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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Regulation of transactivation-independent proapoptotic activity of p53 by FOXO3a
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Regulation of transactivation-independent proapoptotic activity of p53 by FOXO3a

机译：FOXO3a调节p53的非激活依赖的促凋亡活性

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摘要

The tumor suppressor p53 can trigger cell death independently of its transcriptional activity through subcellular translocation and activation of proapoptotic Bcl-2 family members. The regulation of such activity of endogenous p53 in response to stress remains largely unknown. Here we show that nuclear, activated FOX03a could impair p53 transcriptional activity. However, activation of FOX03a either on serum starvation or by expressing a constitutively active form of FOX03a could induce p53-dependent apoptosis, even in cells bearing a transcriptionally inactive form of p53. Furthermore, FOX03a could promote p53 cytoplasmic accumulation by increasing its association with nuclear exporting machinery. Our data also suggest that PUMA and Bax are required for p53-dependent apoptosis in manner that is independent of p53 transcriptional activity.
机译：肿瘤抑制因子p53可以通过亚细胞转运和促凋亡Bcl-2家族成员的激活，独立于其转录活性触发细胞死亡。内源性p53响应压力的这种活性的调节仍然未知。在这里，我们显示核激活的FOX03a可能损害p53转录活性。然而，即使在血清中缺乏转录活性形式的细胞中，通过血清饥饿或表达FOX03a的组成性活性形式来激活FOX03a也会诱导p53依赖性细胞凋亡。此外，FOX03a可以通过增加其与核输出设备的联系来促进p53细胞质的积累。我们的数据还表明，PUMA和Bax以独立于p53转录活性的方式用于p53依赖性凋亡。

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