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Summary Anatomy Item Literature (14667) Expression Attributions Wiki
XB-ANAT-213

Papers associated with central nervous system (and wnk1)

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A minor role of WNK3 in regulating phosphorylation of renal NKCC2 and NCC co-transporters in vivo., Oi K., Biol Open. February 15, 2012; 1 (2): 120-7.              

WNK2 kinase is a novel regulator of essential neuronal cation-chloride cotransporters., Rinehart J., J Biol Chem. August 26, 2011; 286 (34): 30171-80.              

Renal and brain isoforms of WNK3 have opposite effects on NCCT expression., Glover M., J Am Soc Nephrol. June 1, 2009; 20 (6): 1314-22.

Regulation of the expression of the Na/Cl cotransporter by WNK4 and WNK1: evidence that accelerated dynamin-dependent endocytosis is not involved., Golbang AP., Am J Physiol Renal Physiol. December 1, 2006; 291 (6): F1369-76.

Dietary electrolyte-driven responses in the renal WNK kinase pathway in vivo., O'Reilly M., J Am Soc Nephrol. September 1, 2006; 17 (9): 2402-13.

WNK1 affects surface expression of the ROMK potassium channel independent of WNK4., Cope G., J Am Soc Nephrol. July 1, 2006; 17 (7): 1867-74.

WNK1 kinase isoform switch regulates renal potassium excretion., Wade JB., Proc Natl Acad Sci U S A. May 30, 2006; 103 (22): 8558-63.

WNK3 kinase is a positive regulator of NKCC2 and NCC, renal cation-Cl- cotransporters required for normal blood pressure homeostasis., Rinehart J., Proc Natl Acad Sci U S A. November 15, 2005; 102 (46): 16777-82.

WNK1 activates SGK1 by a phosphatidylinositol 3-kinase-dependent and non-catalytic mechanism., Xu BE., J Biol Chem. October 7, 2005; 280 (40): 34218-23.

WNK kinases and the control of blood pressure., Cope G., Pharmacol Ther. May 1, 2005; 106 (2): 221-31.

[WNK1 and WNK4, new players in salt and water homeostasis], Hadchouel J., Med Sci (Paris). January 1, 2005; 21 (1): 55-60.

Molecular pathogenesis of inherited hypertension with hyperkalemia: the Na-Cl cotransporter is inhibited by wild-type but not mutant WNK4., Wilson FH., Proc Natl Acad Sci U S A. January 21, 2003; 100 (2): 680-4.

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