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Home >Products> Reagents >Antibody> LIV-1/SLC39A6 Recombinant Rabbit mAb (SDT-206-84)
LIV-1/SLC39A6 Recombinant Rabbit mAb (SDT-206-84)
LIV-1/SLC39A6 Recombinant Rabbit mAb (SDT-206-84)
Origin of place Singapore
Model S0B0023-10μl
Supplier ANT BIO PTE.LTD.
Price 45
Hits 3
Updated 8/25/2025
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Product Specification


HostRabbit
AntigenLIV-1
SynonymsZinc transporter ZIP6, Estrogen-regulated protein LIV-1, Solute carrier family 39 member 6, Zrt- and Irt-like protein 6, ZIP-6
ImmunogenSynthetic Peptide
LocationCytoplasm, Membrane
AccessionQ13433
Clone NumberSDT-206-84
Antibody TypeRabbit mAb
ApplicationWB, IHC-P
ReactivityHu
Predicted ReactivityOr
PurificationProtein A
Concentration0.5 mg/ml
ConjugationUnconjugated
Physical AppearanceLiquid
Storage Buffer

PBS, 40% Glycerol, 0.05%BSA, 0.03% Proclin 300

Stability & Storage

12 months from date of receipt / reconstitution, -20 °C as supplied

Dilution


applicationdilutionspecies
WB1:1000
IHC-P1:200

Background

Zinc transporter LIV-1 (SLC39A6) is estrogen regulated and present in increased amounts in estrogen receptor-positive breast cancer as well as in tumors that spread to the lymph nodes. The LIV-1 subfamily of ZIP zinc transporters consists of nine human sequences that share considerable homology across transmembrane domains. Many of these sequences have been shown to transport zinc and/or other ions across cell membranes. SLC39A6 is a member of the ZIP family of transporters, which control zinc homeostasis by regulating the influx of zinc from extracellular to intracellular spaces. The zinc transport function of SLC39A6 plays an important role in cellular metabolism. Zinc is required for a variety of cellular processes, including immune activity, protein synthesis, nucleic acid metabolism, cell proliferation, tissue repair and cell division, and low zinc levels can lead to metabolic disorder and inhibit cell growth. Overexpression of SLC39A6 has been related to the progression of several types of cancer, including breast , prostate, pancreatic, cervical and liver cancer, verexpression of SLC39A6 promoted the epithelial-mesenchymal transition (EMT).

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