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WNK4 encodes a member of the WNK family of serine-threonine protein kinases. Additionally we are shipping WNK4 Antibodies (68) and many more products for this protein.
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This study provides substantial new insights into the role of phosphorylation of KLHL3 (show KLHL3 Proteins) in regulating the interaction with WNK4
The distribution of allele frequency and genotype of WNK4 gene Ala589Ser polymorphism showed significant differences between essential hypertension subjects, with or without type 2 diabetes mellitus, and normotensive subjects.
Data indicate that WNK lysine deficient protein kinase 4 protein (WNK4) was degraded not only by proteasomes but also by atypical protein kinase C scaffold protein p62 (p62)-kelch-like 3 protein (KLHL3)-mediated selective autophagy.
this meta-analysis suggested that WNK4 G1155942T and C6749T gene polymorphisms may contribute to the susceptibility and development of hypertension.
Akt (show AKT1 Proteins) and PKA phosphorylated KLHL3 (show KLHL3 Proteins) at S433, and phosphorylation of KLHL3 (show KLHL3 Proteins) by PKA inhibited WNK4 degradation.
WNK4 is a substrate of SFKs and the association of c-Src (show SRC Proteins) and PTP-1D (show PTPN11 Proteins) with WNK4 at Tyr (show TYR Proteins)(1092) and Tyr (show TYR Proteins)(1143) plays an important role in modulating the inhibitory effect of WNK4 on ROMK (show KCNJ1 Proteins)
WNK4 inhibits SNARE (show NAPA Proteins) formation of syntaxin 13 (show STX12 Proteins) with VAMP2 (show VAMP2 Proteins).
Regulation of WNK4 by CUL3 (show CUL3 Proteins) and its relationship to blood pressure regulation and electrolyte homeostasis. [Review]
WNK4 inhibits Large-conductance, Ca(2 )-activated K( ) channel activity, in part, by increasing channel degradation through an ubiquitin-dependent pathway.
analysis of how mutations of KLHL3 (show KLHL3 Proteins) show less ability to ubiquitinate WNK4 because of KLHL3 (show KLHL3 Proteins)'s low stability and/or decreased binding to CUL3 (show CUL3 Proteins) or WNK4
ENaC (show SCNN1A Proteins) and ROMK (show KCNJ1 Proteins) channel activity in kidney tubules are inhibited in TgWnk4(pseudoaldosteronism type II) mice. Wnk4(PHAII)-induced inhibition of ENaC (show SCNN1A Proteins) and ROMK (show KCNJ1 Proteins) may contribute to the suppression of K(+) secretion in the tubules.
Accordingly, medullary WNK4 protein levels were significantly increased in the kidneys of KLHL2 (show KLHL2 Proteins)(-/-) mice. KLHL2 (show KLHL2 Proteins) is indeed a physiological regulator of WNK4 in vivo; however, its function might be different from that of KLHL3 (show KLHL3 Proteins) because KLHL2 (show KLHL2 Proteins) mainly localized in medulla.
The results indicate that quite modest changes in dietary K intake affect plasma [K] and thiazide-sensitive NaCl cotransporter activity. These effects are mediated largely by WNK4, as this kinase exhibits unique Cl-sensitive properties.
the increased NCC (show SLC12A3 Proteins) expression and activation is present in CMA which is highly associated with the enhanced WNK4-SPAK (show STK39 Proteins) signal pathway using WNK4-/- and SPAK (show STK39 Proteins)-/- mice.
increased protein expression levels of WNK1 (show WNK1 Proteins) and WNK4 kinases cause PHAII by KLHL3 (show KLHL3 Proteins) R528H mutation due to impaired KLHL3 (show KLHL3 Proteins)-Cullin3-mediated ubiquitination.
KLHL3 (show KLHL3 Proteins) is phosphorylated at serine 433 in the Kelch domain (a site frequently mutated in hypertension with hyperkalemia) by protein kinase C in cultured cells and that this phosphorylation prevents WNK4 binding and degradation.
WNK4 is the major positive regulator of NCC (show SLC12A3 Proteins) in the kidneys.
WNK1 (show WNK1 Proteins) stimulates the activity of the Na-Cl cotransporter (show SLC12A3 Proteins) via SPAK (show STK39 Proteins), an effect antagonized by WNK4.
in addition to SPAK (show STK39 Proteins) and OSR1 (show OSR1 Proteins), WNK4 is able to anchor itself to the N-terminal domain of NKCC1 (show SLC12A2 Proteins) and to promote cotransporter activation.
SPAK (show STK39 Proteins) deficiency corrects pseudohypoaldosteronism II caused by WNK4 mutation.
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.
WNK lysine deficient protein kinase 4
, protein kinase lysine-deficient 4
, protein kinase with no lysine 4
, serine/threonine-protein kinase WNK4
, protein kinase, lysine deficient 4
, WNK4 Ser/Thr kinase
, protein kinase, lysine-deficient 4