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首页> 外文期刊>Cell Research >p53-independent upregulation of p21WAF1 in NIH 3T3 cells malignantly transformed by mot-2
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p53-independent upregulation of p21WAF1 in NIH 3T3 cells malignantly transformed by mot-2

机译：mot-2恶性转化的NIH 3T3细胞中p21WAF1不依赖p53的上调

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摘要

Mot-2 protein is shown to interact with p53 and inhibit its transcriptional activation function. Most-2 overexpressing stable clones of NIH 3T3 cells were malignantly transformed, however, they had a high level of expression of a p53 downstream gene, p~21WAF1. The present study was undertaken to elucidate possible molecular mechanism (s) of such upregulation. An increased level of p21~WAF1 expression was detected in sta- ble transfectants although an exogenous reporter gene driven by p21~WAF1 promoter exhibited lower activity in these cells suggesting that some post-transcriptional mechanism contributes to upregulation. Western analyses of transient and stable cones revealed that upregulation of p21~WAF` in stable NIH 3T3/mot-2 cells may be mediated by cyclin D1 and cdk-2.
机译：Mot-2蛋白显示与p53相互作用并抑制其转录激活功能。 NIH 3T3细胞的大多数2个过表达的稳定克隆均被恶性转化，但是它们具有p53下游基因p〜21WAF1的高水平表达。进行本研究以阐明这种上调的可能分子机制。在稳定转染子中检测到p21〜WAF1表达水平升高，尽管由p21〜WAF1启动子驱动的外源报告基因在这些细胞中表现出较低的活性，这表明某些转录后机制有助于上调。瞬时和稳定视锥细胞的西方分析表明，稳定的NIH 3T3 / mot-2细胞中p21〜WAF'的上调可能是由细胞周期蛋白D1和cdk-2介导的。

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