E2F1-induced apoptosis:: turning killers into therapeutics

被引:99
|
作者
Stanelle, Jens [1 ]
Puetzer, Brigitte M. [1 ]
机构
[1] Univ Rostock, Dept Vectorol & Expt Gene Therapy, D-18057 Rostock, Germany
关键词
D O I
10.1016/j.molmed.2006.02.002
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The cellular transcription factor E2F1 is part of an antitumor safeguard mechanism: it engages cell-death pathways either alone or in cooperation with p53 to protect organisms from the development of tumors. E2F1 activates downstream factors, which in turn produce secondary changes in gene expression that trigger apoptosis. Although the mechanisms are incompletely understood, several studies have demonstrated that E2F1 is involved in many different aspects of programmed cell death depending on the cellular background. Here, these findings are highlighted in the context of the most recent follow-up studies that have used apoptotic E2F1 genes as new therapeutics or drug targets, thereby providing insight into the basic mechanisms of E2F1-induced apoptosis and its possible clinical implications.
引用
收藏
页码:177 / 185
页数:9
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