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首页> 外文期刊>Molecular and Cellular Biology >Neither macromolecular synthesis nor myc is required for cell death via the mechanism that can be controlled by Bcl-2.
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Neither macromolecular synthesis nor myc is required for cell death via the mechanism that can be controlled by Bcl-2.

机译：通过Bcl-2可以控制的机制，细胞死亡不需要大分子合成或myc。

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Expression of c-myc and macromolecular synthesis have been associated with physiological cell death. We have studied their requirement for the death of factor (interleukin-3)-dependent cells (FDC-P1) bearing an inducible bcl-2 expression construct. FDC-P1 cells expressing bcl-2 turned off expression of c-myc when deprived of interleukin-3 but remained viable as long as bcl-2 was maintained. A subsequent decline in Bcl-2 allowed the cells to undergo apoptosis directly from G0, in the absence of detectable c-myc expression. Thus c-myc expression may lead to apoptosis in some cases but is not directly involved in the mechanism of physiological cell death that can be controlled by Bcl-2. The macromolecular synthesis inhibitors actinomycin D and cycloheximide triggered rapid cell death of FDC-P1 cells in the presence of interleukin-3, but the cells could be protected by Bcl-2. Thus, the cell death machinery can exist in a quiescent state and can be activated by mechanisms that do not require synthesis of RNA or protein.
机译：c-myc的表达和大分子合成与生理细胞死亡有关。我们已经研究了它们对携带诱导型bcl-2表达构建体的因子（白介素3）依赖性细胞（FDC-P1）死亡的要求。当缺乏白细胞介素3时，表达bcl-2的FDC-P1细胞会关闭c-myc的表达，但只要维持bcl-2就会保持活力。随后的Bcl-2下降使细胞直接从G0凋亡，而没有可检测的c-myc表达。因此，在某些情况下，c-myc表达可能导致细胞凋亡，但并不直接参与Bcl-2可以控制的生理细胞死亡机制。大分子合成抑制剂放线菌素D和环己酰亚胺在存在白细胞介素3的情况下触发FDC-P1细胞快速细胞死亡，但该细胞可被Bcl-2保护。因此，细胞死亡机制可以处于静止状态，并且可以通过不需要合成RNA或蛋白质的机制激活。

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