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WNK lysine deficient protein kinase 4

This gene encodes a member of the WNK family of serine-threonine protein kinases. The kinase is part of the tight junction complex in kidney cells, and regulates the balance between NaCl reabsorption and K(+) secretion. The kinase regulates the activities of several types of ion channels, cotransporters, and exchangers involved in electrolyte flux in epithelial cells. Mutations in this gene result in pseudohypoaldosteronism type IIB.[provided by RefSeq, Sep 2009] (from NCBI)
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Top mentioned proteins: SPAK, CAN, V1a, ROMK, OSR1
Papers on WNK4
WNK4 is the major WNK kinase positively regulating NCC in the mouse kidney.
Uchida et al., In Biosci Rep, 21 Apr 2014
However, the role of WNK4 in the regulation of NCC remains controversial.
Structural and biochemical characterisation of the KLHL3-WNK kinase interaction important in blood pressure regulation.
Kurz et al., In Biochem J, 18 Apr 2014
UNLABELLED: With no lysine (K) kinase-1 (WNK1) and WNK4 regulate blood pressure by controlling the activity of ion co-transporters in the kidney.
A Role for the Circadian Clock Protein Per1 in the Regulation of the NaCl Co-transporter (NCC) and the With-no-Lysine Kinase (WNK) Cascade in Mouse Distal Convoluted Tubule Cells.
Gumz et al., United States. In J Biol Chem, 07 Apr 2014
The goal of this study was to test if Per1 regulates sodium transport in the DCT through modulation of NCC and the WNK kinases, WNK1 and WNK4.
Mechanism of Salt-Sensitive Hypertension: Focus on Adrenal and Sympathetic Nervous Systems.
Fujita, Tokyo, Japan. In J Am Soc Nephrol, 27 Mar 2014
Furthermore, these studies point to crucial roles for the Rac1-mineralocorticoid receptor-NCC/ENaC and the renal β-adrenergic stimulant-glucocorticoid receptor-WNK4-NCC pathways in certain rodent models of salt-sensitive hypertension.
Insights in cullin 3/WNK4 and its relationship to blood pressure regulation and electrolyte homeostasis.
Pedraza-Chaverri et al., Mexico. In Cell Signal, 08 Mar 2014
UNLABELLED: One of the most important systems for protein degradation is the ubiquitin-proteasome system (UPS).
FGF23 promotes renal calcium reabsorption through the TRPV5 channel.
Erben et al., Vienna, Austria. In Embo J, 03 Mar 2014
Rather, apical membrane abundance of TRPV5 in renal distal tubules and thus renal calcium reabsorption are regulated by FGF23, which binds the FGF receptor-αKlotho complex and activates a signaling cascade involving ERK1/2, SGK1, and WNK4.
Mineralocorticoid receptor phosphorylation regulates ligand binding and renal response to volume depletion and hyperkalemia.
Lifton et al., New Haven, United States. In Cell Metab, Dec 2013
In volume depletion, angiotensin II and WNK4 signaling decrease MR(S843-P) levels, whereas hyperkalemia increases MR(S843-P).
Effects of angiotensin II on kinase-mediated sodium and potassium transport in the distal nephron.
Hoorn et al., Rotterdam, Netherlands. In Curr Opin Nephrol Hypertens, 2013
RECENT FINDINGS: Ang II can activate the sodium chloride cotransporter (NCC) through phosphorylation by Ste20-related, proline-alanine rich kinase (SPAK), an effect that is independent of aldosterone but dependent on with no lysine kinase 4 (WNK4).
11Beta-hydroxylase deficiency and other syndromes of mineralocorticoid excess as a rare cause of endocrine hypertension.
Koch et al., Jackson, United States. In Horm Metab Res, 2012
Apart from primary aldosteronism, mineralocorticoid excess can be caused by congenital adrenal hyperplasia (CAH) due to mutations of the 11beta-hydroxylase and 17alpha-hydroxylase genes, by inactivating mutations of the glucocorticoid receptor gene (Chrousos syndrome), endogenous hypercortisolism (Cushing's syndrome), by mutations of the 11beta-hydroxysteroid dehydrogenase type 2 gene (apparent mineralocorticoid excess/AME) or licorice/carbenoxolone intake, mutations of the epithelial sodium channel genes (Liddle syndrome), mutations of the mineralocorticoid receptor gene (Geller syndrome), and by mutations in the WNK1, WNK4, KLHL3, CUL3 genes (pseudohypoaldosteronism type 2 or Gordon syndrome).
