John Stokes, M.D. (Full Member)
Director, Division of Nephrology, University of Iowa
Professor, Dept. of Internal Medicine, University of Iowa

http://www.int-med.uiowa.edu/Divisions/Nephrology/Directory/JohnStokes.html

Research Interest    

Dr. Stokes' research addresses the mechanisms whereby ions are translocated across cell membranes and how these processes are regulated. Most recently he has focused on understanding how Na is translocated across the Epithelial Na Channel, (ENaC). This ion channel is composed of three different subunits (alpha, beta, and gamma) and is regulated by steroid hormones as well as by several peptide hormones. Mutations in two of the ENaC subunits can lead to channel activation and are responsible for Liddle Syndrome, which is characterized by hypertension and hypokalemia. Proper regulation of ENaC is critical for both blood pressure regulation and Na and K homeostasis. The molecular interactions responsible for this regulation are being unraveled, and the structural proteins and kinases responsible for efficient channel function are also under investigation. Dr. Stokes' laboratory uses a number of approaches to study this channel, including electrophysiologic analysis of model epithelial monolayers, heterologous expression in Xenopus oocytes, protein overexpression via virus-mediated infection, structure-function analysis, immunofluorescence analysis, genetic engineering and gene targeting, and biochemical analysis of second messengers. Dr. Stokes is the Director of the NIH-supported O'Brien Kidney Research Center at the University of Iowa, which is investigating certain aspects of ENaC regulation. Dr. Stokes is classified under the CF-related component of the Center because of the relevance of his work on ENaC regulation. However, his research is also highly relevant to genetic diseases in the kidney.

Selected Publications:

Husted, R.F., Volk, K.A., Sigmund, R.D., and Stokes, J.B.: Discordant Effects of Corticosteroids and Expression of Subunits on ENaC Activity., Am. J. Physiol. Renal Physiol., Renal, 293:F813-F820, 2007.

Shi, P., Cao, X., Qu. J., Volk, K., Kirby, P., Williamson, R.A., Stokes, J., and Yang, B.: Nephrogenic Diabetes Insipidus in Mice Caused by Deleting C-terminal Tail of Aquaporin-2. Am. J. Physiol. Renal, 292(5):F1344-44, 2007.

Cao, X., Shi, P., Sigmund, R., Husted, R., Sigmund, C.D., Williamson, R., Stokes, J.B., and Yang, B: Mice Heterozygous for Beta-ENaC Deletion Have Defective Potassium Excretion. Am. J. Physiol. Renal, 291(1):F107-15, 2006.

Itani, O., Stokes, J.B., and Thomas, C.P.: Nedd4-2 Isoforms Differentially Associate with ENaC and Regulate Its Activity. Am. J. Physiol. Renal Physiol., 298:F334-F346, 2005.

Publications from Gene Therapy Center

Publications from PubMed