INDUCTION OF APOPTOSIS IN FIBROBLASTS BY C-MYC PROTEIN
INDUCTION OF APOPTOSIS IN FIBROBLASTS BY C-MYC PROTEIN
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DOI：
10.1016/0092-8674(92)90123-t
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发表时间：
1992-04-03
期刊：
影响因子：
64.5
通讯作者：
HANCOCK, DC
中科院分区：
文献类型：
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作者：
EVAN, GI;WYLLIE, AH;HANCOCK, DC
虽然大鼠-1成纤维细胞表达c-myc组成不能逮捕生长在低血清，他们的数量不会增加，因为大量的细胞死亡的文化。我们表明这种细胞死亡依赖于c-myc蛋白的表达，并通过凋亡发生。诱导细胞凋亡所需的c-myc蛋白的区域与共转化、自动调节和抑制分化所需的区域重叠，表明c-myc蛋白的凋亡功能与其其他功能有关。此外，具有较高水平的c-myc蛋白的细胞在血清剥夺时更倾向于细胞死亡。最后，我们表明，失调的c-myc表达诱导细胞凋亡的生长停滞的各种手段，并在细胞周期的各个点。
Although Rat-1 fibroblasts expressing c-myc constitutively are unable to arrest growth in low serum, their numbers do not increase in culture because of substantial cell death. We show this cell death to be dependent upon expression of c-myc protein and to occur by apoptosis. Regions of the c-myc protein required for induction of apoptosis overlap with regions necessary for cotransformation, autoregulation, and inhibition of differentiation, suggesting that the apoptotic function of c-myc protein is related to its other functions. Moreover, cells with higher levels of c-myc protein are more prone to cell death upon serum deprivation. Finally, we demonstrate that deregulated c-myc expression induces apoptosis in cells growth arrested by a variety of means and at various points in the cell cycle.