|Tel||01865 285377, 01865 272432|
- Cantley Group Research Group
PhD, MSc, DIC, BSc (Hons)
RD Lawrence Fellow
I undertook my doctoral studies in the lab of Prof. Dominic Withers at University College London, where I investigated the molecular control of beta cell function by oxygen sensing and insulin signalling pathways. I received my PhD in 2007 and went on to a postdoctoral position at the Garvan Institute of Medical Research, Sydney, where I worked in the lab of Prof. Trevor Biden, and developed my interests in lipid signalling processes in the beta cell. Whilst in Australia I held two consecutive postdoctoral fellowships enabling me to develop my own research direction. I returned to the UK in 2013 to take up my current position as group leader within the Department of Physiology, Anatomy and Genetics at the University of Oxford. I am an RD Lawrence Fellow, funded by Diabetes UK, and a Research Fellow at Wolfson College.
My current research interests revolve around the beta cell: how insulin secretory capacity is matched to demand during health and obesity, and how this fails during type 2 diabetes.
I collaborate with several other research groups including Prof. David James (Garvan Institute, Sydney), Prof. Patrik Rorsman (OCDEM, Oxford), Dr, Anna Gloyn (OCDEM, Oxford) and Prof. Frances Ashcroft (DPAG, Oxford).
Deletion of the von Hippel-Lindau gene in pancreatic beta cells impairs glucose homeostasis in mice.
Cantley J. et al, (2009), J Clin Invest, 119, 125 - 135
Deletion of PKCepsilon selectively enhances the amplifying pathways of glucose-stimulated insulin secretion via increased lipolysis in mouse beta-cells
Cantley J. et al, (2009), Diabetes, 58, 1826 - 1834
Deletion of protein kinase Cδ in mice modulates stability of inflammatory genes and protects against cytokine-stimulated beta cell death in vitro and in vivo.
Cantley J. et al, (2011), Diabetologia, 54, 380 - 389
Pancreatic deletion of insulin receptor substrate 2 reduces beta and alpha cell mass and impairs glucose homeostasis in mice.
Cantley J. et al, (2007), Diabetologia, 50, 1248 - 1256
Lysosomal acid lipase and lipophagy are constitutive negative regulators of glucose-stimulated insulin secretion from pancreatic beta cells.
Pearson GL. et al, (2014), Diabetologia, 57, 129 - 139
Acetyl-CoA carboxylase-1 is a critical regulator of beta cell size and proliferation
Cantley J. et al, (2013), DIABETIC MEDICINE, 30, 8 - 9
Glucose homeostasis in mice is transglutaminase 2 independent.
Iismaa SE. et al, (2013), PLoS One, 8
G protein-coupled receptor (GPR)40-dependent potentiation of insulin secretion in mouse islets is mediated by protein kinase D1.
Ferdaoussi M. et al, (2012), Diabetologia, 55, 2682 - 2692
Oleanolic acid reduces hyperglycemia beyond treatment period with Akt/FoxO1-induced suppression of hepatic gluconeogenesis in type-2 diabetic mice.
Zeng XY. et al, (2012), PLoS One, 7