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首页> 外文会议>Meeting on Cell Signaling World: Signal Transduction Pathways as Therapeutic Targets >Generation of △ TAp73 Proteins by Translation from a Putative Internal Ribosome Entry Site
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Generation of △ TAp73 Proteins by Translation from a Putative Internal Ribosome Entry Site

机译：从假定的内部核糖体进入位点翻译产生△TAp73蛋白。

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摘要

p73 belongs to a family of transcription factors, including p53 and p63, that mediate response to DNA damage and cellular stress by inducing DNA repair, cell cycle arrest, and apoptosis. TP73 gene con tains two promotors and several splice variants resulting in up to 24 possible permutations of p73 proteins which underlies the complexity of the family and its regulatory mechanisms. P73 variants lacking the N terminal, denoted as △TAp73, are not transcriptionally competent and they act in a dominant negative fashion over TAp73. △TAp73 isoforms can be generated by alternative promotor usage, giving rise to △Np73, or alternative splicing of exons 2,3 or 2, and 3 together. Such transcript iso forms potentially produce oncogenic proteins and they were shown to be present in primary tumors and tumor-derived cell lines. We investigated the possibility of additional mechanisms by which p73 protein could be regulated and discovered a putative internal ribosome entry site (IRES) in exon 2. Translation initiation of TAp73 mRNA results in a △Np73-like peptide, thus demonstrating an additional mechanism whereby a △TA p73 protein is produced from a transcript originally generated from the P1 promotor of the p73 gene.
机译：p73属于转录因子家族，包括p53和p63，可通过诱导DNA修复，细胞周期停滞和凋亡来介导对DNA损伤和细胞应激的反应。 TP73基因包含两个启动子和几个剪接变体，导致p73蛋白的多达24种可能的排列，这是该家族及其调控机制的复杂性的基础。缺少N末端的P73变体（表示为ΔTAp73）不具有转录能力，它们以显着的负性方式作用于TAp73。 △TAp73亚型可以通过替代启动子的使用而产生，从而产生△Np73，或者将外显子2,3或2和3拼接在一起。这样的转录本同工型可能产生致癌蛋白，并且显示它们存在于原发性肿瘤和肿瘤衍生的细胞系中。我们研究了通过其他机制调控p73蛋白的可能性，并在外显子2中发现了一个推测的内部核糖体进入位点（IRES）。TAp73mRNA的翻译起始产生了△Np73样肽，因此证明了一种另外的机制△TA p73蛋白是由最初从p73基因的P1启动子产生的转录物中产生的。

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