Regulation of the phosphorylation of elongation factor 2 by MEK-dependent signalling in adult rat cardiomyocytes

被引：43

作者：

Wang, LJ ^{[1
]}

Proud, CG ^{[1
]}

机构：

[1] Univ Dundee, Div Mol Physiol, Fac Life Sci, Dundee DD1 5EH, Scotland

来源：

FEBS LETTERS | 2002年 / 531卷 / 02期

关键词：

translation; elongation; cEF2; MEK; cardiomyocyte; hypertrophy;

D O I：

10.1016/S0014-5793(02)03536-6

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The Gq-coupled agonists phenylephrine and endothelin-1 each activate protein synthesis in cardiomyocytes as part of the programme that leads to cardiac hypertrophy. Here we show that they each induce the dephosphorylation of elongation factor (eEF) 2, a protein that in its dephosphorylated state mediates the translocation step of elongation. The ability of both agonists to induce dephosphorylation of eEF2 requires signalling via the mTOR and NIEK/Erk signalling pathways, but is independent of phosphoinositide 3-kinase. Expression of an activated form of MEK leads to dephosphorylation of eEF2, in an mTOR independent manner, indicating that signalling via MEK/Erk suffices to cause dephosphorylation of eEF2. (C) 2002 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.

引用

页码：285 / 289

页数：5

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