MDMX公司
平方毫米
交易激励
生物
癌症研究
DNA损伤
抑制器
突变体
功能(生物学)
细胞生物学
P53蛋白
细胞凋亡
转录因子
癌症
生物化学
遗传学
DNA
基因
作者
Daniele Bergamaschi,Yardena Samuels,Shan Zhong,Xin Lü
出处
期刊:Oncogene
[Springer Nature]
日期:2005-03-14
卷期号:24 (23): 3836-3841
被引量:8
标识
DOI:10.1038/sj.onc.1208535
摘要
Using various mutants of p53 and mdm2, we demonstrate here that both the DNA binding and transactivation function of p53 are required for ASPP1 and ASPP2 to stimulate the apoptotic functions of p53. Mdm2 and mdmx prevent ASPP1 and ASPP2 from stimulating the apoptotic function of p53 by binding and inhibiting the transcriptional activity of p53. Importantly, mdm2 and mdmx can prevent the stimulatory effects of ASPP1 and ASPP2 without targeting p53 for degradation. These data provide a novel mechanism by which mdm2 and mdmx act as potent inhibitors of p53.
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