As a molecular biologist, I am very interested in understanding mechanisms that maintain genomic stability and how dysfunction in these processes result in human diseases such as cancer and neurodegenerative disorders. My lab focuses on DNA repair pathways that fix damaged DNA and the translesion synthesis process that tolerates DNA damage. It is the dynamism between these two pathways that maintain genomic health.
From a cancer biology perspective, the lab examines some key questions: 1) What factors drive cancer onset? 2) How cancer cells continue to divide unabated and relapse after initial treatment. 3) How therapeutic targeting can rescue the cancer problem. We are specifically studying novel phenotypes of one translesion synthesis protein, REV1, that might help address missing links in understanding cancer etiology. We are also examining how stress factors might influence REV1’s functionality in cancer sustenance and therapy resistance.
The lab also actively explores the consequences of disrupting pathways that maintain genomic health in triplet repeat disorders. We are particularly interested in examining the interplay of stress responses and DNA repair that instigates repetitive DNA instability.
We have recently expanded our investigations of the DNA repair and translesion synthesis pathways during host cell response to virus infections. We have actively pursued how RNA viruses, SARS-CoV-2, and Dengue, impact the DNA damage response, including the expression and function of Double-strand break repair and translesion synthesis proteins.
The lab employs several tools to address these compelling questions, such as tissue culturing, DNA/RNA amplification, microscopy, and other molecular biology methods. We welcome our students, colleagues, and collaborators to join hands in this marvelous adventure!