Mukasa T, Khoroku Y, Tsukahara T, Momoi M Y, Kimura I, Momoi T
Division of Development and Differentiation, National Institute of Neuroscience, NCNP, Tokyo, Japan.
Biochem Biophys Res Commun. 1997 Mar 6;232(1):192-7. doi: 10.1006/bbrc.1997.6234.
P19 EC cells undergoes apoptosis during neuronal differentiation induced by retinoic acid. Two CPP32-like proteases, CPP32 and Mch-3, are expressed in untreated and retinoic acid-treated P19 EC cells. CPP32-like activity is remarkably increased in apoptosis during neuronal differentiation of P19 EC cells. Inhibition of CPP32-like proteases prevents apoptosis, suggesting that activation of CPP32-like proteases play central roles in the apoptosis during neuronal differentiation of P19 EC cells. Wortmannin, PI-3K inhibitor, enhances the CPP32-like activity of the retinoic acid-treated P19 EC cells. PI-3K may be involved in the apoptosis during neuronal differentiation as negative regulator.
P19胚胎癌细胞在视黄酸诱导的神经元分化过程中发生凋亡。两种类CPP32蛋白酶，即CPP32和Mch-3，在未处理的和视黄酸处理的P19胚胎癌细胞中均有表达。在P19胚胎癌细胞神经元分化过程中的凋亡过程中，类CPP32活性显著增加。抑制类CPP32蛋白酶可阻止凋亡，这表明类CPP32蛋白酶的激活在P19胚胎癌细胞神经元分化过程中的凋亡中起核心作用。渥曼青霉素，一种PI-3K抑制剂，可增强视黄酸处理的P19胚胎癌细胞的类CPP32活性。PI-3K可能作为负调节因子参与神经元分化过程中的凋亡。
