets. Evidence for a two-site action of phorbol ester at the level of G-protein function

The Biochemical Journal
S KrishnamurthiV V Kakkar

Abstract

In platelets, and in several other cell systems, pre-treatment with protein kinase C activators such as phorbol 12-myristate 13-acetate (PMA) results in the inhibition of receptor-mediated responses, suggesting that protein kinase C may play an important role in the termination of signal transduction. In the present study, we have attempted to locate the site of action of phorbol ester by comparing thrombin-induced (i.e. receptor-mediated) platelet activation with that induced by guanosine 5'-[gamma-thio]triphosphate (GTP[S]) and NaF, two agents which by-pass the receptor and initiate platelet responses by directly modulating G-protein function. After a 10 s pre-treatment with PMA (16 nM), dense-granule secretion induced by thrombin (0.2 unit/ml), GTP[S] (40 microM) and NaF (30 mM) was potentiated, resulting in a greater than additive response to agent plus PMA. However, after a 5 min pre-treatment, thrombin-induced secretion alone was inhibited, whereas PMA plus GTP[S]/NaF-induced release remained greater than additive. [32P]Phosphatidate formation in response to all three agents, in contrast, was inhibited by 50-70% in PMA (5 min)-treated platelets. That secretion induced by these agents is a protein kinase C-dependent event ...Continue Reading

Citations

May 8, 1999·Pediatric Research·S J IsraelsA McNicol
Feb 7, 2001·The Journal of Clinical Endocrinology and Metabolism·C J TaiP C Leung
Jan 1, 1994·Platelets·J W Heemskerk, S O Sage
Mar 1, 1992·American Journal of Respiratory Cell and Molecular Biology·J G GarciaJ Dominguez
Mar 19, 1991·Biochimica Et Biophysica Acta·E MeldrumA Carozzi
Apr 3, 1991·Biochimica Et Biophysica Acta·Y NozawaK Nagata

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