检测到您当前使用浏览器版本过于老旧,会导致无法正常浏览网站;请您使用电脑里的其他浏览器如:360、QQ、搜狗浏览器的极速模式浏览,或者使用谷歌、火狐等浏览器。
下载Firefoxbat365中文官网登录入口
2013学年春季学期系列学术讲座之十
题目:The molecular mechanism of BRCA1 in DNA damage response and tumor suppression
报告人:Xiaochun Yu
Associate professor, Department of Internal Medicine,
University of Michigan Medical School, Ann Arbor, MI
时间:2013年5月24日(周五),下午13:00-14:30 PM
地点:bat365中文官网登录入口一楼邓祐才报告厅
Abstract:
Normal cells encounter numerous environmental and internal hazards during proliferation. Proper DNA damage response helps cells protect genome integrity. Deregulation of this cellular process results in chromosome instability, and eventually causes cancer. Many tumor suppressors participate in DNA damage response. One typical example is BRCA1 (Breast Cancer Susceptibility Gene 1). Mutation carriers of BRCA1 are predisposed to breast and ovarian cancers, indicating that BRCA1 is a key tumor suppressor. Accumulated evidence suggests that BRCA1 is involved in DNA damage-induced checkpoint activation and DNA damage repair. However, the molecular mechanism by which BRCA1 participates in DNA damage response remains elusive. Here, I will discuss of our recently findings on the role of protein phosphorylation, ubiquitination and PARylation in BRCA1-dependent DNA damage response. In particular, my talk will focus on protein PARylation, a unique posttranslational modification that has been identified for more than 40 years. However, the role of PARylation in response to DNA damage is not clear. Moreover, the inhibitors of protein PARylation can specifically kill tumor cells bearing BRCA1 mutations. Again, the molecular mechanism underlining this interesting phenomenon is not clear. I will present our recent data on the functional interaction between PARylation and BRCA1 during DNA damage response. Our results may explain not only a molecular mechanism of BRCA1 in DNA damage response but also the mechanism by which PARP inhibitors kill breast tumor cells.
联系人:郑晓峰(电话:62755712)
欢迎各位老师和同学积极参加!