Professor of Physiology
Dr. Stanton received his Ph.D. in physiology at Yale University, New Haven, CT in 1980. His postdoctoral training was at Yale University School of Medicine from 1980 to 1983. From 1983 1984 he was Associate Research Scientist in the Department of Physiology at Yale. Dr. Stanton joined the Department of Physiology at Dartmouth as Assistant Professor in 1984. In 1988 he was made Associate Professor of Physiology, and in 1993 Professor. He is Director of the Epithelial Biology Training Program and Director of the Dartmouth Cystic Fibrosis Research Development Program. Dr. Stanton is the Director of the Dartmouth Lung Biology Center
The long-term goal of Dr. Stanton's research is to elucidate the cellular and molecular mechanisms regulating the cystic fibrosis transmembrane conductance regulator (CFTR) Cl- ion channel function in epithelial cells and its role in disease processes. There are three major projects in the laboratory.
- The objective of one study is to elucidate the molecular basis for Cystic Fibrosis. Cystic Fibrosis is an inherited disease manifest by an inability of the trachea and pancreas, to transport NaCl in response to -adrenergic agonists. The most common mutation, ΔF508 CFTR, is a trafficking mutant that fails to leave the endoplasmic reticulum. The long term goal of the project is to identify approaches to allow ΔF508 CFTR to traffic normally and thus, correct the cellular defect in Cystic Fibrosis.
- The goal of the second project in the laboratory is to elucidate why the bacterium Pseudomonas aeruginosa infects airway epithelial cells in patients with Cystic Fibrosis.
- The third project in the laboratory examines how arsenic causes cellular toxicity, diabetes and cancer using the euryhaline fish, Fundulus heteroclitus, as a model organism.
To these ends Dr. Stanton and his colleagues employ a variety of molecular and cell biological approaches including, cDNA cloning, Northern, Southern and Western blot analysis, quantitative real time PCR, siRNA, in situ RT PCR hybridization on tissue sections, immunocytochemistry, confocal microscopy, three dimensional rendering of confocal images and electrophysiological approaches including patch clamp analysis of single ion channels, cRNA expression of channels in Xenopus oocytes and Ussing chamber studies.
Swiatecka-Urban, A., Duhaime, M., Coutermarsh, B., Karlson, K.H., Collawn, J., Milewski, M., Cutting, G.R., Guggino, W.B., Langford, G., and B.A. Stanton BA. PDZ-domain interaction controls the endocytic recycling of the cystic fibrosis transmembrane conductance regulator. J Biol Chem. 18;277(42):40099-10, 2002.
Haggie, P. M., Stanton, B.A. and A. S. Verkman. Increased diffusional mobility of CFTR at the plasma membrane after deletion of its C-terminal PDZ-binding motif. J. Biol. Chem. 279(7):5494-5500, 2004.
Swiatecka-Urban, A., Boyd, C., Coutermarsh, B., Karlson, K., Barnaby, R., Aschenbrenner, L., Langford, G.M., Hasson, T. and B. A. Stanton. Myosin VI regulates endocytosis of the cystic fibrosis transmembrane conductance regulator. J Biol Chem. 279(36):38025-31, 2004.Stanton, B.A. and W. B. Guggino. New insights into cystic fibrosis: molecular switches regulating CFTR. Nature Reviews Molecular Cell Biology, 7(6):426-36, 2006.
Shaw J.R., Gabor K., Hand, E., Lankowski A., Durant L., Thibodeau R., Stanton C. R., Barnaby R.L., Coutermarsh B.A., Karlson K.H., Hamilton J.W., and B.A. Stanton. Role of glucocorticoid receptor in acclimation of killifish (Fundulus heteroclitus) to seawater and effects of arsenic. Am. J. Physiol. Regulatory, Integrative and Comparative Physiology. 292:R1052-60, 2007.
Swiatecka-Urban, A., Talebian, L., Kanno, K., Moreau-Marquis, S., Coutermarsh, B., Hansen, K., Karlson, K.H., Barnaby, R., Cheney, R.E., Langford, G.M., Fukuda, M. and B. A. Stanton. Myosin Vb is required for trafficking of CFTR in Rab11a-specific apical recycling endosomes in polarized human airway epithelial cells. J.Biol. Chem. 282(32):23725-36, 2007.
Moreau-Marquis, S., Bomberger, J.M., Anderson, G.G., Swiatecka-Urban, A., Ye, S., O'Toole, G.A., and B. A. Stanton. The DF508-CFTR mutation results in increased biofilm formation by P. aeruginosa via increasing iron availability. Am. J. Physiology: Lung, Cell and Molecular Physiology. 295(1): L25-37, 2008.
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