Cross-talk between phospholipase C and phosphoinositide 3-kinase signalling pathways
| Autor: | Ian H. Batty, Hickinson Dm, C P Downes |
|---|---|
| Rok vydání: | 1997 |
| Předmět: |
medicine.medical_treatment
Astrocytoma Biochemistry Phosphatidylinositol 3-Kinases Phosphatidylinositol Phosphates GTP-Binding Proteins Phosphoinositide phospholipase C Tumor Cells Cultured medicine Animals Insulin Protein kinase A Receptor Phosphoinositide 3-kinase biology Phospholipase C Chemistry Thrombin Phosphoproteins Cell biology Type C Phospholipases Insulin Receptor Substrate Proteins biology.protein Phosphorylation Signal transduction Signal Transduction |
| Zdroj: | Biochemical Society Transactions. 25:1132-1137 |
| ISSN: | 1470-8752 0300-5127 |
| DOI: | 10.1042/bst0251132 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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