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Dr. Basil Hubbard

Assistant Professor
Pharmacology, University of Alberta
Rm 9-10 Medical Sciences Building, Dept. of Pharmacology, University of Alberta,

Brief Biography:

Dr. Basil P. Hubbard is an Assistant Professor in the Department of Pharmacology at the University of Alberta (UofA). His lab studies biomolecular damage during aging, and develops therapeutics to treat and prevent age-related diseases such as cancer. Prior to joining the Faculty at the UofA, Dr. Hubbard performed post-doctoral work, which focused on improving the specificity of genome engineering tools using continuous directed evolution, at Harvard University in the lab of Dr. David Liu. Dr. Hubbard obtained his PhD from Harvard Medical School in 2011 where working in the lab of Dr. David Sinclair, he studied the biological function of SIRT1, a conserved longevity gene, and described a novel mechanism for how this enzyme can be activated by small-molecule drugs. Dr. Hubbard's research works papers in prestigious journals including Science, Cell, Nature Methods, and Cell Metabolism. His recent research work has been cited over 1000 times in the past 5 years.


Academic positions:

Assistant Professor, University of Alberta


Research interests:

Biological aging is one of the greatest enigmas of the life sciences. While the aging process is ubiquitous in nature, maximum lifespans for different organisms vary widely from a day for the mayfly, to over one thousand years for the bristlecone pine. For model organisms such as yeast, worms, and flies, both lifespan and the onset of age-associated phenotypic changes can be altered experimentally in the laboratory. For mammals such as humans, aging is marked by a complex series of declines in physiological function, and an increase in the incidence of diseases such as cancer, Alzheimer’s, and diabetes. The goal of the Hubbard lab is to identify pharmacological agents to prevent and treat age-related diseases, and promote longevity. To accomplish this objective, we develop biochemical assays to report on the activity of central longevity pathways, and decompose specific aspects of age-related disease into in vitro systems. Using high-throughput small molecule screening and macromolecular protein engineering and evolution, we then attempt to identify agents that can perturb these systems. Positive hits are investigated in vivo for potential therapeutic value, and as tools to garner further insight into the mechanisms underlying age-related disease.


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