Regulation of p53 downstream genes
Regulation of p53 downstream genes
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DOI：
10.1006/scbi.1998.0097
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发表时间：
1998-10-01
影响因子：
14.5
通讯作者：
El-Deiry, WS
中科院分区：
文献类型：
--
作者：
El-Deiry, WS
p53抑癌基因是人类肿瘤中最常见的突变基因，p53蛋白在DNA损伤、缺氧、病毒感染或癌基因激活等不同的检查点激活时稳定，导致不同的生物学效应，如细胞周期阻滞、凋亡、衰老、分化和抗血管生成。稳定的p53蛋白通过磷酸化、去磷酸化和乙酰化被激活，产生有效的序列特异性DNA结合转录因子。p53广泛的生物学效应可以部分地通过其激活许多靶基因的表达来解释，所述靶基因包括p21（WAFI）、GADD 45、14-3-3 σ、bax、Fas/APO 1、KILLER/DR 5、PIG 3、Tsp 1、IGF-BP 3等。这篇综述将集中在p53的转录靶点，它们的调控：p53，以及它们在p53生物学效应中的相对重要性。
The p53 tumor suppressor is the most commonly mutated gene in human cancer, p53 protein is stabilized in response to different checkpoints activated by DNA damage, hypoxia, viral infection, or oncogene activation resulting in diverse biological effects, such as cell cycle arrest, apoptosis, senescence, differentiation and antiangiogenesis. The stable p53 protein is activated by phosphorylation, dephosphorylation and acetylation yielding a potent sequence-specific DNA-binding transcription factor. The wide range of p53's biological effects can in part be explained by its activation of expression of a number of target genes including p21(WAFI), GADD45, 14-3-3 sigma, bax, Fas/APO1, KILLER/DR5, PIG3, Tsp1, IGF-BP3 and others. This review will focus on the transcriptional targets of p53, their regulation: by p53, and their relative importance in carrying out the biological effects of p53.