My research focuses on understanding how cells detect and signal DNA damage and maintain genomic stability. In response to DNA damage or DNA replication problems, cells activate a signaling pathway called the checkpoint to regulate and coordinate various cellular processes to keep the genome stable. The ATR protein kinase is a central player for checkpoint signaling. We are currently investigating how cells recognize different types of DNA damage and activate ATR. We are also studying how activated ATR signals DNA damage in cells and regulates downstream processes such as DNA replication and repair. Given the solid link between loss of genomic stability and cancer development, our study may shed new light on the role of checkpoint as an anti-cancer barrier.