Profile

Background:

I obtained my PhD training at the University of Alberta, Canada, in the Biochemistry department studying signal transduction through the oncogenic Ras proteins. I gained postdoctoral training at the University of British Columbia, Canada, studying mechanisms of neurodegeneration in Huntington disease. Further postdoctoral experience was gained at the Cancer Research UK London Research Institute where I began my research in the cell biology of autophagy.

Research:

We study a pathway called autophagy that enables a cell to degrade its cytoplasmic components.  During autophagy, intercellular proteins and organelles are captured by newly-forming membranes to produce autophagosomes which subsequently fuse with lysosomes.  In mammalian cells, autophagy helps clear proteins and organelles that have become damaged through normal turnover, forming an important route for combating cellular ageing and stress.  Autophagy is also activated following nutrient starvation and the recycling of cellular protein into amino acids helps maintain metabolism.  Current evidence suggests that autophagy plays multiple roles in cancer.  At early stages, autophagy could prevent cancer by buffering metabolic stress thereby preventing oncogenic mutations.  In other situations, autophagy can help maintain the health of cancer cells targeted by chemotherapy, thereby preventing the full clearance of cancer cells.

My previous work studied how levels of autophagy are controlled by signal transduction pathways.  We have been particularly interested in the ULK (uncoordinated-51 like kinase) family of proteins that function downstream of mTORC1 (mammalian target-of-rapamycin complex 1) to regulate autophagy.  We are continuing to study signalling mechanisms of the mTORC1-ULK pathway with the goal of developing strategies that can be applied to slow down the growth of cancer cells.

Teaching:

I teach 2nd year undergraduate Nutritional Biochemistry and Protein structure, 3rd year Laboratories and 4th year Biochemistry on the Molecular mechanisms of disease.