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由磷脂酰肌醇-3-羟基激酶介导的血小板衍生生长因子和胰岛素依赖性pp70S6k激活

PDGF- and insulin-dependent pp70S6k activation mediated by phosphatidylinositol-3-OH kinase.

作者信息

Chung J, Grammer T C, Lemon K P, Kazlauskas A, Blenis J

机构信息

Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115.

出版信息

Nature. 1994 Jul 7;370(6484):71-5. doi: 10.1038/370071a0.

Abstract

Platelet-derived growth factor receptor (PDGF-R) phosphorylation at tyrosines 740/751 and insulin receptor phosphorylation of insulin receptor substrate-1 effects the recruitment and activation of phosphatidylinositol-3-OH kinase (PI(3)K). Changes in PI(3)K activity correlate with cell growth but its downstream signal transducers are unknown. Activation of the 70/85K S6 kinases (pp70S6k) by serine phosphorylation results in 40S ribosomal protein S6 phosphorylation and is important for G1 cell-cycle transition in a variety of cells. Although receptor tyrosine kinases activate the microtubule-associated protein kinase cascade through SH2-/SH3-adaptor proteins, Sos and c-Ras, it is unclear how tyrosine kinases are coupled to the pp70S6k phosphorylation cascade. Here we report that PI(3)K mediates PDGF or insulin receptor signalling to pp70S6k. PI(3)K-mediated activation of pp70S6k is independent of conventional protein kinase C isoforms. Additionally, rapamycin blocks pp70S6k activation by all mitogens, without inhibiting PI(3)K, and acts downstream in this signalling system.

摘要

血小板衍生生长因子受体(PDGF-R)在酪氨酸740/751位点的磷酸化以及胰岛素受体底物-1的胰岛素受体磷酸化会影响磷脂酰肌醇-3-羟基激酶(PI(3)K)的募集和激活。PI(3)K活性的变化与细胞生长相关,但其下游信号转导分子尚不清楚。丝氨酸磷酸化激活70/85K S6激酶(pp70S6k)会导致40S核糖体蛋白S6磷酸化,这对多种细胞的G1期细胞周期转换很重要。尽管受体酪氨酸激酶通过SH2-/SH3衔接蛋白、Sos和c-Ras激活微管相关蛋白激酶级联反应,但尚不清楚酪氨酸激酶是如何与pp70S6k磷酸化级联反应偶联的。在此我们报告,PI(3)K介导PDGF或胰岛素受体向pp70S6k的信号传导。PI(3)K介导的pp70S6k激活不依赖于传统的蛋白激酶C亚型。此外,雷帕霉素可阻断所有促细胞分裂剂对pp70S6k的激活,而不抑制PI(3)K,并且在该信号系统中作用于下游。

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