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首页> 外文期刊>Molecular and Cellular Biology >Polypyrimidine Tract-Binding Protein Enhances the Internal Ribosomal Entry Site-Dependent Translation of p27Kip1 mRNA and Modulates Transition from G1 to S Phase
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Polypyrimidine Tract-Binding Protein Enhances the Internal Ribosomal Entry Site-Dependent Translation of p27Kip1 mRNA and Modulates Transition from G1 to S Phase

机译：聚嘧啶区结合蛋白增强p27Kip1 mRNA的内部核糖体进入位点依赖翻译并调节从G1到S期的过渡

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The p27Kip1 protein plays a critical role in the regulation of cell proliferation through the inhibition of cyclin-dependent kinase activity. Translation of p27Kip1 is directed by an internal ribosomal entry site (IRES) in the 5′ nontranslated region of p27Kip1 mRNA. Here, we report that polypyrimidine tract-binding protein (PTB) specifically enhances the IRES activity of p27Kip1 mRNA through an interaction with the IRES element. We found that addition of PTB to an in vitro translation system and overexpression of PTB in 293T cells augmented the IRES activity of p27Kip1 mRNA but that knockdown of PTB by introduction of PTB-specific small interfering RNAs (siRNAs) diminished the IRES activity of p27Kip1 mRNA. Moreover, the G1 phase in the cell cycle (which is maintained in part by p27Kip1) was shortened in cells depleted of PTB by siRNA knockdown. 12-O-Tetradecanoylphorbol-13-acetate (TPA)-induced differentiation in HL60 cells was used to examine PTB-induced modulation of p27Kip1 protein synthesis during differentiation. The IRES activity of p27Kip1 mRNA in HL60 cells was increased by TPA treatment (with a concomitant increase in PTB protein levels), but the levels of p27Kip1 mRNA remained unchanged. Together, these data suggest that PTB modulates cell cycle and differentiation, at least in part, by enhancing the IRES activity of p27Kip1 mRNA.
机译：p27 Kip1 蛋白通过抑制细胞周期蛋白依赖性激酶活性，在调节细胞增殖中起关键作用。 p27 Kip1 的翻译由p27 Kip1 mRNA 5'非翻译区的内部核糖体进入位点（IRES）指导。在这里，我们报道聚嘧啶束结合蛋白（PTB）通过与IRES元件的相互作用特异性增强p27 Kip1 mRNA的IRES活性。我们发现，在体外翻译系统中添加PTB和在293T细胞中过度表达PTB可以增强p27 Kip1 mRNA的IRES活性，但是通过引入PTB特异性小干扰RNA（siRNAs）可以抑制PTB ）降低了p27 Kip1 mRNA的IRES活性。而且，在通过siRNA敲低而耗尽PTB的细胞中，细胞周期的G 1 期（部分由p27 Kip1 维持）缩短了。用12- O -十四碳酰佛波醇-13-乙酸酯（TPA）诱导的HL60细胞分化，以研究PTB诱导的分化过程中p27 Kip1 蛋白质合成的调控。 TPA处理可增加HL60细胞中p27 Kip1 mRNA的IRES活性（同时增加PTB蛋白水平），但p27 Kip1 mRNA的水平却保持不变。总之，这些数据表明，PTB至少部分地通过增强p27 Kip1 mRNA的IRES活性来调节细胞周期和分化。

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