Replacement Assistant Professor
Room: 850 Peter Morand, Room 225
Office: 613-562-5800 ext. 8234
Work E-mail: email@example.com
Dr Wheaton teaches, develops curricula and facilitates pedagogical strategies in the translational and molecular medicine (TMM) undergraduate program. This includes courses on the aging process, biochemistry, cancer biology, genomic instability, molecular biology, and inquiry-based research laboratories. In addition, Dr Wheaton has taught pre-med biochemistry in the Ottawa-Shanghai joint school of Medicine and is a faculty member in the Science Education Alliance-Phage Hunters Advancing Genomics and Evolutionary Science (SEA PHAGES) program. His current educational focus is improving active learning opportunities to enhance student conceptual understanding and application of scientific principles.
Dr Wheaton has explored the molecular changes in normal cells as they undergo the aging process and during the suppression of cancer. This research centered on cellular senescence, which is a permanent exit from the cell cycle as the result of genome instability, DNA damage or oncogenic stress. Specifically, this involved defining how the regulatory network of the tumor suppressor p53 controls cellular senescence as a result of the aging process. Dr. Wheaton is also interested in how p53 related mechanisms contribute to the childhood premature aging syndrome, Hutchinson-Gilford progeria.
Undergraduates interested in joining the TMM undergraduate program or enrolling in general entry TMM courses are welcome to contact Dr. Wheaton for details.
- Hutchinson-Gilford Progeria Syndrome. Wheaton K. In: Gu D., Dupre M. (eds) Encyclopedia of Gerontology and Population Aging. Springer, Cham (2019). https://link.springer.com/referenceworkentry/10.1007/978-3-319-69892-2_53-1
- Progerin-Induced Replication Stress Facilitates Premature Senescence in Hutchinson-Gilford Progeria Syndrome. Wheaton K, Campuzano D, Ma W, Sheinis M, Ho B, Brown GW, & Benchimol S. Mol Cell Biol. 2017 Jun 29;37(14).https://www.ncbi.nlm.nih.gov/pubmed/28483909
- UbE2E1/UBCH6 Is a Critical in Vivo E2 for the PRC1-catalyzed Ubiquitination of H2A at Lys-119. Wheaton K, Sarkari F, Stanly Johns B, Davarinejad H, Egorova O, Kaustov L, Raught B, Saridakis V, Sheng Y. J Biol Chem. 2017 Feb 17;292(7):2893-2902. https://www.ncbi.nlm.nih.gov/pubmed/28073915
- Assaily W, Rubinger DA, Wheaton K, Lin Y, Ma W, Xuan W, Brown-Endres L, Tsuchihara K, Mak TW, Benchimol S. ROS-mediated p53 induction of Lpin1 regulates fatty acid oxidation in response to nutritional stress. Mol Cell. 2011 Nov 4;44(3):491-501 https://www.ncbi.nlm.nih.gov/pubmed/22055193
- BTG2 antagonizes Pin1 in response to mitogens and telomere disruption during replicative senescence. Wheaton K, Muir J, Ma W, Benchimol S. Aging Cell. 2010 Oct;9(5):747-60. https://www.ncbi.nlm.nih.gov/pubmed/20569234
- Protein kinase C delta blocks immediate-early gene expression in senescent cells by inactivating serum response factor. Wheaton K, Riabowol K. Mol Cell Biol. 2004 Aug;24(16):7298-311. https://www.ncbi.nlm.nih.gov/pubmed/15282327