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2. Plasminogen deficiency does not prevent sodium retention in a genetic mouse model of experimental nephrotic syndrome. (10th June 2020)

4. Urokinase‐type plasminogen activator (uPA) is not essential for epithelial sodium channel (ENaC)‐mediated sodium retention in experimental nephrotic syndrome. (20th May 2019)

5. Zymogen‐locked mutant prostasin (Prss8) leads to incomplete proteolytic activation of the epithelial sodium channel (ENaC) and severely compromises triamterene tolerance in mice. (11th March 2021)