Cross-talk between phospholipase C and phosphoinositide 3-kinase signalling pathways
Cross-talk between phospholipase C and phosphoinositide 3-kinase signalling pathways
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DOI：
10.1042/bst0251132
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发表时间：
1997-11-01
影响因子：
3.9
通讯作者：
Downes, CP
中科院分区：
文献类型：
--
作者：
Batty, IH;Hickinson, DM;Downes, CP
1321N1 星形细胞瘤细胞已被证明是一个有价值的模型系统，可用于研究两个主要 PtdIns (4, 5) P2 利用信号通路之间的相互作用，因为它们拥有分别引起 PI 3 激酶和 G 蛋白依赖性 PLC 独立激活的受体群。 PLC的激活通过至少两种机制下调PI 3-激酶，涉及抑制IRS-1相关的PI 3-激酶和急性激活PtdIns (3,4,5) P3 5-磷酸酶。 PKB 是胰岛素信号通路中重要的早期 PI 3 激酶依赖性成分，也可被 PLC 偶联激动剂下调。胰岛素对 PKB 的激活似乎涉及一种新型 PtdIns (3,4,5) P3 依赖性蛋白激酶，我们将其命名为 PDK1。 PtdIns (3,4,5) P3 刺激的磷酸化和 PDK1 激活 PKB 的分子机制目前正在研究中。
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.