R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.
ZIP14/SLC39A14 (E3H7D) Rabbit mAb #24161
Filter:
- WB
- IP
- IF
Supporting Data
| 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 mAb 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).
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).
- Zhao, N. et al. (2010) J Biol Chem 285, 32141-50.
- McCabe, S. et al. (2023) Comput Struct Biotechnol J 21, 2332-2338.
- Maxel, T. et al. (2019) Sci Rep 9, 8589.
- Hendrickx, G. et al. (2018) PLoS Genet 14, e1007321.
- Tuschl, K. et al. (2016) Nat Commun 7, 11601.
- Hutchens, S. et al. (2023) Am J Physiol Gastrointest Liver Physiol 325, G251-G264.
- Liu, Q. et al. (2023) J Biol Chem 299, 105078.
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For Research Use Only. Not For Use In Diagnostic Procedures.
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