Mouse models of Mdm2 and Mdm4 and their clinical implications

查看全文 作　　者：Shunbin [1]Xiong

机构地区：[1]Department of Genetics,The University of Texas M.D.Anderson Cancer Center

出　　处：《Chinese Journal of Cancer》索引2013年第32卷第7期,共5页

摘　　要：Mdm2 and Mdm4 are two key negative regulators of the tumor suppressor p53.Deletion of either Mdm2 or Mdm4 induces p53-dependent early embryonic lethality in knockout mouse models.The tissuespecific deletion of Mdm2 induces p53-dependent apoptosis,whereas the deletion of Mdm4 induces both p53-dependent apoptosis and cell cycle arrest.Compared to Mdm4 deletion,Mdm2 deletion causes more severe phenotypic defects.Disrupting the Mdm2 and Mdm4 interaction using knockin mice models causes embryonic lethality that can be completely rescued by the concomitant loss of p53,suggesting that Mdm2 and Mdm4 heterodimerization is critical to inhibit p53 activity during embryogenesis.Overexpression of Mdm2 and Mdm4 in mice induces spontaneous tumorigenesis,which clearly indicates that Mdm2 and Mdm4 are bona fide oncogenes.Studies from these mouse models strongly suggest that blocking Mdm2and Mdm4-mediated p53 inhibition is an appealing therapeutic strategy for cancer patients with wild-type p53 alleles. 关键词：MDM2 e模型 MDM2 小鼠模型诱导表达 CL 细胞周期阻滞胚胎发育过程

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Mouse models of Mdm2 and Mdm4 and their clinical implications

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