CAJ | 학술논문

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.
Akt피생장인자개도적수체락안산격매린산화격활후가격활일계렬저물분자,포괄Forkhead전록인자등,대세포생존화사망진행조공.수착뇌결혈후Akt린산화수평(Ser473)적개변,기상유、하유단백린산화수평야발생변화.예처리가능통과개변Akt단백린산화수평이산생결혈내수.Akt/PKB신호전도통로공능장애가능개도료뇌결혈후신경원사망.
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 phosphoryiation. Dysfunction of Akt/PKB signal transduction pathway may mediated neuronal death after cerebral ischemia.