David K. Cortez, Ph.D.

Associate Professor of Biochemistry

Ph.D., Duke University, 1997 (Molecular Cancer Biology)

Cells respond to genotoxic stress by activating signaling pathways that regulate the cell cycle, DNA repair, transcription, and apoptosis. The ataxia-telangiectasia mutated (ATM) and ATM-and Rad3 related (ATR) protein kinases are at the apex of these pathways. These proteins phosphorylate the checkpoint kinases Chk1 and Chk2 and regulate numerous tumor suppressor proteins including p53 and the breast and ovarian susceptibility protein BRCA1. Studies in this laboratory aim to identify components of these DNA damage response pathways and to understand how they work in a coordinated manner to prevent cancer by regulating the cell cycle, promoting DNA repair, or initiating apoptosis. The long-term goal is to understand how cells preserve genomic integrity and determine the role of genomic instability in tumorigenesis.

Recent Publications

Myers JS, Zhao R, Xu X, Ham AJ, Cortez D. Cyclin-dependent kinase 2 dependent phosphorylation of ATRIP regulates the G2-M checkpoint response to DNA damage. Cancer Res. 2007 67:6685-90.

Chen X, Zhao R, Glick GG, Cortez D. Function of the ATR N-terminal domain revealed by an ATM/ATR chimera. Exp Cell Res. 2007 313:1667-74.

Ball HL, Ehrhardt MR, Mordes DA, Glick GG, Chazin WJ, Cortez D. Function of a conserved checkpoint recruitment domain in ATRIP proteins. Mol Cell Biol. 2007 27:3367-77.

Lovejoy CA, Lock K, Yenamandra A, Cortez D. DDB1 maintains genome integrity through regulation of Cdt1. Mol Cell Biol. 2006 26:7977-90.

Myers JS, Cortez D. Rapid activation of ATR by ionizing radiation requires ATM and Mre11. J Biol Chem. 2006 281:9346-50.

Related Links
Cortez Research Laboratory