Alessi D R, Downes C P
Department of Biochemistry, MSI/WTB Complex, Dow Street, Dundee DD1 5EH, UK.
Biochim Biophys Acta. 1998 Dec 8;1436(1-2):151-64. doi: 10.1016/s0005-2760(98)00133-7.
This review focuses on the recent advances made in our understanding of the mechanism by which insulin induces the activation of PI 3-kinase(s) whose role is to generate 3-phosphoinositide lipids which are the second messenger of the insulin signalling pathway. The mechanism by which these signalling molecules induce the activation of downstream signalling pathways leading to the activation of protein kinase B (PKB, also known as Akt) and other kinases is also discussed. PKB is likely to be a major mediator of many of the physiological responses of a cell to insulin and likely physiological cellular targets of this enzyme are highlighted.
本综述着重介绍了我们在理解胰岛素诱导PI 3激酶激活机制方面的最新进展,PI 3激酶的作用是生成3-磷酸肌醇脂质,而3-磷酸肌醇脂质是胰岛素信号通路的第二信使。本文还讨论了这些信号分子诱导下游信号通路激活,进而导致蛋白激酶B(PKB,也称为Akt)和其他激酶激活的机制。PKB可能是细胞对胰岛素许多生理反应的主要介质,本文还强调了该酶可能的生理细胞靶点。