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ATP耗竭可增加成年心肌细胞中延伸因子eEF2的磷酸化,且与mTOR信号传导的抑制无关。

ATP depletion increases phosphorylation of elongation factor eEF2 in adult cardiomyocytes independently of inhibition of mTOR signalling.

作者信息

McLeod Laura E, Proud Christopher G

机构信息

Division of Molecular Physiology, Faculty of Life Sciences, University of Dundee, DD1 5EH, Dundee, UK.

出版信息

FEBS Lett. 2002 Nov 20;531(3):448-52. doi: 10.1016/s0014-5793(02)03582-2.

Abstract

Translation elongation consumes a high proportion of cellular energy and can be regulated by phosphorylation of elongation factor eEF2 which inhibits its activity. We have studied the effects of ATP depletion on the phosphorylation of eEF2 in adult rat ventricular cardiomyocytes. Energy depletion rapidly leads to inhibition of protein synthesis and increased phosphorylation of eEF2. Stimulation of the AMP-activated protein kinase also causes increases eEF2 phosphorylation. Only at later times is an effect on mTOR signalling observed. These data suggest that energy depletion leads to inhibition of protein synthesis through phosphorylation of eEF2 independently of inhibition of mTOR signalling.

摘要

翻译延伸消耗细胞能量的很大一部分,并且可以通过抑制延伸因子eEF2活性的磷酸化来调节。我们研究了ATP耗竭对成年大鼠心室心肌细胞中eEF2磷酸化的影响。能量耗竭迅速导致蛋白质合成受到抑制以及eEF2磷酸化增加。激活AMP活化蛋白激酶也会导致eEF2磷酸化增加。仅在较晚时候才观察到对mTOR信号传导的影响。这些数据表明,能量耗竭通过eEF2的磷酸化导致蛋白质合成受到抑制,而与mTOR信号传导的抑制无关。

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