Home Primary Antibodies SLC12A3 Antibody [G5P18]

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SLC12A3 Antibody [G5P18]

Cat.No.: F4003

    Application: Reactivity:
    • F4003-wb
      Lane 1: Mouse kidney

    Usage Information

    Dilution
    1:1000
    1:100
    Application
    WB, IHC
    Reactivity
    Human, Mouse, Rat
    Source
    Rabbit Monoclonal Antibody
    Storage Buffer
    PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3
    Storage (from the date of receipt)
    -20°C (avoid freeze-thaw cycles), 2 years
    Predicted MW Observed MW
    113 kDa 150 kDa,36 kDa
    *Why do the predicted and actual molecular weights differ?
    The following reasons may explain differences between the predicted and actual protein molecular weight.
    Post-translational modifications(e.g., phosphorylation, glycosylation); Splice variants and isoforms; Relative charge; Multimerization.

    Datasheet & SDS

    Biological Description

    Specificity
    SLC12A3 Antibody [G5P18] detects endogenous levels of total SLC12A3 protein.
    Clone
    G5P18
    Synonym(s)
    NCC; TSC; SLC12A3; Solute carrier family 12 member 3; Na-Cl cotransporter; Na-Cl symporter; Thiazide-sensitive sodium-chloride cotransporter
    Background
    SLC12A3, encoding the thiazide-sensitive Na-Cl cotransporter (NCC) within the SLC12 cation-chloride cotransporter family, mediates electroneutral apical sodium and chloride reabsorption exclusively in the distal convoluted tubule to fine-tune renal salt excretion and maintain extracellular volume. NCC operates through an alternating access mechanism where conserved transmembrane helices coordinate Na+ and Cl- binding in outward-open conformation, undergoing WNK kinase-dependent phosphorylation at the C-terminal regulatory domain that relieves autoinhibition and recruits 14-3-3 scaffolds to stabilize plasma membrane residency; SPAK/OSR1 kinases activated by upstream WNK1/4 sensing low intracellular Cl- phosphorylate NCC at critical serines/threonines, doubling transport velocity while trafficking motifs govern basolateral recycling via endosomal sorting. This pathway integrates dietary salt variation with hormonal fine-tuning, where angiotensin II sustains NCC via AT1R-PLCβ-PKC cascade, while aldosterone indirectly amplifies through serum/glucocorticoid kinase activation of NCC phosphorylation cascades. NCC handles 5-10% of filtered sodium load as the final rheostat preventing natriuresis under hypovolemia, positioning it as the primary thiazide target for hypertension management and essential readout for researchers modeling tubulopathy in kidney organoids or quantifying phosphoregulation via tubule-specific phosphoantibodies. Inactivating mutations disrupt folding/trafficking, causing Gitelman syndrome with profound salt wasting, hypokalemic alkalosis, hypomagnesemia, and secondary hyperaldosteronism that paradoxically lowers blood pressure through volume contraction.
    References
    • https://pubmed.ncbi.nlm.nih.gov/24310820/
    • https://pubmed.ncbi.nlm.nih.gov/27872838/

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