Juan Codina, PhD
Professor, Internal Medicine/Nephrology/Molecular Medicine
Telephone: 336-713-7212
Fax:
Email: jcodina@wfubmc.edu
Education:
1975 - M.S. in Biology, University of Barcelona, Spain
1979 - Ph.D. in Biochemistry (Endocrinology), University of Barcelona, Spain
Current Research:
Studies in our laboratory focus on the role of a family of transporters in the kidney which function to absorb potassium and acidify the urine. Because of this function these transporters have been named H+,K+-ATPases, and they are localized in specialized cells in collecting duct segments of the kidney, as well as, in collecting cells in culture. Previously, we have shown that the kidney plays a major role in potassium balance and acid-base balance. We have studied a transporter in the kidney which absorbs potassium, and secretes acid, and is known as the H+,K+-ATPase. The form in the stomach is the major means of secreting acid and initiates digestion of food. The kidney form is not like the stomach form but responds to low levels of potassium in the blood (chronic hypokalemia), and an acidic blood pH (chronic acidosis). This regulatory response occurs in specific regions of the kidney. Uncertainties remain with respect to participation of specific forms of this transporter in reabsorption of potassium and secretion of acid. Since these transporters in kidney cannot be defined by sensitivity to drugs or inhibitors, as there are none specific, it is not known with certainty if modulations in transport and the well established physiologic responses are a result of regulation of these transporters or other transporters which have not yet been discovered. These studies will allow us to find new ways the kidney regulates potassium and pH balance of the blood and may allow description of abnormalities in tubular function that result in diseases characterized by abnormal responses by these regulatory functions.
Recent Publications:
Codina, J., Li J., Hong, Y. and DuBose, T.D.Jr. “The g-Na+,K+-ATPase subunit assembles selectively with a1/b1-Na+,K+-ATPase but not with the colonic H+,K+-ATPase” Kidney Int., 3, 967-974, 2002.
Li, J., Codina, J., Petroska, E., Werle, M.J. and DuBose, T.D.Jr. “The carboxy-terminus of the colonic H+,K+-ATPase a-subunit is required for stable b-subunit assembly and function”. Kidney Int., 65, 1301-1310, 2004.
Li, J., Codina, J., Petroske, E., Werle, M.J., Willingham, M.C. and DuBose, T.D.Jr. “The Effect of b-Subunit Assembly on Function and Localization of the colonic H+,K+-ATPase a-subunit” Kidney Int., 66, 1068-1075, 2004.
Codina, J., Li. And DuBose, T.D.Jr. “A Carboxy-Terminus Motif of HKa2 is Necessary for Assembly and Function”. Kidney Int., 66, 2283-2292, 2004.
Codina, J., Li, J. and DuBose, T.D. Jr. “CD63 interacts with the carboxy-terminus of the colonic H+,K+-ATPase to increase plasma membrane localization and Rb+-uptake”. Am. J. Physiol., 288, C1279-1286, 2005.
Publications:
For a listing of additional publications, refer to PubMed, a service provided by the National Library of Medicine