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ZIP14/SLC39A14 (E3H7D) Rabbit Monoclonal Antibody #24161

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  • WB
  • IP
  • IF

    Product Specifications

    REACTIVITY H M R Mk
    SENSITIVITY Endogenous
    MW (kDa) 55-65
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    • IF-Immunofluorescence 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 
    • Mk-Monkey 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:50
    Immunofluorescence (Immunocytochemistry) 1:800 - 1:1600

    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

    ZIP14/SLC39A14 (E3H7D) Rabbit Monoclonal Antibody recognizes endogenous levels of total ZIP14/SLC39A14 protein.

    Species Reactivity:

    Human, Mouse, Rat, Monkey

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Leu282 of human ZIP14/SLC39A14 protein.

    Background

    Solute carrier (SLC) family member Zrt- and Irt-like protein 14 (ZIP14) is a transmembrane metal ion symporter encoded by the gene SLC39A14. ZIP14 functions as a plasma membrane transporter of zinc and manganese, and as an endosomal promoter of intracellular uptake of iron from transferrin (1). In liver, ZIP14 localizes to the basolateral membrane of hepatocytes, transporting manganese from the blood for eventual delivery to the bile duct (2). In pancreatic beta cells, SLC39A14 expression is glucose-sensitive and plays a key role in zinc-dependent insulin secretion (3).

    The reported ZIP14 L441R mutation (L438R in mice) disrupts plasma membrane presentation of the transporter, causing intracellular accumulation of zinc in osteoblasts, characterized by excessive bone overgrowth (4).

    SLC39A14 mutation or knockdown can cause manganese dyshomeostasis, resulting in childhood-onset dystonia-Parkinsonism (5). The activity of liver-expressed ZIP14/SLC39A14, intestinal SLC39A10, and blood-brain barrier ZIP8/SLC39A8 all contribute to manganese homeostasis during neuronal development (6,7).

    Alternate Names

    cig19; HCIN; HMNDYT2; KIAA0062; LIV-1 subfamily of ZIP zinc transporter 4; LZT-Hs4; Metal cation symporter ZIP14; NET34; S39AE; SLC39A14; solute carrier family 39 (metal ion transporter), member 14; solute carrier family 39 (zinc transporter), member 14; Solute carrier family 39 member 14; Zinc transporter ZIP14; ZIP-14; ZIP14; Zrt- and Irt-like protein 14; Zrt-, Irt-like protein 14

    For Research Use Only. Not for Use in Diagnostic Procedures.
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