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WNK4 encodes a member of the WNK family of serine-threonine protein kinases. Additionally we are shipping WNK4 Antibodies (65) and WNK4 Proteins (4) and many more products for this protein.
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 ELISA Kits) and PKA phosphorylated KLHL3 at S433, and phosphorylation of KLHL3 by PKA inhibited WNK4 degradation.
WNK4 is a substrate of SFKs and the association of c-Src (show SRC ELISA Kits) and PTP-1D (show PTPN11 ELISA Kits) with WNK4 at Tyr (show TYR ELISA Kits)(1092) and Tyr (show TYR ELISA Kits)(1143) plays an important role in modulating the inhibitory effect of WNK4 on ROMK (show KCNJ1 ELISA Kits)
WNK4 inhibits SNARE (show NAPA ELISA Kits) formation of syntaxin 13 (show STX12 ELISA Kits) with VAMP2 (show VAMP2 ELISA Kits).
Regulation of WNK4 by CUL3 (show CUL3 ELISA Kits) 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 less ability to ubiquitinate WNK4 because of KLHL3's low stability and/or decreased binding to CUL3 (show CUL3 ELISA Kits) or WNK4
WNK4 inhibits ENaC (show SCNN1A ELISA Kits) channel activity independently of Nedd4-2-mediated ENaC (show SCNN1A ELISA Kits) ubiquitination.
KLHL3 is a substrate adaptor for WNK4 in a ubiquitin E3 ligase complex
increased protein expression levels of WNK1 and WNK4 kinases cause PHAII by KLHL3 R528H mutation due to impaired KLHL3-Cullin3-mediated ubiquitination.
KLHL3 is phosphorylated at serine 433 in the Kelch domain (a site frequently mutated in hypertension with hyperkalemia) by protein kinase C (show PKC ELISA Kits) in cultured cells and that this phosphorylation prevents WNK4 binding and degradation.
WNK4 is the major positive regulator of NCC (show SLC12A3 ELISA Kits) in the kidneys.
WNK1 (show WNK1 ELISA Kits) stimulates the activity of the Na-Cl cotransporter (show SLC12A3 ELISA Kits) via SPAK (show STK39 ELISA Kits), an effect antagonized by WNK4.
in addition to SPAK (show STK39 ELISA Kits) and OSR1 (show OSR1 ELISA Kits), WNK4 is able to anchor itself to the N-terminal domain of NKCC1 (show SLC12A2 ELISA Kits) and to promote cotransporter activation.
SPAK (show STK39 ELISA Kits) deficiency corrects pseudohypoaldosteronism II caused by WNK4 mutation.
Activation of the renal Na+:Cl- cotransporter by angiotensin II is a WNK4-dependent process.
data suggest that WNK4 inhibits NCC (show SLC12A3 ELISA Kits) protein through activating the MAPK (show MAPK1 ELISA Kits) ERK1/2 (show MAPK1/3 ELISA Kits) signaling pathway.
these results suggest that these PHAII-causing mutations disrupt a Ca(2 (show CA2 ELISA Kits)+)-sensing mechanism around the acidic motif necessary for the regulation of WNK4 kinase activity by Ca(2 (show CA2 ELISA Kits)+) ions.
Immunolocalization of WNK4 in mouse kidney.
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