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首页> 外文期刊>Cell biology international. >ChIP (chromatin immunoprecipitation) analysis demonstrates co-ordinated binding of two transcription factors to the promoter of the p53 tumour-suppressor gene.
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ChIP (chromatin immunoprecipitation) analysis demonstrates co-ordinated binding of two transcription factors to the promoter of the p53 tumour-suppressor gene.

机译：ChIP（染色质免疫沉淀）分析表明两个转录因子与p53肿瘤抑制基因的启动子协同结合。

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摘要

p53 is a tumour-suppressor protein that plays a role in many cellular processes, including regulation of the cell cycle, DNA repair, transcriptional regulation of genes, chromosomal segregation, cell senescence and apoptosis. The protein's role as a transcription factor has shown that deregulated transcription, whether increased or decreased, has the potential to contribute to the formation of human cancers. It was previously reported that binding of two transcription factors, C/EBPbeta and RBP-Jkappa, to a regulatory site on the p53 promoter regulates its activity, in vitro, in a cell cycle-dependent manner. C/EBPbeta is a CCAAT enhancer-binding protein that is a member of the basic leucine zipper transcription factor (bZIP) family that plays an important role in mediating cell proliferation, differentiation and can also be involved in inflammatory responses, metabolism, cellular transformation, oncogene-induced senescence and tumorigenesis. RBP-Jkappa participates in the transcriptional regulation of target genes by interacting with the cytoplasmic domain of the Notch receptors. When RBP-Jkappa is released, transcriptional repression of its target genes occurs through the recruitment of co-repressor complexes and prevents transcription from occurring. Our reports, here and previously published, show that repression of p53 by RBP-Jkappa and activation of p53 by C/EBPbeta through differential binding of these two factors indicates a type of co-operative regulation in p53 expression. Here, we demonstrate through the use of chromatin immunoprecipitation (ChIP) assays that the co-ordinated binding of these two factors to the p53 promoter occurs in vivo and serves to regulate p53's activity during the cell cycle.
机译：p53是一种肿瘤抑制蛋白，在许多细胞过程中都起作用，包括细胞周期调节，DNA修复，基因转录调节，染色体分离，细胞衰老和凋亡。该蛋白质作为转录因子的作用表明，转录失调，无论增加还是减少，都有可能促进人类癌症的形成。以前有报道说，两种转录因子C / EBPbeta和RBP-Jkappa与p53启动子上的调节位点的结合在体外以细胞周期依赖性方式调节其活性。 C / EBPbeta是一种CCAAT增强子结合蛋白，是基本亮氨酸拉链转录因子（bZIP）家族的成员，在介导细胞增殖，分化中也起着重要作用，还可以参与炎症反应，代谢，细胞转化，癌基因诱导的衰老和肿瘤发生。 RBP-Jkappa通过与Notch受体的胞质结构域相互作用，参与靶基因的转录调控。当RBP-Jkappa释放时，其靶基因的转录抑制通过募集共阻遏物复合物而发生，并阻止了转录的发生。我们在这里和先前发表的报告显示，RBP-Jkappa对p53的阻遏作用以及C / EBPbeta通过这两个因素的差异结合对p53的激活表明了p53表达中的一种合作调节。在这里，我们通过染色质免疫沉淀（ChIP）分析的使用证明这两个因子与p53启动子的协同结合在体内发生，并在细胞周期中起到调节p53活性的作用。

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