Author: Glover Mark Mercier Zuber Annie Figg Nikki O’Shaughnessy Kevin M.
Publisher: NRC Research Press
ISSN: 1205-7541
Source: Canadian Journal of Physiology and Pharmacology, Vol.88, Iss.10, 2010-10, pp. : 986-995
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Abstract
Cation transport in the distal mammalian nephron relies on the SLC12 family of membrane cotransporters that include the thiazide-sensitive Na+-Cl- cotransporter (NCC). NCC is regulated through a scaffold of interacting proteins, including the WNK kinases, WNK 1 and WNK 4, which are mutated in the hypertensive Gordon’s syndrome. Dynamic regulation of NCC function by kinases must involve dephosphorylation by phosphatases, as illustrated by the role of PP1 and PP2B in the regulation of KCC members of the SLC12 family. There are 2 phosphorylation-controlled regulatory pathways for NCC: type 1, mediated by WNK4 and affecting trafficking to the surface membrane, and type 2, affecting intrinsic transporter kinetics by phosphorylation of conserved N-terminal S/T amino acids. Using the
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