WNK Lysine Deficient Protein Kinase 4 (WNK4) ELISA Kits

WNK4 encodes a member of the WNK family of serine-threonine protein kinases. Additionally we are shipping WNK4 Antibodies (68) and WNK4 Proteins (5) and many more products for this protein.

list all ELISA KIts Gene Name GeneID UniProt
Anti-Human WNK4 WNK4 65266 Q96J92
Anti-Mouse WNK4 WNK4 69847 Q80UE6
Anti-Rat WNK4 WNK4 287715 Q7TPK6
How to order from antibodies-online
  • +1 877 302 8632
  • +1 888 205 9894 (toll-free)
  • Order online
  • orders@antibodies-online.com

More ELISA Kits for WNK4 Interaction Partners

Human WNK Lysine Deficient Protein Kinase 4 (WNK4) interaction partners

  1. This study provides substantial new insights into the role of phosphorylation of KLHL3 in regulating the interaction with WNK4

  2. 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.

  3. 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.

  4. this meta-analysis suggested that WNK4 G1155942T and C6749T gene polymorphisms may contribute to the susceptibility and development of hypertension.

  5. Akt (show AKT1 ELISA Kits) and PKA phosphorylated KLHL3 at S433, and phosphorylation of KLHL3 by PKA inhibited WNK4 degradation.

  6. 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)

  7. WNK4 inhibits SNARE (show NAPA ELISA Kits) formation of syntaxin 13 (show STX12 ELISA Kits) with VAMP2 (show VAMP2 ELISA Kits).

  8. Regulation of WNK4 by CUL3 (show CUL3 ELISA Kits) and its relationship to blood pressure regulation and electrolyte homeostasis. [Review]

  9. WNK4 inhibits Large-conductance, Ca(2 )-activated K( ) channel activity, in part, by increasing channel degradation through an ubiquitin-dependent pathway.

  10. 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

Mouse (Murine) WNK Lysine Deficient Protein Kinase 4 (WNK4) interaction partners

  1. However, phosphorylation of SPAK (show STK39 ELISA Kits) and NCC (show SLC12A3 ELISA Kits) at distal convoluted tubules were almost completely absent even in WNK4(-/-)KLHL3(R528H/R528H) mice. In conclusion, increased WNK1 (show WNK1 ELISA Kits) was unable to compensate for WNK4 deficiency and phosphorylate the NCC (show SLC12A3 ELISA Kits), indicating that WNK4 is indispensable for the onset of PHAII.

  2. ENaC (show SCNN1A ELISA Kits) and ROMK (show KCNJ1 ELISA Kits) channel activity in kidney tubules are inhibited in TgWnk4(pseudoaldosteronism type II) mice. Wnk4(PHAII)-induced inhibition of ENaC (show SCNN1A ELISA Kits) and ROMK (show KCNJ1 ELISA Kits) may contribute to the suppression of K(+) secretion in the tubules.

  3. Accordingly, medullary WNK4 protein levels were significantly increased in the kidneys of KLHL2(-/-) mice. KLHL2 is indeed a physiological regulator of WNK4 in vivo; however, its function might be different from that of KLHL3 because KLHL2 mainly localized in medulla.

  4. 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.

  5. the increased NCC (show SLC12A3 ELISA Kits) expression and activation is present in CMA which is highly associated with the enhanced WNK4-SPAK (show STK39 ELISA Kits) signal pathway using WNK4-/- and SPAK (show STK39 ELISA Kits)-/- mice.

  6. increased protein expression levels of WNK1 and WNK4 kinases cause PHAII by KLHL3 R528H mutation due to impaired KLHL3-Cullin3-mediated ubiquitination.

  7. 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.

  8. WNK4 is the major positive regulator of NCC (show SLC12A3 ELISA Kits) in the kidneys.

  9. 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.

  10. 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.

WNK4 Antigen Profile

Antigen Summary

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.

Gene names and symbols associated with WNK4

  • WNK lysine deficient protein kinase 4 (WNK4) antibody
  • WNK lysine deficient protein kinase 4 (Wnk4) antibody
  • 2010002J11Rik antibody
  • Ac2-059 antibody
  • Pha2b antibody
  • Prkwnk4 antibody
  • WNK4 antibody

Protein level used designations for WNK4

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

454699 Pan troglodytes
490959 Canis lupus familiaris
100139742 Bos taurus
100617641 Monodelphis domestica
65266 Homo sapiens
69847 Mus musculus
287715 Rattus norvegicus
Did you look for something else?