Srinivasan A, Roth K A, Sayers R O, Shindler K S, Wong A M, Fritz L C, Tomaselli K J
IDUN Pharmaceuticals, Inc., La Jolla, California 92037, USA.
Cell Death Differ. 1998 Dec;5(12):1004-16. doi: 10.1038/sj.cdd.4400449.
Activation of caspase-3 requires proteolytic processing of the inactive zymogen into p18 and p12 subunits. We generated a rabbit polyclonal antiserum, CM1, which recognizes the p18 subunit of cleaved caspase-3 but not the zymogen. CM1 demonstrated an apparent specificity for activated caspase-3 by specifically immunolabelling only apoptotic but not necrotic cortical neurons in vitro. In the embryonic mouse nervous system, CM1 immunoreactivity was detected in neurons undergoing programmed cell death and was markedly increased in Bcl-xL-deficient embryos and decreased in Bax-deficient embryos. CM1 immunoreactivity was absent in the nervous system of caspase-3-deficient mouse embryos and in neurons cultured from caspase-3-deficient mice. Along with neuronal somata, extensive neuritic staining was seen in apoptotic neurons. These studies indicate that caspase-3 is activated during apoptosis in the developing nervous system in vivo and that CM1 is a useful reagent for its in situ detection.
半胱天冬酶-3的激活需要将无活性的酶原进行蛋白水解加工成p18和p12亚基。我们制备了一种兔多克隆抗血清CM1,它能识别裂解的半胱天冬酶-3的p18亚基,但不能识别酶原。CM1通过在体外仅特异性免疫标记凋亡而非坏死的皮质神经元,显示出对活化的半胱天冬酶-3具有明显的特异性。在胚胎小鼠神经系统中,在经历程序性细胞死亡的神经元中检测到CM1免疫反应性,并且在Bcl-xL缺陷胚胎中明显增加,而在Bax缺陷胚胎中减少。在半胱天冬酶-3缺陷小鼠胚胎的神经系统以及从半胱天冬酶-3缺陷小鼠培养的神经元中未检测到CM1免疫反应性。除了神经元胞体,在凋亡神经元中还可见广泛的神经突染色。这些研究表明,在体内发育中的神经系统的凋亡过程中半胱天冬酶-3被激活,并且CM1是用于其原位检测的有用试剂。