Deen

Research interests include physiology, molecular, cellular and structural biology of protein routing and regulation of water homeostasis . Major current projects of his group include investigations on the molecular and cellular mechanisms causing the mis-sorting of Aquaporin-2 water channels and vasopressin V2 receptors mutants in congenital and acquired Nephrogenic Diabetes Insipidus, a disease with extensive water loss, and how to correction of these conditions might be approached. These issues are addressed using numerous sophisticated molecular and cell biological techniques, in vitro and in vivo. Cell permeable (ant)agonist to rescue V2R mutants and compounds that specifically inhibit AQP function are among his current fascinations as a molecular physiologist.

Peter Deen is an associate professor at the department of Physiology.

• Fabra M, Raldúa D, Power DM, Deen PM, Cerdà J. Marine fish egg hydration is aquaporin-mediated. Science. 307:545, 2008.

• de Mattia F, Savelkoul PJ, Kamsteeg EJ, Konings IB, van der Sluijs P, Mallmann R, Oksche A, Deen PM. Lack of Arginine Vasopressin-Induced Phosphorylation of Aquaporin-2 Mutant AQP2-R254L Explains Dominant Nephrogenic Diabetes Insipidus. J Am Soc Nephrol. 16:2872-80, 2005. 

• Robben JH, Knoers NV, Deen PM. Characterization of vasopressin V2 receptor mutants in nephrogenic diabetes insipidus in a polarized cell model. Am J Physiol Renal Physiol. 289:F265-72, 2005.

• de Mattia F, Savelkoul PJ, Bichet DG, Kamsteeg EJ, Konings IB, Marr N, Arthus MF, Lonergan M, van Os CH, van der Sluijs P, Robertson G, Deen PM. A novel mechanism in recessive Nephrogenic Diabetes Insipidus: wild-type Aquaporin-2 rescues the apical membrane expression of intracellularly retained AQP2-P262L. Hum Mol Genet. 13:3045-56, 2004.