mProX™ Human WNK4 Stable Cell Line

Sub Cat	Product Name	Target Protein Species	Host Cell Type	Assay Types	Inquiry	Datasheet
S01YF-1222-KX528	Magic™ Human WNK4 in Vitro Assay	Human		Kinase Assay

Product Information

Target Family

Kinases/Enzyme

Target Protein Species

Human

Host Cell Type

HEK293;CHO-K1;DLD-1

Target Classification

Kinase Cell Lines

Target Research Area

Cardiovascular Research

Related Diseases

Pseudohypoaldosteronism, Type Iib; Pseudohypoaldosteronism

Gene ID

Human:65266

UniProt ID

Human:Q96J92

Product Properties

Biosafety Level

Level 1

Activity

Yes

Quantity

10⁶ cells per vial

Applications

The applications of WNK4 include its association with familial hyperkalemia and hypertension (FHHt), proximal renal tubular acidosis, and epileptic seizures. WNK4 mutations have been identified in individuals with FHHt, and the mechanism of hyperchloremic acidosis in FHHt is believed to involve the proximal renal tubule. Additionally, the activation of the WNK4-SPAK pathway through the calcium-sensing receptor (CaSR) has implications in renal salt handling and the regulation of sodium chloride cotransporter (NCC) activity. The degradation of WNK4 by KLHL3-CUL3 E3 ligase is affected by potassium levels, and the neddylation and autophagy pathway may play a role in this process. Furthermore, a novel KLHL3-interacting motif in the C-terminal region of WNK4 has been identified, which may contribute to the degradation of WNK4 by KLHL3. Finally, pseudohypoaldosteronism type II (PHAII), which is associated with WNK4 mutations, has been classified as type IV renal tubular acidosis based on laboratory findings.

Protocols

Please visit our protocols page.

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FAQ

chat Taylor Williams (Verified Customer)

How does WNK4 influence acute respiratory distress syndrome (ARDS)? Jun 30 2022

chat Patrick Liam (Creative Biolabs Scientific Support)

WNK4 plays a role in improving alveolar fluid clearance in ARDS, primarily through the upregulation of the epithelial sodium channel (ENaC). Jun 30 2022

chat Taylor Miller (Verified Customer)

What is the role of WNK4 in familial hyperkalemic hypertension (FHHt)? Jun 01 2023

chat Patrick Liam (Creative Biolabs Scientific Support)

WNK4 is implicated in the pathogenesis of FHHt, with its activation leading to hyperkalemia [2]. Jun 01 2023

Published Data

Fig.1 Conducting a Western blot analysis to examine the levels of endogenous β-Catenin after suppressing WNK1 and/or WNK4 expression in DLD1 cells.

Analysis through Western blotting was conducted to assess the impact of WNK1 and WNK4 knockdown on endogenous β-Catenin levels in DLD1 cells. The simultaneous depletion of both WNK1 and WNK4 resulted in a notable decrease in β-Catenin levels in not only DLD1 cells but also HCT116 cells.

Ref: Sato, Atsushi, et al. "WNK regulates Wnt signalling and β-Catenin levels by interfering with the interaction between β-Catenin and GID." Communications biology 3.1 (2020): 666.

Pubmed: 33184430

DOI: 10.1038/s42003-020-01386-2

Research Highlights

Shirin, Neta. et al. "Association of Familial Hyperkalemia and Hypertension (FHHt) with proximal renal tubular acidosis and epileptic seizures." Nephron, 2023.
The inherited disease Familial Hyperkalemic Hypertension (FHHt) is characterized by high levels of potassium, hypertension, and acidic blood caused by a hyperactive sodium chloride co-transporter in the renal distal tubule. Mutations in WNK1, WNK4, KLHL3, or Cul3 can lead to FHHt. However, the exact mechanism for the hyperchloremic acidosis seen in FHHt is not fully understood. This study aims to investigate the underlying cause of this acidosis. Analysis of the genetic mutations and other factors that contribute to FHHt may provide new insights into its pathogenesis.
Shirin, Neta. et al. "Association of Familial Hyperkalemia and Hypertension (FHHt) with proximal renal tubular acidosis and epileptic seizures." Nephron, 2023.
Pubmed: 37666233 DOI: 10.1159/000531868

Chávez-Canales, María, Janeth Alejandra García, and Gerardo Gamba. "Regulation of the WNK4-SPAK-NCC pathway by the calcium-sensing receptor." Current Opinion in Nephrology and Hypertension 32.5 (2023): 451-457.
The regulation of the sodium chloride cotransporter (NCC) in the distal convoluted tubule (DCT) is essential for maintaining proper salt balance in the kidneys. Recent studies have revealed that the calcium-sensing receptor (CaSR) is responsible for activating NCC through the WNK4-SPAK pathway, which operates independently of the Renin-Angiotensin-Aldosterone system. This review explores the latest findings on the mechanism by which CaSR controls NCC activity through the WNK4-SPAK pathway and its potential implications for both physiological and therapeutic purposes.
Chávez-Canales, María, Janeth Alejandra García, and Gerardo Gamba. "Regulation of the WNK4-SPAK-NCC pathway by the calcium-sensing receptor." Current Opinion in Nephrology and Hypertension 32.5 (2023): 451-457.
Pubmed: 37530086 DOI: 10.1097/MNH.0000000000000915