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NIH 3T3 cells malignantly transformed by mot-2 show inactivation and cytoplasmic sequestration of the p53 protein

机译:mot-2恶性转化的NIH 3T3细胞显示出p53蛋白的失活和细胞质隔离

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In previous studies we have reported that a high level of expression of mot-2 protein results in malignant trans- formation of NIH 3T3 cells as analyzed by anchorage inde- pendent grwoth and nude mice assays[Kaul et al., Onco- gene, 17,907-11, 1998]. Mot-2 was found to interact with tumor suppressor protein p53. The transient overexpres- sion of mot-2 inhibitory to transcriptional activation function of p53[Wadhwa et al., J.Biol. Chem., 273, 29586- 91,1998). We demonstrate here that mot-2 transfected stable clone of NIH 3T3 that showed malignant properties indeed show inactivation of p53 function as assayed by exogeneous p53 dependent reporter.
机译:在先前的研究中,我们已经报道了mot-2蛋白的高水平表达会导致NIH 3T3细胞发生恶性转化,这是通过锚定独立的生长激素和裸鼠实验进行了分析[Kaul等,Onco-gene,17,907 -11,1998]。发现Mot-2与肿瘤抑制蛋白p53相互作用。 mot-2对p53转录激活功能的抑制作用瞬时过度表达[Wadhwa等,生物化学杂志。 Chem。,273,29586-91,1998)。我们在这里证明了mot-2转染的显示出恶性特性的NIH 3T3稳定克隆确实显示了p53功能的失活,如通过外源性p53依赖性报道分子所检测的。

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