Sen Prosenjit, Mukherjee Sebanti, Ray Doel, Raha Sanghamitra
Crystallography and Molecular Biology Division, Saha Institute of Nuclear Physics, 1/AF Bidhan Nagar, Calcutta, India.
Mol Cell Biochem. 2003 Nov;253(1-2):241-6. doi: 10.1023/a:1026020101379.
Akt/PKB is a serine/threonine kinase, which controls vital cellular functions such as cell survival/apoptosis, cell cycle progression and glucose metabolism. Akt/PKB acts down-stream from growth factors and hormones and is a key mediator of their pro-survival, proliferative and metabolic effects. Akt/PKB carries out these diverse tasks through phosphorylation of a number of cellular substrates. The substrates of Akt/PKB, which promote the inhibition of apoptosis after being phosphorylated by Akt, include the Forkhead transcription factors and the Bcl-2 family member Bad. The cyclin dependent kinase inhibitors are substrates of Akt which when phosphorylated relinquish their inhibitory influence on cell cycle progression. Akt mediates many of the stimulatory effects of insulin on glucose metabolism through deactivation of glycogen synthase kinase, activation of phosphofructokinase, and modulation of glucose transporter activity. Consequently, Akt can be implicated in the pathological processes, which are associated with defects in regulation of apoptosis/survival and energy metabolism.
Akt/PKB是一种丝氨酸/苏氨酸激酶，它控制着诸如细胞存活/凋亡、细胞周期进程和葡萄糖代谢等重要的细胞功能。Akt/PKB在生长因子和激素的下游发挥作用，是它们促存活、增殖和代谢作用的关键介质。Akt/PKB通过磷酸化多种细胞底物来执行这些不同的任务。Akt/PKB的底物在被Akt磷酸化后促进凋亡抑制，包括叉头转录因子和Bcl-2家族成员Bad。细胞周期蛋白依赖性激酶抑制剂是Akt的底物，磷酸化后它们会放弃对细胞周期进程的抑制作用。Akt通过使糖原合酶激酶失活、激活磷酸果糖激酶和调节葡萄糖转运蛋白活性来介导胰岛素对葡萄糖代谢的许多刺激作用。因此，Akt可能参与了与凋亡/存活调节和能量代谢缺陷相关的病理过程。
