John Brumell, PhD
Dr. Brumell’s research examines the host-pathogen interface and employs genetic and cell biological approaches to understand these infections and their outcomes. This research focuses primarily on Salmonella and Listeria, which are common pathogens and powerful model organisms for the study of infection.
- Salmonella exploits host Rho GTPase signalling pathways through the phosphatase activity of SopB. Truong D, Boddy KC, Canadien V, Brabant D, Fairn GD, D'Costa VM, Coyaud E, Raught B, Pérez-Sala D, Park WS, Heo WD, Grinstein S, Brumell JH. Cell Microbiol. 2018
- Type I interferon promotes cell-to-cell spread of Listeria monocytogenes. Osborne SE, Sit B, Shaker A, Currie E, Tan JM, van Rijn J, Higgins DE, Brumell JH. Cell Microbiol. 2017
- Autophagy proteins are not universally required for phagosome maturation. Cemma M, Grinstein S, Brumell JH. Autophagy. 2016
- Salmonella Disrupts Host Endocytic Trafficking by SopD2-Mediated Inhibition of Rab7. D'Costa VM, Braun V, Landekic M, Shi R, Proteau A, McDonald L, Cygler M, Grinstein S, Brumell JH. Cell Rep. 2015
- Listeria monocytogenes exploits efferocytosis to promote cell-to-cell spread. Czuczman MA, Fattouh R, van Rijn JM, Canadien V, Osborne S, Muise AM, Kuchroo VK, Higgins DE, Brumell JH. Nature. 2014