INDUCTION OF APOPTOSIS IN FIBROBLASTS BY IL-1-BETA-CONVERTING ENZYME, A MAMMALIAN HOMOLOG OF THE C-ELEGANS CELL-DEATH GENE CED-3
INDUCTION OF APOPTOSIS IN FIBROBLASTS BY IL-1-BETA-CONVERTING ENZYME, A MAMMALIAN HOMOLOG OF THE C-ELEGANS CELL-DEATH GENE CED-3
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DOI：
10.1016/0092-8674(93)90486-a
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发表时间：
1993-11-19
期刊：
影响因子：
64.5
通讯作者：
YUAN, JY
中科院分区：
文献类型：
--
作者：
MIURA, M;ZHU, H;YUAN, JY
哺乳动物白细胞介素-1 β转化酶（ICE）与C.线虫细胞死亡基因ced-3。我们在这里表明，小鼠ICE（mICE）基因或C。线虫ced-3基因导致Rat-1细胞经历程序性细胞死亡。在mICE和CED-3之间同源的区域中的点突变消除了mICE和ced-3引起细胞死亡的能力。由mICE引起的细胞死亡可以通过crmA基因（ICE的特异性抑制剂）以及bcl-2（可以防止程序性细胞死亡的哺乳动物致癌基因）的过表达来抑制。我们的研究结果表明，ICE可能在哺乳动物发育过程中起作用，导致程序性细胞死亡。
The mammalian interleukin-1beta-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.