p53 and little brother p53/47: linking IRES activities with protein functions
p53 and little brother p53/47: linking IRES activities with protein functions
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DOI：
10.1038/onc.2009.138
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发表时间：
2009-07-01
期刊：
影响因子：
8
通讯作者：
Das, S.
中科院分区：
文献类型：
--
作者：
Grover, R.;Candeias, M. M.;Das, S.
肿瘤抑制基因p53代表了基因调控的范例。其响应于DNA损伤条件的快速诱导归因于p53蛋白的半衰期增加和p53 mRNA的翻译增加。最近的进展，我们的理解转录后调控的p53包括内部核糖体进入位点（IRES）内的p53 mRNA的发现。这些IRES元件调节全长以及N末端截短的同种型p53/47的翻译。p53/47同种型通过在p53 ORF内存在的内部AUG密码子处的交替起始产生。本文就翻译调控机制在p53功能调控中的作用作一综述。我们在这里详细讨论了不同的细胞应激途径如何触发p53 mRNA的帽依赖性和帽非依赖性翻译的改变，以及p53亚型的相对表达水平的变化如何导致更分化的p53活性。Oncogene（2009）28，2766-2772; doi：10.1038/onc.2009.138; 2009年6月1日在线发表
The tumor suppressor p53 represents a paradigm for gene regulation. Its rapid induction in response to DNA damage conditions has been attributed to both increased half-life of p53 protein and also increased translation of p53 mRNA. Recent advances in our understanding of the post-transcriptional regulation of p53 include the discovery of internal ribosome entry sites (IRESs) within the p53 mRNA. These IRES elements regulate the translation of the full length as well as the N-terminally truncated isoform, p53/47. The p53/47 isoform is generated by alternative initiation at an internal AUG codon present within the p53 ORF. The aim of this review is to summarize the role of translational control mechanisms in regulating p53 functions. We discuss here in detail how diverse cellular stress pathways trigger alterations in the cap-dependent and cap-independent translation of p53 mRNA and how changes in the relative expression levels of p53 isoforms result in more differentiated p53 activity. Oncogene (2009) 28, 2766-2772; doi:10.1038/onc.2009.138; published online 1 June 2009