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神经生长因子和表皮生长因子可诱导PC12细胞中的蛋白质合成及真核起始因子2B(eIF2B)激活。

Nerve and epidermal growth factor induce protein synthesis and eIF2B activation in PC12 cells.

作者信息

Kleijn M, Welsh G I, Scheper G C, Voorma H O, Proud C G, Thomas A A

机构信息

Department of Molecular Cell Biology, Utrecht University, Padualaan 8, 3584 CH Utrecht, The Netherlands.

出版信息

J Biol Chem. 1998 Mar 6;273(10):5536-41. doi: 10.1074/jbc.273.10.5536.

Abstract

The regulation of protein synthesis and of eukaryotic initiation factor eIF2B was studied in PC12 cells. An increase in protein synthesis was observed after nerve growth factor (NGF) and epidermal growth factor (EGF) treatment of PC12 cells, and this increase coincided with activation of eIF2B. Growth factor addition in the presence of the phosphatidylinositol-3'-OH kinase inhibitor wortmannin showed that both NGF- and EGF-induced protein synthesis and eIF2B activation were phosphatidylinositol-3'-OH kinase dependent. The EGF-induced stimulation of protein synthesis and activation of eIF2B was dependent upon FK506-binding protein-rapamycin-associated protein, as shown with the immunosuppressant rapamycin, whereas NGF induction was partially dependent upon FK506-binding protein-rapamycin-associated protein. The activities of two kinases that act on eIF2B, glycogen synthase kinase-3 and casein kinase II, were measured to assess their potential roles in the activation of eIF2B in PC12 cells. Inactivation of glycogen synthase kinase-3 was seen in response to both NGF and EGF and this coincided with activation of eIF2B. However, inactivation of glycogen synthase kinase-3 was not rapamycin sensitive, in contrast to the activation of eIF2B. This indicates the involvement of another protein kinase or regulatory mechanism in the eIF2B activation. Both growth factors activated casein kinase II. However, the time course of its activation and its insensitivity to wortmannin and rapamycin suggest that casein kinase II does not play a major regulatory role in eIF2B activation under these conditions.

摘要

在PC12细胞中研究了蛋白质合成及真核起始因子eIF2B的调控。在用神经生长因子(NGF)和表皮生长因子(EGF)处理PC12细胞后,观察到蛋白质合成增加,且这种增加与eIF2B的激活同时发生。在磷脂酰肌醇-3'-OH激酶抑制剂渥曼青霉素存在的情况下添加生长因子表明,NGF和EGF诱导的蛋白质合成及eIF2B激活均依赖于磷脂酰肌醇-3'-OH激酶。免疫抑制剂雷帕霉素显示,EGF诱导的蛋白质合成刺激及eIF2B激活依赖于FK506结合蛋白-雷帕霉素相关蛋白,而NGF诱导则部分依赖于FK506结合蛋白-雷帕霉素相关蛋白。检测了作用于eIF2B的两种激酶即糖原合酶激酶-3和酪蛋白激酶II的活性,以评估它们在PC12细胞中eIF2B激活中的潜在作用。在对NGF和EGF的反应中均可见糖原合酶激酶-3失活,且这与eIF2B的激活同时发生。然而,与eIF2B的激活相反,糖原合酶激酶-3的失活对雷帕霉素不敏感。这表明在eIF2B激活中涉及另一种蛋白激酶或调节机制。两种生长因子均激活了酪蛋白激酶II。然而,其激活的时间进程及其对渥曼青霉素和雷帕霉素的不敏感性表明,在这些条件下酪蛋白激酶II在eIF2B激活中不发挥主要调节作用。

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