mProX™ Human WNK2 Stable Cell Line

Sub Cat	Product Name	Target Protein Species	Host Cell Type	Assay Types	Inquiry	Datasheet
S01YF-1222-KX526	Magic™ Human WNK2 in Vitro Assay	Human		Kinase Assay

Product Information

Target Family

Kinases/Enzyme

Target Protein Species

Human

Host Cell Type

HEK293;CHO-K1;HT29

Target Classification

Kinase Cell Lines

Target Research Area

Metabolic Research

Related Diseases

Hypomagnesemia 4, Renal; Suprasellar Meningioma

Gene ID

Human:65268

UniProt ID

Human:Q9Y3S1

Product Properties

Biosafety Level

Level 1

Activity

Yes

Quantity

10⁶ cells per vial

Applications

WNK2 (With no Lysine [K] kinase 2) has various applications in different fields. In the field of ion homeostasis and cell volume regulation, overactivation of WNK2 can lead to pseudohypoaldosteronism type II (Gordon syndrome) characterized by hyperkalemia and high blood pressure. WNK2 has also been shown to be required for the development of the nervous system in mice, zebrafish, and flies, as well as the cardiovascular system of mice and fish. Additionally, WNK2 and its homolog in Drosophila (Wnk) modulate canonical Wnt signaling. The C-terminal domain of WNK2, which has been shown to promote phase transitions in cell culture, is required for viability in vivo. Furthermore, WNK2 has been identified as a potential germline mutation associated with serrated polyposis syndrome, and it has been implicated in the progression of clear cell renal carcinoma. These findings suggest that WNK2 plays diverse roles in various biological processes and diseases, making it a promising target for further research and potential therapeutic interventions.

Protocols

Please visit our protocols page.

Customer Reviews

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FAQ

chat Skyler Brown (Verified Customer)

Could WNK2 mutations be associated with serrated polyposis syndrome? Sep 05 2021

chat Patrick Liam (Creative Biolabs Scientific Support)

Germline mutations in WNK2 have been identified in cases of serrated polyposis syndrome, suggesting a potential association. Sep 05 2021

chat Casey Johnson (Verified Customer)

How does WNK2 affect ovarian cancer progression? Nov 06 2021

chat Patrick Liam (Creative Biolabs Scientific Support)

WNK2 is targeted by microRNA-324-3p, which suppresses ovarian cancer progression by inhibiting the WNK2/RAS pathway. Nov 06 2021

Published Data

Fig.1 Knockdown WNK2 in HT-29 cells.

In assessing the specificity of the protein band identified by the anti-WNK2 serum, HT29 cells underwent transfection with either a control small interfering RNA (siGFP) or two distinct WNK2-specific small interfering RNAs (siRNAs). After 24 hours post-transfection, the presence of WNK2 was examined using both western blot analysis (top panels) and RT-PCR (bottom panels).

Ref: Moniz, S., et al. "Protein kinase WNK2 inhibits cell proliferation by negatively modulating the activation of MEK1/ERK1/2." Oncogene 26.41 (2007): 6071-6081.

Pubmed: 17667937

DOI: 10.1038/sj.onc.1210706

Research Highlights

Yarikipati, Prathibha. et al. "Unanticipated domain requirements for Drosophila Wnk kinase in vivo." PLoS genetics, 2023.
The role of WNK (With no Lysine [K]) kinases has been widely studied and are known to play a critical role in maintaining ion homeostasis and regulating cell volume. However, overactivation of these kinases leads to pseudohypoaldosteronism type II (Gordon syndrome), a medical condition characterized by high blood pressure and hyperkalemia. More recent studies have shown that WNK family members are also necessary for proper development of the nervous and cardiovascular systems in mice, zebrafish, and flies. Additionally, it has been discovered that WNK2 in humans and Drosophila Wnk are involved in modulating canonical Wnt signaling.
Yarikipati, Prathibha. et al. "Unanticipated domain requirements for Drosophila Wnk kinase in vivo." PLoS genetics, 2023.
Pubmed: 37819975 DOI: 10.1371/journal.pgen.1010975

L Stockley, Tracy. et al. "CANTRK: A Canadian Ring Study to Optimize Detection of NTRK Gene Fusions by Next-Generation RNA Sequencing." The Journal of molecular diagnostics : JMD, 2023.
The Canadian NTRK (CANTRK) study was conducted as an interlaboratory comparison ring study in order to optimize the testing for neurotrophic receptor tyrosine kinase (NTRK) fusions among Canadian laboratories. Sixteen diagnostic laboratories participated by utilizing next-generation sequencing (NGS) for the detection of NTRK1, NTRK2, or NTRK3 fusions. Each laboratory was provided with 12 formalin-fixed, paraffin-embedded tumor samples containing unique NTRK fusions, as well as two control samples (one ALK and one ROS1). All laboratories followed validated protocols for NGS fusion detection, including the use of various panels such as Oncomine Comprehensive Assay v3, Oncomine Focus Assay, Oncomine Precision Assay, AmpliSeq for Illumina Focus, TruSight RNA Pan-Cancer Panel, FusionPlex Lung, and QIAseq Multimodal Lung. One sample had to be excluded from analysis due to sample quality issues. Out of the remaining 13 samples, 6 of the 11 NTRK fusions and both control fusions were successfully detected by all laboratories. However, two fusions (WNK2::NTRK2 and STRN3::NTRK2) were not detected by 10 laboratories using the Oncomine Comprehensive or Focus panels, as these panels did not contain WNK2 and STRN3 in their designs. Additionally, two challenging fusions (TPM3::NTRK1 and LMNA::NTRK1) were found to have bioinformatics issues when using the AmpliSeq for Illumina Focus panel. One laboratory also had difficulty detecting a low-level ETV6::NTRK3 fusion using the TruSight Pan-Cancer Panel. Panels that were able to detect all fusions included FusionPlex Lung, Oncomine Precision, and QIAseq Multimodal Lung. Overall, the CANTRK study demonstrated the competency of Canadian laboratories in detecting NTRK fusions by NGS using various panels, and also identified some key areas for improvement in NTRK fusion testing.
L Stockley, Tracy. et al. "CANTRK: A Canadian Ring Study to Optimize Detection of NTRK Gene Fusions by Next-Generation RNA Sequencing." The Journal of molecular diagnostics : JMD, 2023.
Pubmed: 36586421 DOI: 10.1016/j.jmoldx.2022.12.004