My lab uses mouse genetic modeling and molecular and cellular techniques to study basic biochemical pathways of relevance to aging biology.
I. Aging is often accompanied by increases in inflammation. A major interest of the lab is how perturbations in the regulation of autophagy and mitochondrial dynamics in cells are linked to inflammation. One project in the lab focuses on a family of interferon-gamma and LPS regulated proteins, the Immunity Related GTPases (IRGs). The lab has shown that mice and cells lacking one of these proteins, Irgm1, have excessive inflammatory responses that are accompanied by decreases in autophagy and mitophagy, and altered cellular metabolism. IRG genes in human (IRGM) have been linked to several inflammatory diseases including Crohn’s disease and sepsis. Current work in the lab focuses on their role in those diseases using bacterial and relevant mouse models.
II. Altered expression of the cytokine Transforming Growth Factor beta (TGF-b) has been linked with a number of aging processes, including stem cell and neural function. TGF-b is consequently a therapeutic target for a number of age-related diseases. The lab is studying a novel regulator of TGF-b expression called P311, which drives TGF-b translation. Mice have been created that lack P311 and are being used to address the role of P311 in a number of physiological processes.
Education and Training
- Ph.D., Duke University, 1995