p53肿瘤抑制基因:G1生长阻滞和细胞凋亡的中介。

Experientia Pub Date : 1996-10-31 DOI:10.1007/BF01920109
E Yonish-Rouach
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引用次数: 21

摘要

肿瘤抑制基因p53在保护细胞免受DNA损伤方面起着重要作用。该蛋白在辐射或基因毒性物质的作用下被激活,也可能通过其他信号被激活,导致细胞周期G1期的生长停滞或细胞凋亡。虽然已经证明p53作为序列特异性转录激活因子的功能对于诱导生长停滞是必要的,但p53介导的细胞凋亡机制尚不清楚。似乎在某些条件下,G1检查点的激活会阻止细胞凋亡,但细胞环境可能会改变p53激活的结果,导致细胞死亡。P53也可能通过多种途径直接诱导细胞凋亡,这些途径可能是转录依赖的,也可能是独立的。G1阻滞或细胞凋亡的结果取决于一个复杂的调控信号网络。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The p53 tumour suppressor gene: a mediator of a G1 growth arrest and of apoptosis.

The tumour suppressor gene p53 plays a major role in the protection of cells from DNA damage. Activation of the protein in response to irradiation or genotoxic agents, and possibly by other signals, results in growth arrest at the G1 phase of the cell cycle or in apoptosis. While it has been shown that the ability of p53 to function as a sequence-specific transcriptional activator is necessary for the induction of growth arrest, the mechanism of p53-mediated apoptosis is not yet clear. It appears that under some conditions activation of the G1 checkpoint will prevent apoptosis, but the cellular environment may alter the result of p53 activation towards cell death. p53 may also directly induce apoptosis through several pathways, which may be transcriptionally dependent or independent. The outcome-a G1 arrest or apoptosis-will depend on a complex network of regulatory signals.

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