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首页> 外文期刊>Genomics >Cloning of the rat beta-catenin gene (Ctnnb1) promoter and its functional analysis compared with the Catnb and CTNNB1 promoters.
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Cloning of the rat beta-catenin gene (Ctnnb1) promoter and its functional analysis compared with the Catnb and CTNNB1 promoters.

机译：与Catnb和CTNNB1启动子相比，大鼠β-catenin基因（Ctnnb1）启动子的克隆及其功能分析。

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Considerable recent interest has focused on the stabilization and accumulation of beta-catenin protein in human and animal tumors and the corresponding activation of downstream beta-catenin/TCF/LEF target genes. However, there is only sparse information on the regulation of beta-catenin expression at the transcriptional level and its possible involvement in physiological and pathophysiological processes. We report here the cloning and characterization of a 3.6-kb promoter fragment from the rat beta-catenin gene, Ctnnb1, and its comparison with corresponding promoters from the mouse and human genes, Catnb and CTNNB1. Several AP1 binding sites were confirmed in the promoters of all three species using mobility shift and reporter assays, and one putative TCF/LEF site also was observed in the promoter of CTNNB1. Subsequently, protein/DNA array analyses identified numerous other transcription factors through their high-affinity binding to the Ctnnb1 promoter, including E2F1, NFkappaB, MEF1, Pax5, ISRE2, Smad3/4, GATA, and ZIC. The strong binding of E2F1 and NFkappaB is especially noteworthy, because the former transcription factor is regulated by cyclin D1, a downstream target of beta-catenin/TCF/LEF signaling, whereas the latter transcription factor has been implicated in cross talk results are discussed in terms of their implications for human cancer development and specifically the various tumors in which beta-catenin mRNA is overexpressed, as well as for embryonic development, when reversible changes in beta-catenin expression occur in response to secreted Wnt ligands. The findings reported here should provide important avenues for further research focused on the regulation of Ctnnb1 activity, including the ability of beta-catenin/Tcf downstream targets to modulate beta-catenin expression at the transcriptional level.
机译：最近的关注集中在人和动物肿瘤中β-catenin蛋白的稳定和积累以及下游β-catenin/ TCF / LEF靶基因的相应激活上。但是，在转录水平上有关β-catenin表达的调控及其可能参与生理和病理生理过程的信息很少。我们在这里报告从大鼠β-catenin基因Ctnnb1的3.6 kb启动子片段的克隆和表征，并将其与来自小鼠和人类基因Cantb和CTNNB1的相应启动子进行比较。使用迁移率变化和报道分子分析在所有三个物种的启动子中确认了几个AP1结合位点，并且在CTNNB1的启动子中还观察到一个推定的TCF / LEF位点。随后，蛋白质/ DNA阵列分析通过与Ctnnb1启动子的高亲和力结合，鉴定了许多其他转录因子，包括E2F1，NFkappaB，MEF1，Pax5，ISRE2，Smad3 / 4，GATA和ZIC。 E2F1和NFkappaB的强结合尤其值得注意，因为前者的转录因子受细胞周期蛋白D1的调控，而后者是β-catenin/ TCF / LEF信号传导的下游靶标，而后者的转录因子已涉及相声结果。当它们对分泌的Wnt配体产生可逆变化时，β-catenin表达发生可逆变化时，它们对人类癌症发展的影响，尤其是β-cateninmRNA过表达的各种肿瘤，以及对胚胎发育的影响。此处报道的发现应为进一步研究集中于Ctnnb1活性的研究提供重要途径，包括调节β-catenin/ Tcf下游靶标在转录水平上调节β-catenin表达的能力。

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