GAIN OF FUNCTION MUTATIONS IN P53
GAIN OF FUNCTION MUTATIONS IN P53
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DOI：
10.1038/ng0593-42
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发表时间：
1993-05-01
期刊：
影响因子：
30.8
通讯作者：
LEVINE, AJ
中科院分区：
文献类型：
--
作者：
DITTMER, D;PATI, S;LEVINE, AJ
我们报告说，鼠或人突变型p53蛋白在细胞中的表达没有内源性p53蛋白赋予这些细胞新的或额外的表型。在缺乏p53的细胞系中表达的突变型p53蛋白导致在裸鼠中增强的致瘤潜力（（10）3细胞）或在琼脂细胞培养物中增强的平板接种效率（人SAOS-2细胞）。此外，突变的人p53等位基因，不像野生型p53蛋白，也可以增强测试基因的表达调节的多药耐药性增强子-启动子元件。这些数据表明，除了先前显示的与该肿瘤抑制基因中的突变相关的功能丧失之外，还与p53突变相关的功能获得。
We report that the expression of murine or human mutant p53 proteins in cells with no endogenous p53 proteins confers new or additional phenotypes upon these cells. Mutant p53 proteins expressed in cell lines lacking p53 resulted in either enhanced tumorigenic potential in nude mice ((10)3 cells) or enhanced plating efficiency in agar cell culture (human SAOS-2 cells). Also, mutant human p53 alleles, unlike the wild-type p53 protein, could also enhance the expression of a test gene regulated by the multi-drug resistance enhancer-promoter element. These data demonstrate a gain of function associated with p53 mutations in addition to the loss of function shown previously to be associated with mutations in this tumour suppressor gene.