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Mol Biol Cell. 2005 Nov;16(11):5087-93. Epub 2005 Aug 17.

The C-terminal tail of the polycystin-1 protein interacts with the Na,K-ATPase alpha-subunit.

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1
Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT 06510, USA.

Abstract

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 alpha-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.

PMID:
16107561
PMCID:
PMC1266409
DOI:
10.1091/mbc.E05-03-0200
[Indexed for MEDLINE]
Free PMC Article
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