Product Description
Size: 5µg / 10µg
Recombinant mouse WNK4 protein is a Mouse Fragment protein, in the 1 to 441 aa range, expressed in Baculovirus infected Sf9 cells, with >85%, suitable for SDS-PAGE, FuncS.
Key facts
Purity:>85% Densitometry,
Expression system:Baculovirus infected Sf9 cells,
Tags:GST tag N-Terminus,
Applications:FuncS, SDS-PAGESee reactivity dataSee the reactivity data table below for information on validated species and application combinations.,
Biologically active:Yes,
Biological activity:The specific activity of ab206027 was determined to be 1.5 nmol/min/mg.,
Accession:Q80UE6,
Animal free:No,
Carrier free:No,
Species:Mouse,
Storage buffer:pH: 7.5Constituents: 25% Glycerol (glycerin, glycerine), 0.87% Sodium chloride, 0.79% Tris HCl, 0.31% Glutathione, 0.004% (R*,R*)-1,4-Dimercaptobutan-2,3-diol, 0.003% EDTA, 0.002% PMSF
Properties and Storage Information:
Shipped at conditions-Dry Ice, Appropriate short-term storage conditions--80°C, Appropriate long-term storage conditions--80°C, Aliquoting information-Upon delivery aliquot, Storage information-Avoid freeze / thaw cycle
Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
WNK4 also known as With No Lysine [K] Kinase 4 is a serine/threonine-protein kinase weighing approximately 135 kDa. Mechanically WNK4 plays a role in regulating the activity of ion channels and transporters especially those involved in the transport of sodium potassium and chloride ions. It is widely expressed in the kidney particularly in the distal convoluted tubules and connecting tubules where it modulates ion balance across cell membranes.
Biological function summary
WNK4 is important in maintaining electrolyte homeostasis and blood pressure regulation. It acts as a central regulator in maintaining sodium and potassium balance influencing channels like the sodium chloride co-transporter (NCC) and the epithelial sodium channel (ENaC). WNK4 often functions as part of complexes that include other kinases like WNK1 and WNK3 which modulate its activity and function.
Pathways
WNK4 is integral to the signaling cascades that control renal sodium and potassium excretion mostly through the WNK-SPAK/OSR1-NCC pathway. In this pathway WNK4 influences the activity of SPAK and OSR1 which subsequently affects NCC. Additionally WNK4 interacts with other proteins such as KLHL3 and CUL3 acting as regulators of ion transport and blood pressure.
WNK4 mutations link to pseudohypoaldosteronism type II (PHAII) a genetic disorder causing hyperkalemia and hypertension. Aberrant WNK4 activity can alter ion channel regulation contributing to the pathology of hypertension through its interaction with proteins like NCC. Disruption in WNK4 signaling and expression mediated by mutations or environmental factors provides insight into the development and potential treatment of hypertension.
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Collaboration
Tony Tang
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