Xiaohua Wu, PhD

Professor
Department of Molecular Medicine
California Campus



Scripps Research Joint Appointments

Faculty, Graduate Program

Research Focus

DNA double-strand break repair and cell cycle checkpoints in mammalian cells

Gross chromosomal arrangements (GCRs) are hall markers of cancer cells, and DNA double-stand breaks (DSBs) are the major cause of cancer-associated genome instability. Unrepaired DSBs can lead to chromosomal breakage and cell death, while incorrectly repaired DSBs would lead to genome instability. The research interest of my laboratory is to understand the molecular mechanisms underlying the function of DNA damage checkpoint and DSB repair to maintain genome stability and prevent cancer and aging. We have established novel EGFP-based DSB repair assays and chromosomal translocation mouse models to investigate the mechanisms underlying DSB repair and chromosomal rearrangement. We are also interested in understanding the role of the breast cancer suppressor BRCA1, and other disease-linked and genome-stability maintenance genes, such as Nbs1, Mre11 and CtIP, in the maintenance of genome stability.


Education

Ph.D. (Moleculary Biology; Genetics), Brandeis University, 1995
B.S. (Genetics), Fudan University, 1987

Professional Experience

Postdoctoral Fellow, Department of Cancer Biology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA, 1996-20012017-2017 Associate Professor, Molecular Medicine, Scripps Research
2007-2017 Associate Professor, Molecular and Experimental Medicine (MEM), Scripps Research
2002-2007 Assistant Professor, Molecular and Experimental Medicine (MEM), Scripps Research
1996-2001 Postdoctoral Associate with Dr. David M. Livingston, Harvard Medical School, Harvard University
1995-1996 Postdoctoral Fellow, Brandeis University

Awards & Professional Activities

New Scholar in Aging, Ellison Medical Foundation

Selected References

All Publications

Hailong Wang, H., Li, Y., Truong, L.N., Shi,L.Z., Hwang, P.Y.H., He, J., Cho, M.J., Li, H., Negrete, A., Shiloach, J., Berns, M.W., Shen, B., Chen, L. and Wu, X. (2014) CtIP maintains stability at common fragile sites and inverted repeats by end resection-independent endonuclease activity. Molecular Cell 54:1012-1021.

Truong, L., Li, Y., Shi, L., Hwang, P., He, J., Wang, H., Razavian, N., Berns, M., and Wu, X. (2013) Microhomology-mediated End Joining and Homologous Recombination share the initial end resection step to repair DNA double-strand breaks in mammalian cells. Proceedings of the National Academy of Sciences (PNAS) 110:7720-7725.

Wang, H., Shi, L.Z., Wong, C.C., Han, X., Hwang, P.Y., Truong, L.N., Zhu, Q., Shao, Z., Chen, D.J., Berns, M.W., Yates JR 3rd, Chen L, Wu X. (2013) The interaction of CtIP and Nbs1 connects CDK and ATM to regulate HR-mediated double-strand break repair. PLoS Genetics 9:e1003277.

Liu E., Lee A.Y., Chiba T., Olson E. Sun P. and Wu X. (2007) ATR-mediated S-phase checkpoint prevents DNA rereplication in mammalian cells when the licensing control is disrupted. Journal of Cell Biology 179: 643-657.

Olson E., Nievera C.J., Liu E., Lee A.Y., Chen L. and Wu X. (2007) The Mre11 complex mediates the S-phase checkpoint through an interaction with RPA. Molecular and Cellular Biology 27: 6053-6067.