Ballard Darby J, Peng Hao-Yun, Das Jugal Kishore, Kumar Anil, Wang Liqing, Ren Yijie, Xiong Xiaofang, Ren Xingcong, Yang Jin-Ming, Song Jianxun
Department of Microbial Pathogenesis and Immunology, Texas A&M University Health Science Center, Bryan, TX, United States.
Department of Biochemistry and Biophysics, Texas A&M University, College Station, TX, United States.
Front Mol Biosci. 2021 Aug 31;8:727863. doi: 10.3389/fmolb.2021.727863. eCollection 2021.
Eukaryotic Elongation Factor-2 Kinase (eEF2K) acts as a negative regulator of protein synthesis, translation, and cell growth. As a structurally unique member of the alpha-kinase family, eEF2K is essential to cell survival under stressful conditions, as it contributes to both cell viability and proliferation. Known as the modulator of the global rate of protein translation, eEF2K inhibits eEF2 (eukaryotic Elongation Factor 2) and decreases translation elongation when active. eEF2K is regulated by various mechanisms, including phosphorylation through residues and autophosphorylation. Specifically, this protein kinase is downregulated through the phosphorylation of multiple sites mTOR signaling and upregulated the AMPK pathway. eEF2K plays important roles in numerous biological systems, including neurology, cardiology, myology, and immunology. This review provides further insights into the current roles of eEF2K and its potential to be explored as a therapeutic target for drug development.
真核生物延伸因子2激酶(eEF2K)作为蛋白质合成、翻译和细胞生长的负调节因子。作为α激酶家族结构独特的成员,eEF2K在应激条件下对细胞存活至关重要,因为它有助于细胞活力和增殖。作为蛋白质翻译全局速率的调节因子,eEF2K在激活时抑制eEF2(真核生物延伸因子2)并降低翻译延伸。eEF2K受多种机制调节,包括通过残基的磷酸化和自磷酸化。具体而言,这种蛋白激酶通过mTOR信号传导的多个位点的磷酸化而下调,并通过AMPK途径上调。eEF2K在众多生物系统中发挥重要作用,包括神经学、心脏病学、肌学和免疫学。本综述进一步深入探讨了eEF2K的当前作用及其作为药物开发治疗靶点的潜在探索价值。