《生命科学》 2006, 18(2):

细胞周期蛋白依赖性激酶活化激酶(CAK)的研究进展

储 琳^1,2，钱 旻¹，严缘昌^2,3*

1华东师范大学生命科学学院，上海200062；2中国科学院上海生命科学研究院生物化学与细胞生物学研究所，上海200031；3 上海高校模式生物E-研究院，上海200031

摘　要：摘　要：细胞周期蛋白依赖性激酶(CDKs)的基本功能是对细胞周期进行调控。CDKs的激活需要与特异性亚基cyclins结合，并被CDK7-cyclin H-MAT1三元复合物(CAK)磷酸化。此外，CDK7-cylin H-MAT1还是转录因子ⅡH(TFⅡH)的亚基组成部分，磷酸化RNA聚合酶Ⅱ(RNAPⅡ)大亚基的羧基末端结构域(CTD)。CAK因为在细胞周期过程中的重要作用，而受到越来越广泛的关注。本文主要就CAK自身活性调节及其对细胞周期的调控进展作一综述。
关键词：CAK；CDK；CTD；磷酸化

Advances in the studies of cyclin dependent kinase-activating kinase (CAK)

CHU Lin^1,2, QIAN Min¹, YAN Yuan-Chang^2,3*

1 School of Life Science, East China Normal University, Shanghai 200062, China; 2 Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China; 3 Model Organism Division,

Abstract: Abstract: Cell cycle progression is regulated by cyclin dependent kinases (CDKs). The activity of CDKs is tightly controlled by several mechanisms, including binding of subunits to CDKs (cyclins), and phosphorylation by CDK7-cyclin H-MAT1(CAK). Besides, CAK complex is a component of transcription factor Ⅱ(TFⅡH) and phosphorylates the carboxy-terminal domain (CTD) of the largest subunit of RNA polymeraseⅡ(RNAPⅡ). Because of pivotal function of CAK in cell cycle, broad attention has arisen. This review focuses on the regulation of CAK activity via its three subunits and its regulation on the cell cycle progression.
Key words: CAK; CDK; CTD; phosphorylation