报  告  人：梁世康教授

报告题目：非同源末端连接的分子机制和基于结构的小分子药物研发

报告时间：10 月20日（周二）下午4：30

报告地点：计算机楼313会议室

报告摘要：DNA is the main carrier of human genetic information and must be delivered intact and undamaged to the next generation to sustain hereditary and health. However, DNA damage is inevitable. A single human cell experiences tens of thousands of DNA lesions every day. Among different types of DNA damage, DNA double-strand break (DSB) is the most lethal one. Mis-repaired or un-repaired DSBs can easily result in huge genome instability and cell death.

There are two major pathways to respond to and repair DSBs: Homologous Recombination (HR) and Non-Homologous End Joining (NHEJ). HR requires DNA end resection and sister chromatid for template-guided repair. Unlike HR, NHEJ has no requirement of template and is active throughout the whole cell cycle. NHEJ is commonly considered as the fast and efficient repair pathway. In humans, NHEJ is the preferred DSB repair pathway, with the indispensable core components of Ku70/80, DNA-PKcs, XLF, XRCC4, and DNA Ligase IV. Among them, DNA-PKcs is the key kinase subunit and cancer drug target. Our research has been focusing on the molecular mechanisms of structure-based NHEJ drug development, spatial organisation, and regulation.

个人简介：梁世康博士，香港大学李嘉诚医台湾av女优生物医学台湾av女优助理教授（Tenure-Track）。本科阶段就读于复旦大学和英国伯明翰大学，获伯明翰大学理学学士（一等荣誉）学位，并于英国剑桥大学获哲学博士学位。曾在剑桥大学生物化学系、剑桥大学心肺研究所及英国皇家帕普沃思医院从事博士后研究。研究方向包括人类DNA损伤应答与修复、蛋白质-蛋白质及蛋白质-核酸相互作用、多组分大分子复合物的组装与调控、整合生物物理学、生物化学与结构生物学、冷冻电镜、人工智能辅助的结构导向药物发现及AI for Science。在Nature、Nature Structural & Molecular Biology等期刊发表代表性论文。主持或参与国家自然科学基金、香港研究资助局及联合研究项目，担任《Genome Instability & Disease》青年编委