Regulation and roles of elongation factor 2 kinase

被引:75
|
作者
Proud, Christopher G. [1 ]
机构
[1] Univ Southampton, Ctr Biol Sci, Southampton SO17 1BJ, Hants, England
基金
英国惠康基金; 英国生物技术与生命科学研究理事会;
关键词
eEF2; mRNA translation; nutrient; protein synthesis; synaptic plasticity; tumour; PROTEIN-SYNTHESIS; CRYSTAL-STRUCTURE; TRANSLATION; ACTIVATION; DOMAIN; PHOSPHORYLATION; INHIBITION; RAPAMYCIN; LEADS; MTOR;
D O I
10.1042/BST20140323
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
Eukaryotic elongation factor 2 kinase (eEF2K) belongs to the small family of atypical protein kinases termed a-kinases, and is the only calcium/calmodulin (Ca/CaM)-dependent member of that group. It phosphorylates and inactivates eEF2, to slow down the rate of elongation, the stage in mRNA translation that consumes almost all the energy and amino acids consumed by protein synthesis. In addition to activation by Ca/CaM, eEF2K is also regulated by an array of other regulatory inputs, which include inhibition by the nutrient-and growth-factor activated signalling pathways. Recent evidence shows that eEF2K plays an important role in learning and memory, processes that require the synthesis of new proteins and involve Ca-mediated signalling. eEF2K is activated under conditions of nutrient and energy depletion. In cancer cells, or certain tumours, eEF2K exerts cytoprotective effects, which probably reflect its ability to inhibit protein synthesis, and nutrient consumption, under starvation conditions. eEF2K is being evaluated as a potential therapeutic target in cancer.
引用
收藏
页码:328 / 332
页数:5
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