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WNK4 encodes a member of the WNK family of serine-threonine protein kinases. Zusätzlich bieten wir Ihnen WNK4 Proteine (6) und viele weitere Produktgruppen zu diesem Protein an.
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Human Polyclonal WNK4 Primary Antibody für EM, IHC - ABIN153223
Wilson, Disse-Nicodème, Choate, Ishikawa, Nelson-Williams, Desitter, Gunel, Milford, Lipkin, Achard, Feely, Dussol, Berland, Unwin, Mayan, Simon, Farfel, Jeunemaitre, Lifton: Human hypertension caused by mutations in WNK kinases. in Science (New York, N.Y.) 2001
Zeige alle 7 Referenzen für 153223
This study provides substantial new insights into the role of phosphorylation of KLHL3 (zeige KLHL3 Antikörper) 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 Antikörper) and PKA phosphorylated KLHL3 (zeige KLHL3 Antikörper) at S433, and phosphorylation of KLHL3 (zeige KLHL3 Antikörper) by PKA inhibited WNK4 degradation.
WNK4 is a substrate of SFKs and the association of c-Src (zeige SRC Antikörper) and PTP-1D (zeige PTPN11 Antikörper) with WNK4 at Tyr (zeige TYR Antikörper)(1092) and Tyr (zeige TYR Antikörper)(1143) plays an important role in modulating the inhibitory effect of WNK4 on ROMK (zeige KCNJ1 Antikörper)
WNK4 inhibits SNARE (zeige NAPA Antikörper) formation of syntaxin 13 (zeige STX12 Antikörper) with VAMP2 (zeige VAMP2 Antikörper).
Regulation of WNK4 by CUL3 (zeige CUL3 Antikörper) 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 (zeige KLHL3 Antikörper) show less ability to ubiquitinate WNK4 because of KLHL3 (zeige KLHL3 Antikörper)'s low stability and/or decreased binding to CUL3 (zeige CUL3 Antikörper) or WNK4
However, phosphorylation of SPAK (zeige STK39 Antikörper) and NCC (zeige SLC12A3 Antikörper) at distal convoluted tubules were almost completely absent even in WNK4(-/-)KLHL3 (zeige KLHL3 Antikörper)(R528H/R528H) mice. In conclusion, increased WNK1 (zeige WNK1 Antikörper) was unable to compensate for WNK4 deficiency and phosphorylate the NCC (zeige SLC12A3 Antikörper), indicating that WNK4 is indispensable for the onset of PHAII.
ENaC (zeige SCNN1A Antikörper) and ROMK (zeige KCNJ1 Antikörper) channel activity in kidney tubules are inhibited in TgWnk4(pseudoaldosteronism type II) mice. Wnk4(PHAII)-induced inhibition of ENaC (zeige SCNN1A Antikörper) and ROMK (zeige KCNJ1 Antikörper) 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 Antikörper)(-/-) mice. KLHL2 (zeige KLHL2 Antikörper) is indeed a physiological regulator of WNK4 in vivo; however, its function might be different from that of KLHL3 (zeige KLHL3 Antikörper) because KLHL2 (zeige KLHL2 Antikörper) 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 Antikörper) expression and activation is present in CMA which is highly associated with the enhanced WNK4-SPAK (zeige STK39 Antikörper) signal pathway using WNK4-/- and SPAK (zeige STK39 Antikörper)-/- mice.
increased protein expression levels of WNK1 (zeige WNK1 Antikörper) and WNK4 kinases cause PHAII by KLHL3 (zeige KLHL3 Antikörper) R528H mutation due to impaired KLHL3 (zeige KLHL3 Antikörper)-Cullin3-mediated ubiquitination.
KLHL3 (zeige KLHL3 Antikörper) is phosphorylated at serine 433 in the Kelch domain (a site frequently mutated in hypertension with hyperkalemia) by protein kinase C (zeige PKC Antikörper) in cultured cells and that this phosphorylation prevents WNK4 binding and degradation.
WNK4 is the major positive regulator of NCC (zeige SLC12A3 Antikörper) in the kidneys.
WNK1 (zeige WNK1 Antikörper) stimulates the activity of the Na-Cl cotransporter (zeige SLC12A3 Antikörper) via SPAK (zeige STK39 Antikörper), an effect antagonized by WNK4.
in addition to SPAK (zeige STK39 Antikörper) and OSR1 (zeige OSR1 Antikörper), WNK4 is able to anchor itself to the N-terminal domain of NKCC1 (zeige SLC12A2 Antikörper) and to promote cotransporter activation.
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