pAkt在衰老细胞中的核转位

Nuclear Translocation of pAkt in Senescent Cells

磷脂酰肌醇3-激酶(PI3K)/蛋白激酶B(PKB,又称为Akt)/叉头转录因子(FOXO)信号通路在从酵母菌到小鼠的寿命以及衰老的调节上都起着非常重要的作用.有研究发现,血清可以激活年轻细胞、衰老细胞胞浆内的Akt,并且年轻细胞核内磷酸化Akt(pAkt)增多,而衰老细胞核内pAkt没有增多.为了研究衰老细胞膜是否发生转位受损,即pAkt能否通过衰老细胞核膜进入核内,通过激光共聚焦显微镜(CLSM)、Western印迹等实验方法,发现衰老细胞胞浆中pAkt可以进入核内,进入核内的pAkt很快被去磷酸化灭活.

The phosphatidylinositol-3 kinase/Akt/FOXO signaling pathway is critically involved in controling the senescence and life span in organisms ranging from yeast to mice. Serum stimulation has been reported to increase the cytoplasmic Akt activity in both early passage and senescent ceils. However,the increase of active Akt in the nucleus was only observed in the nuclear extracts from early passage cells, exhibited. To investigate whether the nuclear membranes of senescent cells is impaired, thus altered pAkt translocation through nuclear membrane and lead to very little active Akt in nuclear extracts of the senescence ceils following serum stimulation, we used Confocol laser scanning microscopy, and Western blot to demonstrate that cytoplasmic pAkt is able to enter the nuclei of senescent cells, but rapidly inactivated afterwards.