Cross-talk between phospholipase C and phosphoinositide 3-kinase signalling pathways

Biochemical Society Transactions
Ian H BattyC Peter Downes

Abstract

1321N1 astrocytoma cells have proved a valuable model system in which to study interactions between two major PtdIns (4,5) P2-utilizing signaling pathways, since they possess receptor populations which elicit independent activation of PI 3-kinase and a G-protein-dependent PLC respectively. Activation of PLC down-regulates PI 3-kinase by at least two mechanisms involving inhibition of IRS-1-associated PI 3-kinase and acute activation of a PtdIns (3,4,5) P3 5-phosphatase. PKB, which is an important early PI 3-kinase-dependent component of insulin signalling pathways, is also down-regulated by PLC-coupled agonists. The activation of PKB by insulin appears to involve a novel PtdIns (3,4,5) P3-dependent protein kinase, which we have named PDK1. The molecular mechanisms underlying PtdIns (3,4,5) P3-stimulated phosphorylation and activation of PKB by PDK1 are currently under investigation.

Citations

Jul 20, 2011·Biochimica Et Biophysica Acta·Takashi UenoEiki Kominami
Mar 29, 2013·International Journal of Molecular Sciences·Elmar PeschkeEckhard Mühlbauer
Dec 17, 2003·Journal of Cell Science·Keqiang Ye, Solomon H Snyder

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