Receptor stimulated accumulation of phosphatidylinositol (3,4,5)-trisphosphate by G-protein mediated pathways in human myeloid derived cells.
1993; Springer Nature; Volume: 12; Issue: 6 Linguagem: Inglês
10.1002/j.1460-2075.1993.tb05880.x
ISSN1460-2075
AutoresLen Stephens, A. Eguinoa, Shawn Corey, Trevor Jackson, Phillip T. Hawkins,
Tópico(s)Drug Transport and Resistance Mechanisms
ResumoPhosphoinositide 30H-kinase (PI3K) activities are thought to be critical regulatory enzymes in a new intracellular signalling pathway, the activation of which results in the rapid accumulation of a putative signalling molecule, phosphatidylinositol (3,4,5)-trisphosphate [PtdIns(3,4,5) P3]. To date, activation of PI3K has always correlated with its recruitment into complexes containing protein tyrosine kinases (PTK). Here we report that agonists which utilize G-protein mediated transduction pathways can stimulate very rapid and large accumulations of PtdIns(3,4,5)P3 via a novel mechanism, possibly involving direct coupling between the G-protein and a PI3K activity. In addition, some of these agonists also stimulate small increases in PI3K activity in anti-phosphotyrosine and anti-src-type PTK antibody directed immunoprecipitates, indicating activation of PI3K via a 'conventional' PTK mediated mechanism; these pathways however, play only a minor role in the initial, agonist sensitive production of PtdIns(3,4,5)P3 in myeloid derived cells.
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