交易激励
生物
突变体
癌变
端粒酶逆转录酶
分子生物学
基因
突变
端粒酶
癌症研究
基因表达
遗传学
作者
Mariano J. Scian,Katherine E. Stagliano,Debabrita Deb,Michelle A. E. Anderson,Evie H. Carchman,Anindita Das,Kristoffer Valerie,Swati Palit Deb,Sumitra Deb
出处
期刊:Oncogene
[Springer Nature]
日期:2004-04-12
卷期号:23 (25): 4430-4443
被引量:108
标识
DOI:10.1038/sj.onc.1207553
摘要
We have studied the mechanism of mutant p53-mediated oncogenesis using several tumor-derived mutants. Using a colony formation assay, we found that the majority of the mutants increased the number of colonies formed compared to the vector. Expression of tumor-derived p53 mutants increases the rate of cell growth, suggesting that the p53 mutants have 'gain of function' properties. We have studied the gene expression profile of cells expressing tumor-derived p53-D281G to identify genes transactivated by mutant p53. We report the transactivation of two genes, asparagine synthetase and human telomerase reverse transcriptase. Quantitative real-time PCR confirms this upregulation. Transient transfection promoter assays verify that tumor-derived p53 mutants transactivate these promoters significantly. An electrophoretic mobility shift assay shows that tumor-derived p53-mutants cannot bind to the wild-type p53 consensus sequence. The results presented here provide some evidence of a possible mechanism for mutant p53-mediated transactivation.
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