Dr. Samuel Bunting

Cells are constantly exposed to damage, but some cells repair damage and continue growing normally, while other cells suffer apoptosis, senescence or become malignant. The biological reasons for these differing responses to stress are not clear. The goal of my research program is to show why different cells respond differently to stress, with the goal of reprogramming cells so that they repair damage in an advantageous way.We study these questions in mice using a variety of molecular and biochemical techniques with a particular focus on DNA repair. By using genetically-targeted mouse strains, we aim to explore the full complexity of mechanisms regulating the response to damage in a long-lived mammalian species with significant homology to humans.I am an instructor in the Rutgers/UMDNJ Molecular Biosciences Program within the Cell and Developmental Biology and Biochemistry Programs.