- Glitsch Group Research Group
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.
Reciprocal regulation of two G protein-coupled receptors sensing extracellular concentrations of Ca2+ and H.
Wei WC. 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
Lack of kinase regulation of canonical transient receptor potential 3 (TRPC3) channel-dependent currents in cerebellar Purkinje cells.
Nelson C. and Glitsch MD., (2012), J Biol Chem, 287, 6326 - 6335
Protons and Ca2+: ionic allies in tumor progression?
Glitsch M., (2011), Physiology (Bethesda), 26, 252 - 265
Muscle dysfunction caused by a KATP channel mutation in neonatal diabetes is neuronal in origin.
Clark RH. et al, (2010), Science, 329, 458 - 461