摘要
磷脂酰肌醇3-激酶(PI3-K/Akt)途径是细胞内重要的促细胞存活通路之一,PI3-K被细胞外信号活化后,激活下游蛋白激酶Akt。在阿尔茨海默病(AD)的发病过程中,凋亡相关基因Bad、GSK-3、转录因子家族、caspases家族等参与了神经元的凋亡,导致神经元的大量丢失。而活化的Akt通过磷酸化Bad、GSK-3、转录因子家族、IB、caspases等使促凋亡基因失活,从而起到抑制神经元凋亡及促进神经元存活的作用,进而减少AD神经元的大量丢失,改善AD的病理变化。
Phosphatidylinositol 3-kinase/Akt （PI3-K/Akt）signaling is one of the important intracellular signal pathways of promoting cell survival. Akt is a downstream protein kinase of PI3-K, which is activated by extracellular signals. In the process of Alzhimer disease （AD）, apoptosis-related genes such as Bad, GSK-3β , transcription factor family, caspases induce neurons apoptosis, but activated Akt adjusts the activation forms of apoptosis-related genes through phosphorylation to inhibit neurons apoptosis and promote neurons survival to reduce neurons massive loss and improve the pathological changes of Alzheimer＇s disease.
出处
《解剖科学进展》
CAS
2008年第3期331-333,共3页
Progress of Anatomical Sciences
基金
辽宁省自然科学基金资助项目(NO.20062088)
