Bcl-2 prevents death of factor-deprived cells but fails to prevent apoptosis in targets of cell mediated killing.
Bcl-2 prevents death of factor-deprived cells but fails to prevent apoptosis in targets of cell mediated killing.
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Bcl-2 可防止缺乏因子的细胞死亡，但无法防止细胞介导杀伤靶标的细胞凋亡。
DOI：
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发表时间：
1992
影响因子：
4.4
通讯作者：
Irving L. Weissman
中科院分区：
文献类型：
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作者：
David L. Vaux;Hector L. Aguila;Irving L. Weissman
“程序性细胞死亡”用于描述被细胞毒性 T 细胞或生长因子剥夺杀死的细胞的死亡。尽管bcl-2可以防止缺乏生长因子的细胞死亡，但它无法保护细胞免遭T细胞杀伤。尽管有 bcl-2 表达，靶细胞的 DNA 仍被降解为核小体大小的片段。因此，因子剥夺诱导的细胞凋亡的早期步骤与细胞毒性 T 细胞触发的细胞凋亡的早期步骤不同，尽管它们具有共同的最终途径，即 DNA 降解和细胞质膜完整性丧失。
'Programmed cell death' has been used to describe the death of cells killed by cytotoxic T cells or growth factor deprivation. Although bcl-2 can prevent death of cells deprived of growth factor, it failed to protect cells against T cell killing. In spite of bcl-2 expression, the DNA of targeted cells was degraded into nucleosome-sized fragments. Therefore the early steps in apoptosis induced by factor deprivation differ from those triggered by cytotoxic T cells, although they share a common final pathway featuring degradation of the DNA and loss of cytoplasmic membrane integrity.