Associate Professor of Biomedical Science
Maike Glitsch gained a degree in Biological Sciences in 1995 (University of Göttingen and Max Planck Institute for biophysical Chemistry in Göttingen, Germany) and a Doctorate in Biology (University of Göttingen and Max Planck Institute for biophysical Chemistry in Göttingen, Germany; thesis on cellular neuroscience) in 1998. She then came to Oxford as a post-doctoral fellow on a Human Frontiers of Sciences Program Long Term Fellowship, and was subsequently funded by the Wellcome Trust and Royal Society. She has since been appointed as University Lecturer in Biomedical Sciences and Tutorial Fellow in Medicine at St. Hilda’s College Oxford.
Maike Glitsch’s research interests centre around communication between cells in the mammalian brain and, more recently, the involvement of certain channels and receptors in neuronal development in health and disease. In particular, her group is currently focussing on the role of intracellular calcium in development of the cerebellum, a region of the brain involved in motor coordination and learning. Inappropriate proliferation of certain cells in the cerebellum leads to the formation of tumours. Using electrophysiology, calcium imaging and molecular biology, they are trying to understand differences in calcium signalling between healthy and cancerous human brain tissue.
Coincidence Detection of Membrane Stretch and Extracellular pH by the Proton-Sensing Receptor OGR1 (GPR68).
Wei W-C. et al, (2018), Curr biol
Gordon Research Conference on Ca2+ Signalling 2017 Editorial.
Glitsch MD., (2018), J physiol, 596, 2661 - 2662
Functional expression of calcium-permeable canonical transient receptor potential 4-containing channels promotes migration of medulloblastoma cells.
Wei W-C. et al, (2017), J physiol, 595, 5525 - 5544
Reciprocal regulation of two G protein-coupled receptors sensing extracellular concentrations of Ca2+ and H.
Wei W-C. et al, (2015), Proc natl acad sci u s a, 112, 10738 - 10743
Extracellular acidosis impairs P2Y receptor-mediated Ca(2+) signalling and migration of microglia.
Langfelder A. et al, (2015), Cell calcium, 57, 247 - 256