Physiology and Biophysics Discipline
Dr. Neil Bradbury received his PhD in medical biochemistry from the University of Wales, Cardiff in 1987. Prior to that, he received a bachelor’s degree (Hons) in biochemistry from the University of St. Andrews in Scotland.
Dr. Bradbury is a member of the American Physiological Society.
Dr. Bradbury's research interests lie in the area of regulation of membrane protein trafficking in polarized epithelia. We have used the chloride channel protein CFTR as a paradigm for the cAMP dependent regulation of apical membrane endocytic events. We are interested in the protein-protein interactions between adaptins, clathrin, and CFTR involved in the endocytic internalization of CFTR. Interest also lies in the cAMP-dependent protein kinase (PKA) regulation of CFTR channel activity and trafficking and its mediation by binding of PKA to subcellular anchor proteins (AKAPs).
Dey, I and Bradbury N.A. (2018) Physiology of the Gut: Experimental Models for Investigating Intestinal Fluid and Electrolyte Transport. DOI:
Bridges R.J. and Bradbury N.A. (2018) Cystic Fibrosis, Cystic Fibrosis Transmembrane Conductance Regulator and Drugs: Insights from Cellular Trafficking.
Bradbury, Neil. (2017). All Cells Have a Sex. In: Legato M.J. (ed.) Principles of Gender-Specific Medicine: Gender in the Genomic Era: Third Edition. Academic Press pp. 269-290. .
Dey I. and Bradbury N.A. (2017) Activation of TPA-response element present in human Lemur Tyrosine Kinase 2 (lmtk2) gene increases its expression.
Bradbury N.A. (2017) Attention span during lectures: 8 seconds, 10 minutes, or more?
Bradbury N.A. (2016). CFTR and Cystic Fibrosis: A Need for Personalized Medicine. In: Hamilton K., Devor D. (eds) Ion Channels and Transporters of Epithelia in Health and Disease. Physiology in Health and Disease. Springer, New York, NY pp. 773-802.
Dey I., Shah K., and Bradbury N.A. (2016) Natural Compounds as Therapeutic Agents in the Treatment Cystic Fibrosis.
Butler E.C. and Bradbury N.A. (2015) Signal dependent ER export of lemur tyrosine kinase 2.
Jai Y., Shah K., Bridges R.J., and Bradbury N.A. (2015) Evidence against resveratrol as a viable therapy for the rescue of defective ΔF508 CFTR.
Shah K. and Bradbury N.A. (2015) Lemur Tyrosine Kinase 2, a novel target in prostate cancer therapy.
White C., Nixon A., and Bradbury N.A. (2015) Determining Membrane Protein Topology Using Fluorescence Protease Protection (FPP).
Shah K., Cheng Y., Hahn B., Bridges R., and Bradbury N.A., Mueller D.M. (2015) Synonymous codon usage affects the expression of wild type and F508del CFTR.
Shah K. and Bradbury N.A. (2015) Kinase modulation of androgen receptor signaling: implications for prostate cancer.
Huang H., Shah K., and Bradbury N.A., Li C., White C. (2014) Mcl-1 promotes lung cancer cell migration by directly interacting with VDAC to increase mitochondrial Ca2+ uptake and reactive oxygen species generation.
Shah K., McCormack C.E., and Bradbury N.A. (2013) Do you know the sex of your cells?
Nixon A., Jia Y., White C., and Bradbury N.A. (2012) Determination of the membrane topology of lemur tyrosine kinase 2 (LMTK2) by fluorescence protease protection.
Young, A., Abban, C.Y., Gentzsch, M., Menes, P.I., Bridges, R.J. and Bradbury N.A. (2009). Dynasore inhibits the removal of wild-type and mutant CFTR from the cell surface.
Silvis, M.R., Bertrand, C., Ameen, N., Golin-Bisello, F., Butterworth, M., Frizzell, R.A. and Bradbury, N.A. (2009). Rab11b regulates apical recycling of CFTR in polarized epithelial cells.
Abban, C.Y., Bradbury, N.A. and Meneses, P.I. (2008). HPV16 and BPV1 infection can be blocked by the dynamin inhibitor dynasore.
Ameen, N., Silvis, M.R., and Bradbury, N.A. (2007) Endocytic trafficking of CFTR in health and disease.
Oztan, A., Silvis, M., Weisz, O.A., Bradbury, N.A., Hsu, S-C., Goldenring, J.R., Yeamon, C., and Apodaca, G. (2007). Exocyst requirement for endocytic traffic directed toward the apical pole of polarized MDCK cells.
Silvis, M.R., Picciano, J.A., Bertrand, C., Weixel, K., Bridges, R.J. and Bradbury, N.A. (2003). A mutation in the cystic fibrosis transmembrane conductance regulator generates a novel internalization sequence and enhances endocytic rates.
Weixel, K.M. and Bradbury, N.A. (2001). µ2 binding directs the cystic fibrosis transmembrane conductance regulator to the clathrin-mediated endocytic pathway.
Bradbury, N.A. (2001). cAMP signaling cascades and CFTR: is there more to learn?
Weixel, K.M. and Bradbury, N.A. (2001). Endocytic adaptor complexes bind the C-terminal domain of CFTR.
Sun, F., Hug, M., Bradbury, N.A. and Frizzell, R.A. (2000). E3KARP mediates the association of ezin and PKA with CFTR in airway cells.
Singh, A.K., Schultz, B.D., Katzenellenbogen, J.A., Price, E.M., Bridges, R.J. and Bradbury, N.A. (2000). Estrogen inhibition of CFTR-mediated chloride secretion.
Weixel, K. and Bradbury, N.A. (2000). The carboxyl terminus of CFTR binds the endocytic adaptor complex AP-2.
Bradbury, N.A., Clark, J.A.,Watkins, S.C., Widnell, C., Smith, H.S., and Bridges, R.J. (1999). Characterization of the internalization pathways of the cystic fibrosis transmembrane conductance regulator (CFTR).
Bradbury N.A. (1999). Role of intracellular CFTR in acidification. (Invited Review Article)
Bradbury, N.A., and Bridges R.J. (1994) Role of membrane trafficking in plasma membrane solute transport. (Invited Review Article)