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Receptor stimulated accumulation of phosphatidylinositol (3,4,5)‐trisphosphate by G‐protein mediated pathways in human myeloid derived cells.
Author(s) -
Stephens L.,
Eguinoa A.,
Corey S.,
Jackson T.,
Hawkins P.T.
Publication year - 1993
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1002/j.1460-2075.1993.tb05880.x
Subject(s) - biology , phosphatidylinositol , myeloid cells , g protein , signal transduction , microbiology and biotechnology , receptor , inositol , gq alpha subunit , biochemistry
Phosphoinositide 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.