Pkd1 mouse models

We have introduced lox P sites into introns 2 and 4 of the mouse Pkdl gene which allows its regulated inactivation. Mutations in human PKD1 account for at-85% of all cases of human autosomal dominant polycystic kidney disease. We have shown that we can recapitulate a human-like disease presentation using inducible Cre-recombinases. This model is a powerful tool for studying the pathophysiology of the disease, determining the normal function of the Pkdl gene product, and for testing potential therapies.

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