G. Angus McQuibban

Associate Professor

Address

University of Toronto
Faculty of Medicine, Department of Biochemistry
MaRS Centre, West Tower
661 University Ave., Suite 1500, Rm 1536
Toronto, ON M5G 1M1

Lab	McQuibban Mitophagy Laboratory
Lab Phone	416-978-5873
Office Phone	416-978-6820
Email	angus.mcquibban@utoronto.ca

After completing an undergraduate degree and M.Sc. (Biochemistry) at the University of Toronto, I moved to Vancouver to pursue a Ph.D. (Biochemistry and Molecular Biology). My work focused on identifying novel substrates for a class of proteases (MMPs) that contribute to cancer metastasis. I discovered that inflammatory chemokines were a new family of substrates for this enzyme family. After completing my Ph.D. I moved to England for my PDF at the MRC-Laboratory of Molecular Biology in Cambridge. I continued my work of proteolysis, but this time working with a new family of proteases, called Rhomboids. There I revealed their important activity within mitochondria. I started my lab ‘back home’ in 2005, and since, my research interests have focused on mitochondrial quality control, and how dysregulation leads to human disease. My lab currently balances basic science projects with translational studies and small molecule screening to develop novel therapeutics in neurodegenerative disease.

In the News

Research Lab

Learn more: McQuibban Mitophagy Laboratory

Research Description

Mitochondrial Quality Control Pathways and Human Neurodegenerative Disease

Understanding Mitochondrial Dysfunction in Human Neurodegenerative Diseases

Mitochondria have long been known as ‘the powerhouse of the cell’ and while this is true, ongoing studies of mitochondrial function have revealed that these organelles orchestrate and regulate critically important signalling pathways. Not only do mitochondria regulate overall cellular metabolism, they also form an important platform for apoptosis and as such are key regulators of cellular health.

In the lab, we focus on a newly identified pathway that regulates the overall health of the mitochondrial network. Mitophagy, the removal of damaged mitochondria by autophagy, is responsible for maintaining mitochondrial health.

We have an intense interest in understanding how mitophagy impacts health outcomes in human neurodegenerative diseases, most notably Parkinson disease (PD).

Our research focuses on the proteostasis pathways that regulate mitochondrial turnover during cellular stress. We have identified proteases that are key regulators of mitophagy, and have linked them to the eitiology of PD.