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WNK lysine deficient protein kinase 3

This gene encodes a protein belonging to the 'with no lysine' family of serine-threonine protein kinases. These family members lack the catalytic lysine in subdomain II, and instead have a conserved lysine in subdomain I. This family member functions as a positive regulator of the transcellular Ca2+ transport pathway, and it plays a role in the increase of cell survival in a caspase-3-dependent pathway. Alternative splicing results in multiple transcript variants. [provided by RefSeq, May 2010] (from NCBI)
Top mentioned proteins: WNK4, SPAK, PAK1, OSR1, V1a
Papers on WNK3
Unique chloride-sensing properties of WNK4 permit the distal nephron to modulate potassium homeostasis.
Ellison et al., Portland, United States. In Kidney Int, Oct 2015
Kinase assay studies showed that chloride inhibits WNK4 kinase activity at lower concentrations than it inhibits activity of WNK1 or WNK3.
Kelch-Like Protein 2 Mediates Angiotensin II-With No Lysine 3 Signaling in the Regulation of Vascular Tonus.
Uchida et al., Tokyo, Japan. In J Am Soc Nephrol, Sep 2015
Previously, we identified the WNK3-STE20/SPS1-related proline/alanine-rich kinase-Na/K/Cl cotransporter isoform 1 phosphorylation cascade in vascular smooth muscle cells and found that it constitutes an important mechanism of vascular constriction by angiotensin II (AngII).
Renal NCC is unchanged in the midpregnant rat and decreased in the late pregnant rat despite avid renal Na+ retention.
Baylis et al., Gainesville, United States. In Am J Physiol Renal Physiol, Aug 2015
We also measured mRNA expression of NCC and members of the SPAK/NCC regulatory kinase network, serum and glucocorticoid-regulated kinase (SGK)1, total with no lysine kinase (WNK)1, WNK3, and WNK4.
Inhibition of WNK3 Kinase Signaling Reduces Brain Damage and Accelerates Neurological Recovery After Stroke.
Sun et al., Boston, United States. In Stroke, Jul 2015
BACKGROUND AND PURPOSE: WNK kinases, including WNK3, and the associated downstream Ste20/SPS1-related proline-alanine-rich protein kinase (SPAK) and oxidative stress responsive 1 (OSR1) kinases, comprise an important signaling cascade that regulates the cation-chloride cotransporters.
WNK-SPAK-NCC cascade revisited: WNK1 stimulates the activity of the Na-Cl cotransporter via SPAK, an effect antagonized by WNK4.
Hadchouel et al., Mexico. In Hypertension, 2014
Moreover, WNK4 decreases the WNK1 and WNK3-mediated activation of NCC.
WNK3 abrogates the NEDD4-2-mediated inhibition of the renal Na+-Cl- cotransporter.
Gamba et al., Lausanne, Switzerland. In Am J Physiol Renal Physiol, 2014
The serine/threonine kinase WNK3 and the ubiquitin-protein ligase NEDD4-2 are key regulators of the thiazide-sensitive Na+-Cl- cotransporter (NCC), WNK3 as an activator and NEDD2-4 as an inhibitor.
Modulation of NCC activity by low and high K(+) intake: insights into the signaling pathways involved.
Gamba et al., Mexico. In Am J Physiol Renal Physiol, 2014
This suggests that for NCC activation by ANG II, integrity of the WNK4/SPAK pathway is required, whereas for the low-K(+) diet, SPAK phosphorylation occurred despite the absence of WNK4, suggesting the involvement of another WNK (WNK1 or WNK3).
N-terminal serine dephosphorylation is required for KCC3 cotransporter full activation by cell swelling.
Gamba et al., Mexico. In J Biol Chem, 2013
Additionally, WNK3, which inhibits the activity of KCC3, promoted phosphorylation of Ser-96 as well as Thr-991 and Thr-1048.
Dietary salt intake regulates WNK3-SPAK-NKCC1 phosphorylation cascade in mouse aorta through angiotensin II.
Uchida et al., Tokyo, Japan. In Hypertension, 2013
However, a low-salt diet and angiotensin II together did not increase phosphorylation of SPAK and NKCC1 in the aorta in WNK3 knockout mice, indicating that activation of the WNK-SPAK-NKCC1 phosphorylation cascade induced by a low-salt diet and angiotensin II is dependent on WNK3.
With-No-Lysine Kinase 3 (WNK3) stimulates glioma invasion by regulating cell volume.
Sontheimer et al., Birmingham, United States. In Am J Physiol Cell Physiol, 2011
Analysis of the data showed that WNK3 is an essential regulator of NKCC1 and that WNK3 activates NKCC1-mediated ion transport necessary for cell volume changes associated with cell invasion.
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.
Similar effects of all WNK3 variants on SLC12 cotransporters.
Mercado et al., Mexico. In Am J Physiol Cell Physiol, 2011
The Wnk3 protein isoforms have a similar effect on SLC12 cotransporters. NKCC1/2 and NCC were inhibited, even in hypertonicity, while KCCs were activated, even in isotonic conditions.
Altered expression of regulators of the cortical chloride transporters NKCC1 and KCC2 in schizophrenia.
Lewis et al., Pittsburgh, United States. In Arch Gen Psychiatry, 2011
OXSR1 and WNK3 transcripts were substantially overexpressed in subjects with schizophrenia relative to comparison subjects.
WNK3 is a putative chloride-sensing kinase.
Gamba et al., Mexico. In Cell Physiol Biochem, 2010
The with-no-lysine kinase 3 (WNK3) is a serine/threonine kinase that modulates the activity of the electroneutral cation-coupled chloride cotransporters (CCC).
Serum and glucocorticoid-induced kinase (SGK) 1 and the epithelial sodium channel are regulated by multiple with no lysine (WNK) family members.
Cobb et al., Dallas, United States. In J Biol Chem, 2010
Data find that expression of the N termini of all four WNKs results in modest to strong activation of SGK1.
Emerging roles for WNK kinases in cancer.
Jordan et al., Lisbon, Portugal. In Cell Mol Life Sci, 2010
Although most research has focussed on the role of WNK1, WNK3 and WNK4 in regulating different ion transporters in both the kidney and extrarenal tissues, there is growing evidence for additional roles of WNK kinases in various signalling cascades related to cancer.
Molecular physiology of the thiazide-sensitive sodium-chloride cotransporter.
Hoover et al., Chicago, United States. In Curr Opin Nephrol Hypertens, 2009
Another WNK kinase, WNK3, also regulates NCC, activating NCC and antagonizing the effect of WNK4.
Renal and brain isoforms of WNK3 have opposite effects on NCCT expression.
O'Shaughnessy et al., Cambridge, United Kingdom. In J Am Soc Nephrol, 2009
The C-terminal motifs contributed by exons 18 and 22 play an important role in the actions of WNK3 isoforms on NCCT.
The regulation of salt transport and blood pressure by the WNK-SPAK/OSR1 signalling pathway.
Alessi et al., Dundee, United Kingdom. In J Cell Sci, 2008
It has recently been shown that the WNK [with-no-K(Lys)] kinases (WNK1, WNK2, WNK3 and WNK4) have vital roles in the control of salt homeostasis and blood pressure.
Molecular physiology of the WNK kinases.
Lifton et al., New Haven, United States. In Annu Rev Physiol, 2007
The related kinase WNK3 has reciprocal actions on the primary mediators of cellular Cl(-) influx and efflux, effects that can serve to regulate cell volume during growth and in response to osmotic stress as well as to modulate neuronal responses to GABA.
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