Wang Gen-zhu, Qi Xin, Li Jing
Yao Xue Xue Bao. 2015 Jul;50(7):808-13.
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.
真核生物延伸因子2激酶(eEF2K)是一种众所周知的Ca2+/钙调蛋白(CaM)依赖性激酶。eEF2K催化eEF2的磷酸化,随后通过损害其与核糖体结合的能力使eEF2失活,从而对蛋白质合成产生负调节作用。最近在几种恶性肿瘤中发现了eEF2K的高表达。作为参与肿瘤进展的因素,eEF2K成为未来癌症治疗的一个潜在靶点。本文综述了eEF2K与肿瘤的关系以及eEF2K抑制剂的最新研究进展。