Render Target: SSR
Render Timestamp: 2024-11-14T23:09:23.477Z
Commit: 3c1f305a63297e594ac8d7bb5424007d592d68be
XML generation date: 2024-10-03 16:01:10.774
Product last modified at: 2024-10-04T07:01:00.821Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77
R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

WNK1 (F1O3U) Rabbit mAb #62054

Filter:
  • WB
  • IHC
  • IF

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 230
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IHC-Immunohistochemistry 
    • IF-Immunofluorescence 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Simple Western™ 1:10 - 1:50
    Immunohistochemistry (Paraffin) 1:200 - 1:800
    Immunofluorescence (Immunocytochemistry) 1:3200 - 1:6400

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/mL BSA, 50% glycerol, and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    WNK1 (F1O3U) Rabbit mAb recognizes endogenous levels of total WNK1 protein.

    Species Reactivity:

    Human

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the amino terminus of human WNK1 protein.

    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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