Dudley Lamming

Position title: Assistant Professor

Email: dlamming@medicine.wisc.edu

Phone: 608-256-1901 x 12861

Biology of aging and age-related diseases, diabetes, cancer, Alzheimer’s disease

WSM VA Hospital
Ph.D., Harvard University
Research Interests
Biology of aging and age-related diseases, diabetes, cancer, Alzheimer’s disease
Research Fields
Biology of Aging, Cell Signaling, Human and mouse

Research Description:
The Lamming laboratory focuses on the physiological role played by the mechanistic target of rapamycin (mTOR), a protein kinase that through a diverse set of substrates regulates complex cellular processes, including growth, metabolism, and aging. Recent work has shown that rapamycin, an inhibitor of mTOR signaling, can promote health and longevity in model organisms including mammals. Understanding and manipulating the mTOR signaling pathway may provide insight into the treatment of age-related diseases, including diabetes, Alzheimer’s disease, and cancer.

Representative Publications:
Search PubMed for more publications by Dudley Lamming

Lamming, D.W., Mihaylova, M.M., Katajisto, P., Baar, E.L., Yilmaz, O.H., Hutchins, A., Gultekin, Y., Gaither, R., Sabatini, D.M. (2014) Depletion of Rictor, an essential protein component of mTORC2, decreases male lifespan. Aging Cell [Epub ahead of print]

Lamming, D.W., Demirkan, G., Boylan, J.M., Mihaylova, M.M., Peng, T., Ferreira, J., Neretti, N., Salomon, A., Sabatini, D.M., and Gruppuso, P.A. (2014) Hepatic signaling by the mechanistic target of rapamycin complex2 (mTORC2). FASEB J 28(1):300-315.

Lamming, D.W., Ye, L., Astle, M.C., Baur, J.A., Sabatini, D.M., Harrison, D.E., (2013) Young and old genetically heterogeneous HET3 mice on a rapamycin diet are glucose intolerant but insulin sensitive. Aging Cell 12(4): 712-718.

Lamming, D.W, Ye, L., Katajisto, P., Concalves, M.D., Saitoh, M., Stevens, D.M., Davis, J.G., Salmon, A.B., Richardson, A., Ahima, R.S., Guertin, D.A., Sabatini, D.M., Baur, J.A., (2012) Rapamycin-Induced Insulin Resistance Is Mediated by mTORC2 Loss and Uncoupled from Longevity. Science 335:1638-1643.