报告题目：Fanconi Anemia and Complex DNA Lesions
报告人：Dr. Lei Li
Professor, Department of Experimental Radiation Oncology
The University of Texas MD Anderson Cancer Center
时 间：2017年12 月5 日（星期二） 14:30-15:30
Dr. Li’s group has long standing research interests in understanding the molecular mechanisms of genomic instability and tumorigenesis. The maintenance of genomic integrity following DNA damage depends on the coordination of DNA repair with cell cycle checkpoint controls. The integrity of the DNA damage response pathway is crucial for the prevention of neoplastic transformation, as suggested by the fact that many proteins involved in these pathways are tumor suppressors including BRCA1, BRCA2, ATM, RPA1 and FANC family. Efforts by his laboratory over the years have led to the discovery of a recombination-independent repair mechanism of DNA crosslinks and to the functional dissection of the Fanconi anemia pathway.
1. Wang Y, Leung JW, Jiang Y, Lowery MG, Do H, Vasquez KM, Chen J, Wang W, Li L. FANCM and FAAP24 maintain genome stability via cooperative as well as unique functions. Mol Cell 49(5):997-1009, 2013.
2. Li L.BRCA1 forks over new roles in DNA-damage response- before and beyond the breaks. Mol Cell 44(2):174-176, 2011.
3. Shen X, Do H, Li Y, Chung W-H, Tomasz M, deWinter JP, Xia B, Elledge SJ Wang W, Li L. Recruitment of Fanconi anemia and breast cancer proteins to DNA damage sites is differentially governed by replication. Mol Cell 35(5):716-23, 2009.
4. Huang Y, Leung JW, Lowery M, Matsushita N, Wang Y, Shen X, Huong D, Takata M, Chen J,Li L. Modularized Functions of the Fanconi Anemia Core Complex. Cell Rep 7(6):1-9, 2014.
5. Tian Y, Paramasivam M, Ghosal G, Chen D, Shen X, Huang Y, Akhter S, Legerski R, Chen J, Seidman MM, Qin J,Li L. UHRF1 Contributes to DNA Damage Repair as a Lesion Recognition Factor and Nuclease Scaffold.Cell Rep 10(12):1957-66, 2015.