Mukasa T, Urase K, Momoi M Y, Kimura I, Momoi T
Division of Development and Differentiation, National Institute of Neuroscience, NCNP, Tokyo, Japan.
Biochem Biophys Res Commun. 1997 Feb 24;231(3):770-4. doi: 10.1006/bbrc.1996.6002.
We isolated mouse CPP32/apopain cDNA, a mammalian homologue most closely related to Ced-3 in C. elegans, and examined the involvement of CPP32 in the apoptosis of nervous system during development. CPP32 is specifically expressed in the trigeminal (V) ganglia, facio-acoustic (VII-VIII) ganglion complex, and dorsal root ganglia (DRGs) of mouse 10.5-day embryos. CPP32-like proteases are activated during apoptosis of DRG neurons induced by deprivation of NGF and serum. Ac-DEVD-CHO, an inhibitor for CPP32-like proteases, prevents apoptosis of DRG neurons, but Ac-YVAD-CHO, an inhibitor for ICE-like proteases, does not. These results suggest that CPP32 or CPP32-like proteases play a role as central mediator in the apoptosis of DRG neurons induced by lack of neurotrophin signals.
我们分离出了小鼠CPP32/凋亡蛋白酶cDNA，它是一种与秀丽隐杆线虫中的Ced-3最密切相关的哺乳动物同源物，并研究了CPP32在发育过程中神经系统凋亡中的作用。CPP32在10.5天龄小鼠胚胎的三叉神经（V）节、面听神经（VII - VIII）节复合体和背根神经节（DRG）中特异性表达。在由神经生长因子（NGF）和血清剥夺诱导的DRG神经元凋亡过程中，CPP32样蛋白酶被激活。CPP32样蛋白酶的抑制剂Ac-DEVD-CHO可防止DRG神经元凋亡，但ICE样蛋白酶的抑制剂Ac-YVAD-CHO则不能。这些结果表明，CPP32或CPP32样蛋白酶在由神经营养因子信号缺失诱导的DRG神经元凋亡中作为中心介质发挥作用。
