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真核延伸因子2激酶(e EF2K)是一种Ca2+/Ca M依赖性蛋白激酶,e EF2是其已知的唯一底物。e EF2K催化e EF2的Thr56位点发生磷酸化,导致降低e EF2与核糖体的结合能力进而抑制肽链延伸。现已发现,e EF2K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e EF2K可能是一个潜在的肿瘤治疗靶点。本文就e EF2K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。
Eukaryotic elongation factor 2 kinase (e EF2K) is a Ca2 + / Ca M-dependent protein kinase and e EF2 is its only known substrate. e EF2K catalyzes phosphorylation at the Thr56 site of e EF2, resulting in a decrease of e EF2 binding to ribosomes and thus inhibition of peptide chain elongation. It has been found that e EF2K is highly expressed or highly activated in a variety of tumor cells and is involved in the regulation of tumor progression. Thus e EF2K may be a potential therapeutic target for oncology. This article reviews the structure, function, relationship with tumor and the research progress of inhibitors of e EF2K.