Regulation and roles of elongation factor 2 kinase
Regulation and roles of elongation factor 2 kinase
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DOI：
10.1042/bst20140323
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发表时间：
2015-06-01
影响因子：
3.9
通讯作者：
Proud, Christopher G.
中科院分区：
文献类型：
--
作者：
Proud, Christopher G.
真核细胞延伸因子2激酶（eEF 2K）属于称为α-激酶的非典型蛋白激酶的小家族，并且是该组中唯一的钙/钙调蛋白（Ca/CaM）依赖性成员。它磷酸化并使eEF 2失活，以减缓延伸的速率，这是mRNA翻译中消耗蛋白质合成所消耗的几乎所有能量和氨基酸的阶段。除了通过Ca/CaM激活外，eEF 2K还受到一系列其他调节输入的调节，其中包括通过营养和生长因子激活的信号传导途径的抑制。最近的证据表明，eEF 2K在学习和记忆中起着重要作用，这些过程需要合成新的蛋白质并涉及Ca介导的信号传导。eEF 2K在营养和能量耗尽的条件下被激活。在癌细胞或某些肿瘤中，eEF 2K发挥细胞保护作用，这可能反映了其在饥饿条件下抑制蛋白质合成和营养消耗的能力。eEF 2K被评估为癌症的潜在治疗靶点。
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.