Dr. Casey received a B.Sc. (Honours Biochemistry) from Queen's University and Ph.D. (Biochemistry) from University of Toronto. He carried out three years of postdoctoral research at Stanford University. Dr. Casey joined the faculty at University of Alberta in 1996.
Since becoming a faculty member, Dr. Casey received salary support awards from the Medical Research Council of Canada (Scholar) and Alberta Heritage Foundation for Medical Research (Scholar, Senior Scholar, Scientist). Dr. Casey won the Young Investigator awards from the Canadian Physiological Society and Canadian Society for Biochemistry, Molecular and Cellular Biology. In 2016, Dr. Casey received the mentoring award from the Faculty of Medicine and Dentistry.
Dr. Casey was Director of the Membrane Protein Disease Research Group 2008-2017. Currently he leads the International Research Training Group in Membrane Biology, an NSERC-funded program for graduate students and PDFs, working between U of a and Germany's Technical University Kaiserslautern and Saarland University.
Throughout his career, Dr. Casey's research passion has been membrane transport processes.
Dr. Casey's research passion is membrane transport. How do small molecular machines (membrane transport proteins) control the flow of material into and out of cells.
In particular, Dr. Casey's group has studied SLC4 (Solute Carrier family 4). Most of these proteins are bicarbonate transporters. SLC4A1 (also called Band 3 or AE1) is a chloride/bicarbonate exchanger of the the red blood cell membrane. Dr. Casey's group has studied how this protein functions and what goes wrong in disease.
Over the last several years the focus of his group has been corneal blindness. In 2006 Dr. Casey's lab was part of the group that discovered mutations of the gene encoding SLC4A11 cause congenital hereditary endothelial dystrophy, corneal blindness that arises in children. Subsequently their research revealed that SLC4A11 mutations can also cause a common disease, Fuchs endothelial corneal dystrophy.
The Casey lab has been working to understand the normal roles of SLC4A11 and what goes wrong to cause disease. This has led them to identify potential new therapies to treat patients with corneal blindness.
The lab's research is funded by a Project grant from the Canadian Institutes of Health Research (2018-2023) and part of a CREATE training grant from NSERC.
corneal blindness, Fuchs endothelial corneal dystrophy, congenital hereditary endothelial dystrophy, SLC4A11, membrane transport
Yang, Y., Seo-Meyer, P., Lezon-Geyda, K., Badior, K.E., Casey, J.R., Li, J., Reithmeier, R.A.F. and Gallagher, P.G. (2018) A Homozygous Ser725Arg Mutation in the Anion-binding Site of Band 3 (SLC4A1) Abolishes Transport Function Causing Transfusion Dependent Anemia and Distal Renal Tubular Acidosis Blood, 131, 1759-1763.
Alka, K. and Casey, J.R. (2018) Molecular Phenotype of SLC4A11 Missense Mutants: Setting the Stage for Personalized Medicine in Corneal Dystrophies, Human Mutation, 39, 676-690. Featured as cover for this issue of the journal.
Badior, K., Alka, K., and Casey, J.R. (2017) SLC4A11 Three-Dimensional Homology Model Rationalizes Corneal Dystrophy-causing Mutations, Human Mutation, 38, 279-288.
Loganathan, S.K., Lukowski, C.M. and Casey, J.R. (2016) The cytoplasmic domain is essential for transport function of the integral membrane transport protein SLC4A11, Am. J. Physiol., 310, C161-174.
Chiu, A.M., Mandziuk, J.J., Alka, K., Loganathan, S.K., and Casey, J.R. (2015) High Throughput Assay Identifies Glafenine as a Chemical Corrector for the Folding Defect in Corneal Dystrophy-Causing Mutants of SLC4A11, Invest. Opthal. and Vis. Sci., 56, 7739-53. Paper discussed at: http://www.laserbeatsrock.com/#!A-Step-Toward-Restoring-the-Ocular-Tide/cjds/575816d20cf24c9615a4f4f9
Loganathan, S.K., and Casey, J.R. (2014) Corneal Dystrophy-causing SLC4A11 Mutants: Suitability for Folding-Correction Therapy, Human Mutation, 35, 1082-91. (Article selected for a video highlight; See http://www.youtube.com/watch?v=rLvUicNtsoM)
Vilas, G.L., Loganathan, S., Liu J., Riau, A.K., Young, J.D., Mehta, J.S., Vithana, E.N. and Casey, J.R. (2013) Transmembrane water flux through SLC4A11: a route defective in corneal diseases, Human Mol. Genet.,22, 4579-90.
Vithana, E.N, Morgan, P.E., Ramprasad, V., Tan, D.T.H., Yong, V.H.K., Venkataraman, D., Venkatraman, A., Yam, G.H.F., Nagasamy, S., Law, R.W.K., Rajagopal, R., Pang, C.P., Kumaramanickevel, G., Casey, J.R, Aung, T. (2008) SLC4A11 Mutations in Fuchs Endothelial Corneal Dystrophy (FECD) Hum. Mol. Genet., 17, 656-666.
Vithana, E.N. Morgan, P.E., Sundaresan, P., Ebenezer, N., Tan, D.T.H., Anand, S., Khine, K.O., Venkataraman, D., Yong, V., Salto-Tellez, M., Venkataraman, A., Guo, K., Hemadevi, B., Mohamed, M.D., Srinivasan, M., Prajna, V., Khine, M., Casey, J.R., Inglehearn, C.F., & Aung, T. (2006) Mutations in Na+-borate co-transporter SLC4A11 cause recessive Congenital Hereditary Endothelial Dystrophy CHED2 Nature Genetics, 38, 755-7.