报告人简介：魏文毅博士，目前任美国哈佛医学院副教授，2002年获美国布朗大学博士学位，2002-2005年在Dana-Farber肿瘤研究所William Kaelin教授实验室从事研究助理工作，2005-2006年在哈佛医学院担任医学讲师，2006-2012年在哈佛医学院Beth Israel Deaconess Medical Center任助理教授。已在主流期刊包括Nature，Cell, Cancer Cell, J.Exp.Med, Molecular Cell等发表多篇论文。

 

报告摘要：Aberrant cell cycle regulation leads to cancer development. Proper cell cycle transitions are driven by waves of ubiquitin-dependent degradation of key cell cycle regulators by APC or SCF, the two major E3 ligase complexes. The main research in my laboratory at Department of Pathology, BIDMC is focused on understanding how APC and SCF activities contribute towards cell cycle regulation and subsequent tumor formation. More specifically, I am interested in elucidating the underlying mechanisms that timely regulate APC/Cdh1 and various SCF E3 ligase activities in different cell cycle phases. Additionally, I am also interested in understanding whether other layers of crosstalk between the APC and SCF complex exist. Furthermore, I would like to identify novel downstream targets for both APC and SCF complexes, which will help pinpoint their functions in both cell cycle control and tumor formation. To this end, I have developed biochemical purification approaches that would allow me to identify novel downstream targets for APC/Cdh1 and SCF/Fbw7 complexes. I will present new information regarding our dedicated efforts in utilizing multidisciplinary approaches including biochemical and genetic analysis to understand the tumor suppressor role of Cdh1 or Fbw7 and the oncogenic potential of Skp2. These results will help to better understand the multilayer regulation of the delicate proteolysis pathways, which will lead us to the design of more efficient intervention strategies to combat cancer and other diseases.