Director, Centre for Integrative Physiology
- Professor of Physiology
Anant Parekh was a medical student at Oxford University, where he obtained his undergraduate and doctoral degrees (both at University College). He then moved, initially as an Alexander Von Humboldt Scholar, to the Max Planck Institute for biophysical Chemistry in Goettingen, Germany, where he worked in Professor Erwin Neher’s department with Professor Walter Stuehmer and then Professor Reinhold Penner. He moved back to Oxford (Physiology) in 1997 as a Wellcome Trust Career Development Fellow and Sir Edward Abraham Research Fellow at Keble College. He was subsequently awarded a Lister Institute Senior Research Fellowship, Amersham Medical Fellowship (Keble College) and then Monsanto Senior Research Fellowship (Exeter College, Oxford). In 2002, he was appointed to a proleptic University Lectureship (Physiology Department) and Tutorial Fellowship (Lady Margaret Hall). In the same year, he was awarded a personal chair.
Anant Parekh’s research interests are on intracellular calcium signalling and how changes in calcium can engender a wide range of cellular responses. In particular, his work has focussed on store-operated calcium channels in the plasma membrane, how these channels interact with intracellular organelles like mitochondria and how these fundamental elements go awry in human disease. He was awarded the Wellcome Prize in Physiology (2002), India International Foundation Prize (2009), GL Brown Prize from the UK Physiological Society (2012). He is a member of Academia Europaea and is a Fellow of the Academy of Medical Sciences. He was elected Vice-Chair (2015) and Chair (2017) of the Gordon Conference on calcium signalling. He sits on the editorial boards of the Journal of Physiology, Cell Calcium and BMC Physiology.
Store-Operated Ca2+ Channels: Mechanism, Function, Pharmacology, and Therapeutic Targets.
Bakowski D. et al, (2021), Annu Rev Pharmacol Toxicol, 61, 629 - 654
Single-nucleotide polymorphisms in Orai1 associated with atopic dermatitis inhibit protein turnover, decrease calcium entry and disrupt calcium-dependent gene expression.
Yeh Y-C. et al, (2020), Hum Mol Genet, 29, 1808 - 1823
The whole-cell Ca2+ release-activated Ca2+ current, ICRAC , is regulated by the mitochondrial Ca2+ uniporter channel and is independent of extracellular and cytosolic Na.
Samanta K. et al, (2020), J Physiol, 598, 1753 - 1773