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Vol. 16, Issue 11, 5087-5093, November 2005

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The C-Terminal Tail of the Polycystin-1 Protein Interacts with the Na,K-ATPase -Subunit

Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT 06510

Submitted March 10, 2005; Revised July 21, 2005; Accepted August 8, 2005
Monitoring Editor: Guido Guidotti

Polycystin-1 (PC-1) is the product of the PKD1 gene, which is mutated in autosomal dominant polycystic kidney disease. We show that the Na,K-ATPase -subunit interacts in vitro and in vivo with the final 200 amino acids of the polycystin-1 protein, which constitute its cytoplasmic C-terminal tail. Functional studies suggest that this association may play a role in the regulation of the Na,K-ATPase activity. Chinese hamster ovary cells stably expressing the entire PC-1 protein exhibit a dramatic increase in Na,K-ATPase activity, although the kinetic properties of the enzyme remain unchanged. These data indicate that polycystin-1 may contribute to the regulation of Na,K-ATPase activity in kidneys in situ, thus modulating renal tubular fluid and electrolyte transport.

Abbreviations used: ADPKD, autosomal dominant polycystic kidney disease; CHO, Chinese hamster ovary; MDCK, Madin-Darby canine kidney; HA, hemagglutinin; PBS, phosphate-buffered saline; PC-1, polycystin-1.

Address correspondence to: Michael J. Caplan (michael.caplan{at}yale.edu).

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