Mechanisms of sodium-chloride cotransporter modulation by angiotensin II.
Gamba et al., Mexico. In Curr Opin Nephrol Hypertens, 2012
Recent evidence suggests that these effects are achieved through modulation of the With No Lysine kinase 4 (WNK4) and Ste20-related, proline-alanine-rich kinase (SPAK) pathway.
Pathophysiology of salt sensitivity hypertension.
Fujita et al., Tokyo, Japan. In Ann Med, 2012
Renal beta2 adrenoceptor stimulation in the kidney leads to decreased transcription of the gene encoding WNK4, a negative regulator of Na(+) reabsorption through Na(+) -Cl (-) cotransporter in the distal convoluted tubules, resulting in salt-dependent hypertension.
Activation of the renal Na+:Cl- cotransporter by angiotensin II is a WNK4-dependent process.
Gamba et al., Mexico. In Proc Natl Acad Sci U S A, 2012
Activation of the renal Na+:Cl- cotransporter by angiotensin II is a WNK4-dependent process.
KLHL3 mutations cause familial hyperkalemic hypertension by impairing ion transport in the distal nephron.
Jeunemaitre et al., Paris, France. In Nat Genet, 2012
Familial hyperkalemic hypertension (FHHt) is a Mendelian form of arterial hypertension that is partially explained by mutations in WNK1 and WNK4 that lead to increased activity of the Na(+)-Cl(-) cotransporter (NCC) in the distal nephron.
Disease-causing mutations in the acidic motif of WNK4 impair the sensitivity of WNK4 kinase to calcium ions.
Peng et al., Birmingham, United States. In Biochem Biophys Res Commun, 2012
these results suggest that these PHAII-causing mutations disrupt a Ca(2+)-sensing mechanism around the acidic motif necessary for the regulation of WNK4 kinase activity by Ca(2+) ions.
WNK4 inhibits NCC protein expression through MAPK ERK1/2 signaling pathway.
Cai et al., Atlanta, United States. In Am J Physiol Renal Physiol, 2012
data suggest that WNK4 inhibits NCC protein through activating the MAPK ERK1/2 signaling pathway.
Antagonistic regulation of cystic fibrosis transmembrane conductance regulator cell surface expression by protein kinases WNK4 and spleen tyrosine kinase.
Jordan et al., Lisbon, Portugal. In Mol Cell Biol, 2011
Results show that Tyr512 phosphorylation is a novel signal regulating the prevalence of CFTR at the cell surface and that WNK4 and Syk perform an antagonistic role in this process.
The calcineurin inhibitor tacrolimus activates the renal sodium chloride cotransporter to cause hypertension.
Ellison et al., Portland, United States. In Nat Med, 2011
In wild-type mice, the CNI tacrolimus caused salt-sensitive hypertension and increased the abundance of phosphorylated NCC and the NCC-regulatory kinases WNK3, WNK4 and SPAK.
Hypertension associated polymorphisms in WNK1/WNK4 are not associated with hydrochlorothiazide response.
Hui et al., Beijing, China. In Clin Biochem, 2011
hypertension associated polymorphisms in WNK1 and WNK4 may not be predictors for antihypertensive response to diuretics.
Renal nerves, WNK4, glucocorticoids, and salt transport.
Brooks et al., Portland, United States. In Cell Metab, 2011
A study in Nature Medicine (Mu et al., 2011) shows that dietary salt excess, coupled with β-adrenergic stimulation, increases arterial pressure via glucocorticoid receptors and WNK4, suggesting interactions between these systems in the pathogenesis of hypertension.
Epigenetic modulation of the renal β-adrenergic-WNK4 pathway in salt-sensitive hypertension.
Fujita et al., Tokyo, Japan. In Nat Med, 2011
salt loading suppressed renal WNK4 expression, activated the Na(+)-Cl(-) cotransporter and induced salt-dependent hypertension
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