Mechanisms of Nedd4/Nedd4-2-mediated regulation of the epithelial sodium channel [ 2005 - 2007 ]

Research Grant

Researchers: Prof Sharad Kumar (Principal investigator) ,  A/Pr Anuwat Dinudom ,  Prof David Cook

Brief description The epithelial sodium channel (ENaC) is a highly specific ion channel expressed in the apical membrane of some tissues. In the kidney, ENaC activity is responsible for maintaining sodium balance, blood volume and blood pressure. In the lung ENaC function is required for fluid clearance. Abnormal regulation of ENaC is associated with conditions such as hypertension, cystic fibrosis and pulmonary oedema. Delineating the molecular basis of the regulation of ENaC is vital in understanding disease mechanisms and in defining targets for novel therapeutics for the treatment of disorders that arise due to sodium imbalance. Furthermore, ENaC and the molecules involved in the channel regulatory cascade are potential candidate genes in defining the genetic causes of human hypertension and salt wasting disorders. Previous studies from our laboratories and by other groups have shown that Nedd4 and Nedd4-2 proteins are key players in regulating ENaC activity. Our recent NHMRC supported work has identified another important protein, Grk2, as a regulator of ENaC. The work proposed in this application is an extension of our recent findings and will enable us to fully define how Nedd4-Nedd4-2 and Grk2 regulate the activity of ENaC.

Funding Amount $AUD 471,000.00

Funding Scheme NHMRC Project Grants

Notes Standard Project Grant