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Key Documents

SAB3500603

Sigma-Aldrich

Anti-ZIP14 antibody produced in rabbit

affinity isolated antibody, buffered aqueous solution

Synonym(s):

Anti-LZT-Hs4, Anti-NET34, Anti-SLC39A14, Anti-Slc39A14, Anti-Solute carrier family 39 member A14

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

predicted mol wt 54 kDa

species reactivity

human, mouse, rat

technique(s)

ELISA: suitable
immunofluorescence: suitable
immunohistochemistry: suitable
western blot: suitable

NCBI accession no.

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

General description

Solute carrier family 39 member 14 or Zrt- and Irt-like protein 14 (ZIP14), a transmembrane metal ion transporter, is a member of the LIV-1 subfamily. It contains eight transmembrane domains (TMDs), a metalloprotease, and a histidine-rich motif. ZIP14 is majorly expressed in the pancreas, liver, and heart. The ZIP14 gene is mapped to human chromosome 8p21.3.

Immunogen

ZIP14 antibody was raised against a 16 amino acid peptide near the center of human ZIP14.

Application

Anti-ZIP14 antibody produced in rabbit has been used in immunoblotting. 1:2500

Biochem/physiol Actions

Zrt- and Irt-like protein 14 (ZIP14) is a divalent metal transporter specific for zinc (Zn). However, some studies report, it also mediates the transport of manganese (Mn), iron (Fe), and cadmium (Cd). ZIP14 along with ZIP8 are prime Mn2+ importers of the brain′s capillary bed and in human brain microvascular endothelial cells (HBMVEC) in in vitro conditions. Mutations in the ZIP14 gene lead to manganese dyshomeostasis, which in turn results in manganese accumulation in childhood-onset parkinsonism–dystonia patients.

Features and Benefits

Evaluate our antibodies with complete peace of mind. If the antibody does not perform in your application, we will issue a full credit or replacement antibody. Learn more.

Linkage

The action of this antibody can be blocked using blocking peptide SBP3500603.

Physical form

Supplied in PBS with 0.02% sodium azide.

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Pricing

Storage Class Code

10 - Combustible liquids

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

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Stephen R Hennigar et al.
The Journal of nutrition, 146(11), 2167-2173 (2016-11-03)
Hepcidin mediates the hypoferremia of inflammation by inhibiting iron transfer into circulation; however, a regulator for the hypozincemia observed in individuals with acute and chronic inflammatory and infectious diseases is not known. The objective of this study was to determine
Annalisa Palmieri et al.
Cell biology international, 32(7), 733-738 (2008-04-11)
Stem cells derived from human dental pulp are able to differentiate into osteoblasts and are a potential source of autologous bone. The aim of this study was to compare genes differentially expressed in osteoblastoids from human dental pulp (OHDP) to
Ningning Zhao et al.
The Journal of biological chemistry, 285(42), 32141-32150 (2010-08-05)
ZIP14 is a transmembrane metal ion transporter that is abundantly expressed in the liver, heart, and pancreas. Previous studies of HEK 293 cells and the hepatocyte cell lines AML12 and HepG2 established that ZIP14 mediates the uptake of non-transferrin-bound iron
Karin Tuschl et al.
Nature communications, 7, 11601-11601 (2016-05-28)
Although manganese is an essential trace metal, little is known about its transport and homeostatic regulation. Here we have identified a cohort of patients with a novel autosomal recessive manganese transporter defect caused by mutations in SLC39A14. Excessive accumulation of
Brittany L Steimle et al.
The Journal of biological chemistry, 294(50), 19197-19208 (2019-11-09)
Manganese supports numerous neuronal functions but in excess is neurotoxic. Consequently, regulation of manganese flux at the blood-brain barrier (BBB) is critical to brain homeostasis. However, the molecular pathways supporting the transcellular trafficking of divalent manganese ions within the microvascular

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