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生物来源
rabbit
质量水平
偶联物
unconjugated
抗体形式
affinity isolated antibody
抗体产品类型
primary antibodies
克隆
polyclonal
表单
buffered aqueous solution
分子量
predicted mol wt 54 kDa
种属反应性
human, mouse, rat
技术
ELISA: suitable
immunofluorescence: suitable
immunohistochemistry: suitable
western blot: suitable
NCBI登记号
UniProt登记号
运输
dry ice
储存温度
−20°C
靶向翻译后修饰
unmodified
基因信息
human ... SLC39A14(23516)
一般描述
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.
免疫原
ZIP14 antibody was raised against a 16 amino acid peptide near the center of human ZIP14.
应用
Anti-ZIP14 antibody produced in rabbit has been used in immunoblotting. 1:2500
生化/生理作用
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.
特点和优势
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.
联系
The action of this antibody can be blocked using blocking peptide SBP3500603.
外形
Supplied in PBS with 0.02% sodium azide.
免责声明
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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储存分类代码
10 - Combustible liquids
闪点(°F)
Not applicable
闪点(°C)
Not applicable
法规信息
常规特殊物品
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
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
Mutations in SLC39A14 disrupt manganese homeostasis and cause childhood-onset parkinsonism-dystonia.
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
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