摘要
Akt被生长因子介导的受体酪氨酸激酶磷酸化激活后可激活一系列底物分子，包括Forkhead转录因子等，对细胞生存和死亡进行调控。随着脑缺血后Akt磷酸化水平（Ser473）的改变，其上游、下游蛋白磷酸化水平也发生变化。预处理可能通过改变Akt蛋白磷酸化水平而产生缺血耐受。Akt／PKB信号转导通路功能障碍可能介导了脑缺血后神经元死亡。
After being activated by the growth factor-mediated receptor tyrosine kinase phosphorylation, Akt activates a series of substrate molecules, including Forkhead transcription factors etc, which regulate cell survival and death. With the changes of Akt phosphorylation levels （Ser473） after cerebral ischemia, its upstream and downstream protein phosphorylation levels have also changed. Preconditioning may produce ischemic tolerance by changing the levels of Akt protein phosphorylation. Dysfunction of Akt/PKB signal transduction pathway may mediated neuronal death after cerebral ischemia.
出处
《国际脑血管病杂志》
北大核心
2009年第2期149-152,共4页
International Journal of Cerebrovascular Diseases
基金
基金项目：广东省自然科学基金（8151018201000035）
关键词
蛋白质丝氨酸苏氨酸激酶
蛋白质酪氨酸激酶
脑缺血
缺血预处理
protein-serine-threonine kinases
protein-tyrosine kinases
cerebral ischemia
ischemic preconditioning
