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作 者:宋嘉宁 MUHAMMAD Tahir 张文婷[1] 王娟[1] SONG Jianing;MUHAMMAD Tahir;ZHANG Wenting;WANG Juan(College of Environment and Life,Beijing University of Technology,Beijing 100124,China)
机构地区:[1]北京工业大学环境与生命学部,北京100124
出 处:《河北师范大学学报(自然科学版)》2021年第6期612-619,共8页Journal of Hebei Normal University:Natural Science
基 金:国家自然科学基金(91854115)。
摘 要:自噬是细胞在应激过程中为了维持细胞稳态进行自我降解的过程,适度的细胞自噬有利于细胞生存,但是自噬水平过高或过低都会导致细胞内稳态失衡,甚至细胞死亡,且自噬水平变化与癌症等多种疾病相关.激酶在自噬调控通路中必不可少,近年来对于自噬的研究越来越深入,关于调节自噬进程的蛋白激酶研究也更加全面,有些蛋白激酶直接作为自噬核心蛋白发挥作用,比如unc-51样自噬激活蛋白激酶1(ULK1)/自噬相关蛋白1(Atg1)和Ⅲ类磷脂酰肌醇3-激酶(PI3K),还有些蛋白通过磷酸化自噬核心蛋白对自噬进行调控,比如雷帕霉素靶点蛋白(TOR)、AMP激活蛋白激酶(AMPK)、蛋白激酶C(PKC)、丝裂原活化蛋白激酶(MAPK).以细胞自噬为基础,对蛋白激酶,TOR,ULK1/Atg1,MAPK,PI3K,AMPK和PKC的研究现状进行了综述.Autophagy is a process by which cells undergo self-degradation to maintain cell homeostasis during stress.Moderate autophagy is conducive to cell survival,but excessive autophagy can lead to death,and changes in autophagy levels are associated with many diseases such as cancer.Kinases are essential in the autophagy regulatory pathways.Recently,several studies have been conducted to decipher the specific role of protein kinases in the regulation of autophagy.Some protein kinases like ULK1(unc-51 like autophagy activating kinase 1)/Atg1(autophagy-related gene1),and PI3 K(phosphatidylinositol 3-kinase)constitute core autophagy machinery and directly regulate the autophagy.Other kinases like TOR(target of rapamycin),AMPK(AMP-activated protein kinase),PKC(protein kinase C),and MAPK(mitogen activated kinase-like protein)play their role by phosphorylating core protein kinases.This review summarizes the recent knowledge of autophagy regulation by protein kinases,including TOR,ULK1/Atg1,MAPK,PI3 K,AMPK,and PKC.
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