BBS Faculty Member - David Sinclair

David Sinclair

Department of Genetics

Harvard Medical School,
New Research Building, Room 0931B
77 Avenue Louis Pasteur
Boston, MA 02115
Tel: 617-432-3931
Fax: 617-432-6225
Email: david_sinclair@hms.harvard.edu
Lab Members: 8 postdoctoral fellows, 1 lab manager, 4 graduate students, 3 undergraduate students
Visit my lab page here.



Why do we grow old? Why does aging cause disease? Can we slow aging or even reverse it? These are some of the greatest unsolved questions in biology. Advances in technology are allowing us to probe these questions more deeply and more rapidly than ever. By tackling these questions, we aim to develop medicines that may one day prevent and/or treat multiple common diseases at once. Our ultimate goal is to allow people to live healthier, disease-free lives. We focus on genes (e.g. sirtuins) and small molecules (e.g. resveratrol) that mimic exercise and calorie restriction, a diet that slows the pace of aging in animals. We use mouse models to test genes and small molecules for their ability to protect against common age-related diseases such as cancer, heart disease, Alzheimer’s disease, cardiovascular disease, infertility, and type II diabetes. At the cellular level we study epigenetics, cellular metabolism and mitochondrial function, neuroprotection, and cellular senescence. Expertise in the lab ranges from enzymology and biochemistry, to genetics and systems biology, to mouse models and pharmacology. Graduate students in the lab develop a comprehensive set of skills and knowledge about a variety of diseases and their underlying cellular processes, preparing them for a career in academia and/or drug discovery.





Last Update: 6/2/2014



Publications

For a complete listing of publications click here.

 


 

Armour, SM., Bennett, EJ., Braun, CR., Zhang, XY., McMahon, SB., Gygi, SP., Harper, JW., and Sinclair, DA. (2013). A high-confidence interaction map identifies SIRT1 as a mediator of acetylation of USP22 and the SAGA coactivator complex. Molecular Cell Biology, 33(8):1487-502. PMID: 23382074.

Hubbard, BP., Gomes, AP., Dai, H., Li, J., Case, AW, .et al., Perni, RB., Ellis, JL., Vlasuk, GP., and Sinclair, DA. (2013). Evidence for a common mechanism of SIRT1 regulation by allosteric activators.
Science, Vol. 339: 1216-1219.

Gomes, A.P., Price N.L., Lin A.Y, Moslehi, J., Rajman, L., White, J.P., Teodoro, J.S., Wran, C.D., Hubbard, B.P., Mercken, E.M., Palmeira, C., de Cabo, R., Rolo, A.P., Turner, N., Bell, E. and Sinclair, D.A. Declining NAD+ induces a pseudohypoxic state disrupting nuclear-mitochondrial communication during aging.
Cell 2013 155(7):1624-38

Germline energetics, aging, and female infertility. Tilly JL, Sinclair DA.
Cell Metab. 2013 Jun 4;17(6):838-50

North BJ, Rosenberg MA, Jeganathan KB, Hafner AV, Michan S, Dai J, Baker DJ, Cen Y, Wu LE, Sauve AA, van Deursen JM, Rosenzweig A, Sinclair DA. SIRT2 induces the checkpoint kinase BubR1 to increase lifespan.
EMBO J. 2014 May 12.



© 2013 by the President and Fellows of Harvard College