报告题目：Dissection of the MDM2-p53 tumor suppression pathway

主 讲 人：University of North Carolina at Chapel Hill张延平教授

时 间：2016年10月12日13:30

地 点：医学院C108会议室

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医学院

2016年10月9日

主讲嘉宾简介：

The broad goal of my research is to uncover the complex regulatory network surrounding the MDM2/MDMX-p53 tumor suppression pathway, thereby providing a possible means to manipulate p53 function. I have the expertise and leadership skills necessary to successfully carry out the proposed work. Over the past 20 years, I have been involved in various important discoveries of function, mechanism, and regulation of the tumor suppressor p53. I was involved in the discoveries of the ARF-MDM2-p53 signaling pathway, the p53 nucleo-cytoplasmic shuttling, and the first evidences for the ribosomal protein regulation of the MDM2-p53 signaling. I pioneered a paradigm for the in vivo function of MDM2 by developing and characterizing several MDM2 mutant knock-in mouse models and demonstrated the unique function and control mechanism of MDM2 E3 ubiquitin ligase, MDM2 central zinc finger domain, and MDM2-MDMX interaction. I have demonstrated capability in three areas. (1) Identifying and persistently investigating the important questions, (2) Combining multi-disciplinary approaches in our research, and (3) The enthusiasm and collegiality in collaborations with colleagues at the University of North Carolina at Chapel Hill and crossing the world, and in motivating and nurturing young graduate students and postdoctoral fellows. The proposed studies are based on our own observations in mice and cell cultures that suggested a previously unexpected role of MDM2 E3 ligase and its homolog MDMX in regulating p53. My expertise and experience in related areas have fully prepared me to lead and carry out the proposed research. This proposal address important yet understudied issues in tumor metabolism and p53 biology, and I am extremely motivated to perform these studies.