Dudley W. Lamming, Ph.D.
Lab: C4141 VA Hospital (4th floor - C wing)
The Lamming laboratory is primarily focused on understanding the physiological role played by the mechanistic target of rapamycin (mTOR), a protein kinase that, through a diverse set of substrates, regulates 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. As detailed by Dr. Lamming in a recent JCI review - Rapalogs and mTOR inhibitors as anti-aging therapeutics - understanding and manipulating the mTOR signaling pathway may provide insight into the treatment of age-related diseases, including diabetes, Alzheimer's disease, and cancer.
Specific questions of the laboratory include:
- Understanding the physiological role played by mTOR complex 2 (mTORC2) using mouse models;
- Identification of compounds that can selectively regulate either mTORC1 or mTORC2 as possible therapies for age-related diseases and type 2 diabetes;
- Identifying the mechanisms underlying the metabolic consequences of aging.
Postdoctoral, Ph.D. students, M.D. students and undergraduates interested in pursuing research in the Lamming lab should contact Dr. Lamming directly at firstname.lastname@example.org
Selected recent research publications (full publication list):
- Arriola Apelo SI, Neuman JC, Baar EL, Syed FA, Cummings NE, Brar HK, Pumper CP, Kimple ME, Lamming DW. Alternative rapamycin treatment regimens mitigate the impact of rapamycin on glucose homeostasis and the immune system. Aging Cell 2016 Feb;15(1):28-38. doi: 10.1111/acel.12405.
- Baar EL, Carbajal KA, Ong IM, Lamming DW. Sex- and tissue-specific changes in mTOR signaling with age in C57BL/6J mice. Aging Cell 2016; Feb;15(1):155-66. doi: 10.1111/acel.12425.
- Lamming DW, Cummings NE, Rastelli AL, Gao F, Cava E, Bertozzi B, Spelta F, Pili R, Fontana L. Restriction of dietary protein decreases mTORC1 in tumors and somatic tissues of a tumor-bearing mouse xenograft model. Oncotarget Oct 13;6(31):31233-40. doi: 10.18632/oncotarget.5180.
- Lamming DW. (2014) Diminished mTOR signaling: a common mode of action for endocrine longevity factors. Springerplus 3:735. doi: 10.1186/2193-1801-3-735
- Lamming DW, Mihaylova MM, Katajisto P, Baar EL, Yilmaz OH, Hutchins A, Gultekin Y, Gaither R, Sabatini DM. (2014) Depletion of Rictor, an essential protein component of mTORC2, decreases male lifespan. Aging Cell 13(5): 911-7. doi: 10.1111/acel.12256
- 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. (2013) Hepatic signaling by the mechanistic target of rapamycin complex2 (mTORC2). FASEB J 28(1): 300-15. doi: 10.1096/fj.13-23774
- 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.