New insight into the role of MDMX in MDM2-mediated p53 degradation and anti-cancer drug development.

Oncoscience Pub Date : 2021-08-09 eCollection Date: 2021-01-01 DOI:10.18632/oncoscience.542
Jing Yang, Yanping Zhang
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Abstract

Inactivation of the tumor suppressor p53 has been generally accepted as a hallmark of tumor. MDM2 and MDMX, the two closely related proteins are considered to be critical for negatively regulating p53 activity through inhibitory binding to and post-translational modification of the p53 protein. We have demonstrated that MDMX facilitates MDM2-mediated p53 ubiquitination and degradation via recruitment of the ubiquitin-conjugating enzyme UbcH5c to the MDM2-MDMX heterooligomers. Here, we discuss our new findings from genetically engineered mouse models and a potential therapeutic strategy.

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MDMX在mdm2介导的p53降解和抗癌药物开发中的作用的新见解。
肿瘤抑制因子p53的失活已被普遍认为是肿瘤的标志。MDM2和MDMX这两个密切相关的蛋白被认为是通过抑制p53蛋白的结合和翻译后修饰来负性调节p53活性的关键蛋白。我们已经证明,通过在MDM2-MDMX异聚物上募集泛素结合酶UbcH5c, MDMX促进了mdm2介导的p53泛素化和降解。在这里,我们讨论了基因工程小鼠模型的新发现和潜在的治疗策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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