Flynn A, Proud G
Department of Biosciences, University of Kent at Canterbury, UK.
FEBS Lett. 1996 Jul 1;389(2):162-6. doi: 10.1016/0014-5793(96)00564-9.
The cap-binding initiation factor 4E (eIF4E) is regulated by phosphorylation and by the inhibitory binding protein 4E-BP1. Here we show that insulin-induced phosphorylation of eIF4E is not significantly affected by rapamycin, but is sensitive to wortmannin, which inhibits phosphatidylinositol 3'-kinase and blocks the activation of MAP kinase. Since PD098059, an inhibitor of MAP kinase activation, also blocks insulin-induced phosphorylation of eIF4E, the MAP kinase pathway seems to mediate this effect. Phosphorylated eIF4E can still bind to 4E-BP1. These data illustrate that (i) distinct signalling pathways mediate the phosphorylation of eIF4E and 4E-BP1 and (ii) phosphorylation of eIF4E, unlike that of 4E-BP1, does not lead directly to the release of 4E-BP1.
帽结合起始因子4E(eIF4E)受磷酸化作用及抑制性结合蛋白4E - BP1的调控。在此我们表明,胰岛素诱导的eIF4E磷酸化不受雷帕霉素的显著影响,但对渥曼青霉素敏感,渥曼青霉素可抑制磷脂酰肌醇3'-激酶并阻断丝裂原活化蛋白激酶(MAP激酶)的激活。由于MAP激酶激活抑制剂PD098059也能阻断胰岛素诱导的eIF4E磷酸化,MAP激酶途径似乎介导了这一效应。磷酸化的eIF4E仍能与4E - BP1结合。这些数据表明:(i)不同的信号通路介导eIF4E和4E - BP1的磷酸化;(ii)与4E - BP1不同,eIF4E的磷酸化不会直接导致4E - BP1的释放。