Render Target: STATIC
Render Timestamp: 2024-11-05T09:42:31.645Z
Commit: 57f6e368eba1a427377652f2ad915d45d7f340a4
XML generation date: 2024-08-01 15:24:22.032
Product last modified at: 2024-10-22T16:00:10.407Z
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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464

WNK4 Antibody #5713

Filter:
  • WB

    Supporting Data

    REACTIVITY H M R Dg
    SENSITIVITY Endogenous
    MW (kDa) 135-140
    SOURCE Rabbit
    Application Key:
    • WB-Western Blotting 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 
    • Dg-Dog 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    WNK4 Antibody detects endogenous levels of total WNK4 protein.

    Species Reactivity:

    Human, Mouse, Rat, Dog

    The antigen sequence used to produce this antibody shares 100% sequence homology with the species listed here, but reactivity has not been tested or confirmed to work by CST. Use of this product with these species is not covered under our Product Performance Guarantee.

    Species predicted to react based on 100% sequence homology:

    Bovine

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a sythetic peptide corresponding to residues surrounding Lys59 of human WNK4. Antibodies were purified by protein A and peptide affinity chromatography.

    Background

    The WNK [with no lysine (K)] family of serine/threonine kinases is characterized by having a cysteine in place of lysine in subdomain II of its kinase activation domain (1,2). The lysine necessary for phosphoryl transfer is located in an atypical position in the catalytic domain. Four WNK family members have been identified in humans (WNK1-4) and have been implicated in regulating ion permeability (3). Mutations in the WNK1 and WNK4 genes in humans cause pseudohypoaldosteronism type II (PHAII), an autosomal dominant disorder leading to hypertension, hyperkalemia, and renal tubular acidosis (4). WNK4 is specifically expressed in the kidney, whereas WNK1 has a wider distribution but is predominantly expressed in polarized epithelia (1-3). Heterozygous Wnk1 mutations in mice result in a significant decrease in blood pressure, while homozygous mutations are embryonic lethal (5). WNK1 is phosphorylated by Akt at Thr60 (6). In addition, WNK1 may be autophosphorylated at Ser382 in the activation loop, which is thought to be required for its kinase activity (7).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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