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WNK4 encodes a member of the WNK family of serine-threonine protein kinases. Zusätzlich bieten wir Ihnen WNK4 Antikörper (74) und viele weitere Produktgruppen zu diesem Protein an.
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5 WNK4 sites (S47, S64, S1169, S1180, S1196) are phosphorylated downstream of AngII signaling in cultured cells and in vitro by PKC (zeige PRRT2 Proteine) and PKA. Phosphorylation at S64 and S1196 promoted phosphorylation of the WNK4 kinase T-loop at S332 (required for kinase activation) and increased phosphorylation of SPAK (zeige STK39 Proteine). Volume depletion induced phosphorylation of these sites in vivo, predominantly in the distal convoluted tubule.
Modulation of WNK4 activity by [Cl]i can account for its dual role on the NCC (zeige SLC12A3 Proteine), and this has important physiological implications regarding the regulation of extracellular potassium concentration.
This study provides substantial new insights into the role of phosphorylation of KLHL3 (zeige KLHL3 Proteine) 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 (zeige AKT1 Proteine) and PKA phosphorylated KLHL3 (zeige KLHL3 Proteine) at S433, and phosphorylation of KLHL3 (zeige KLHL3 Proteine) by PKA inhibited WNK4 degradation.
WNK4 is a substrate of SFKs and the association of c-Src (zeige SRC Proteine) and PTP-1D (zeige PTPN11 Proteine) with WNK4 at Tyr (zeige TYR Proteine)(1092) and Tyr (zeige TYR Proteine)(1143) plays an important role in modulating the inhibitory effect of WNK4 on ROMK (zeige KCNJ1 Proteine)
WNK4 inhibits SNARE (zeige NAPA Proteine) formation of syntaxin 13 (zeige STX12 Proteine) with VAMP2 (zeige VAMP2 Proteine).
Regulation of WNK4 by CUL3 (zeige CUL3 Proteine) and its relationship to blood pressure regulation and electrolyte homeostasis. [Review]
reduced age-dependent weight gain of WNK1 (zeige WNK1 Proteine) TG mice seems to be related with the decreased Kir6.2 (zeige KCNJ11 Proteine) expression via WNK1 (zeige WNK1 Proteine)- and WNK4-regulated protein stability of Kir6.2 (zeige KCNJ11 Proteine).
WNK4 protein affected the DNA-binding ability of C/EBPbeta (zeige CEBPB Proteine) and thereby reduced PPARgamma (zeige PPARG Proteine) expression. In the WNK4(-/-) mice, PPARgamma (zeige PPARG Proteine) and C/EBPalpha (zeige CEBPA Proteine) expression were decreased in adipose tissues, and the mice exhibited partial resistance to high-fat diet-induced adiposity.
However, phosphorylation of SPAK (zeige STK39 Proteine) and NCC (zeige SLC12A3 Proteine) at distal convoluted tubules were almost completely absent even in WNK4(-/-)KLHL3 (zeige KLHL3 Proteine)(R528H/R528H) mice. In conclusion, increased WNK1 (zeige WNK1 Proteine) was unable to compensate for WNK4 deficiency and phosphorylate the NCC (zeige SLC12A3 Proteine), indicating that WNK4 is indispensable for the onset of PHAII.
ENaC (zeige SCNN1A Proteine) and ROMK (zeige KCNJ1 Proteine) channel activity in kidney tubules are inhibited in TgWnk4(pseudoaldosteronism type II) mice. Wnk4(PHAII)-induced inhibition of ENaC (zeige SCNN1A Proteine) and ROMK (zeige KCNJ1 Proteine) may contribute to the suppression of K(+) secretion in the tubules.
Accordingly, medullary WNK4 protein levels were significantly increased in the kidneys of KLHL2 (zeige KLHL2 Proteine)(-/-) mice. KLHL2 (zeige KLHL2 Proteine) is indeed a physiological regulator of WNK4 in vivo; however, its function might be different from that of KLHL3 (zeige KLHL3 Proteine) because KLHL2 (zeige KLHL2 Proteine) 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 (zeige SLC12A3 Proteine) expression and activation is present in CMA which is highly associated with the enhanced WNK4-SPAK (zeige STK39 Proteine) signal pathway using WNK4-/- and SPAK (zeige STK39 Proteine)-/- mice.
increased protein expression levels of WNK1 (zeige WNK1 Proteine) and WNK4 kinases cause PHAII by KLHL3 (zeige KLHL3 Proteine) R528H mutation due to impaired KLHL3 (zeige KLHL3 Proteine)-Cullin3-mediated ubiquitination.
KLHL3 (zeige KLHL3 Proteine) 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 (zeige SLC12A3 Proteine) in the kidneys.
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