Miura M, Zhu H, Rotello R, Hartwieg E A, Yuan J
Cardiovascular Research Center, Massachusetts General Hospital, Charlestown 02129.
Cell. 1993 Nov 19;75(4):653-60. doi: 10.1016/0092-8674(93)90486-a.
The mammalian interleukin-1 beta-converting enzyme (ICE) has sequence similarity to the C. elegans cell death gene ced-3. We show here that overexpression of the murine ICE (mICE) gene or of the C. elegans ced-3 gene causes Rat-1 cells to undergo programmed cell death. Point mutations in a region homologous between mICE and CED-3 eliminate the ability of mICE and ced-3 to cause cell death. The cell death caused by mICE can be suppressed by overexpression of the crmA gene, a specific inhibitor of ICE, as well as by bcl-2, a mammalian oncogene that can act to prevent programmed cell death. Our results suggest that ICE may function during mammalian development to cause programmed cell death.
哺乳动物白细胞介素-1β转化酶（ICE）与秀丽隐杆线虫细胞死亡基因ced-3具有序列相似性。我们在此表明，小鼠ICE（mICE）基因或秀丽隐杆线虫ced-3基因的过表达会导致大鼠-1细胞发生程序性细胞死亡。mICE和CED-3之间同源区域的点突变消除了mICE和ced-3导致细胞死亡的能力。mICE引起的细胞死亡可被ICE的特异性抑制剂crmA基因的过表达以及bcl-2（一种可防止程序性细胞死亡的哺乳动物癌基因）抑制。我们的结果表明，ICE可能在哺乳动物发育过程中发挥作用导致程序性细胞死亡。
