王根柱, 戚欣, 李静. 真核延伸因子2激酶与肿瘤J. 药学学报, 2015,50(7): 808-813.
引用本文: 王根柱, 戚欣, 李静. 真核延伸因子2激酶与肿瘤J. 药学学报, 2015,50(7): 808-813.
WANG Gen-zhu, QI Xin, LI Jing. Eukaryotic elongation factor 2 kinase and cancerJ. Acta Pharmaceutica Sinica, 2015,50(7): 808-813.
Citation: WANG Gen-zhu, QI Xin, LI Jing. Eukaryotic elongation factor 2 kinase and cancerJ. Acta Pharmaceutica Sinica, 2015,50(7): 808-813.

真核延伸因子2激酶与肿瘤

Eukaryotic elongation factor 2 kinase and cancer

  • 摘要: 真核延伸因子2激酶 (eEF2K) 是一种Ca2+/CaM依赖性蛋白激酶, eEF2是其已知的唯一底物。eEF2K催化eEF2的Thr56位点发生磷酸化, 导致降低eEF2与核糖体的结合能力进而抑制肽链延伸。现已发现, eEF2K在多种肿瘤细胞中高表达或高度活化, 参与肿瘤进程的调控, 因此eEF2K可能是一个潜在的肿瘤治疗靶点。本文就eEF2K的结构、功能、与肿瘤的关系及其抑制剂的研究进展进行综述。

     

    Abstract: Eukaryotic elongation factor 2 kinase (eEF2K) is well known as a Ca2+/calmodulin (CaM)-dependent kinase. eEF2K catalyzes the phosphorylation of eEF2 and subsequently inactivates eEF2 by impairing its ability to bind to the ribosome, thereby negatively modulates protein synthesis. The high expression of eEF2K has been found recently in several types of malignancies. As participating in the progress of tumor, eEF2K emerges a potential target for future cancer therapy. The relationship between eEF2K and tumor, and the latest progress of eEF2K inhibitors were summarized in this article.

     

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