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SLC39A8 encodes a member of the SLC39 family of solute-carrier genes, which show structural characteristics of zinc transporters. Additionally we are shipping SLC39A8 Antibodies (30) and many more products for this protein.
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ZIP8 reclaims Mn from bile and regulates whole-body Mn homeostasis.
Intravitreal holo-transferrin (show Tf Proteins) injection decreased Zip 14 (show SLC39A14 Proteins) protein levels. These data indicate that Zip8 and Zip14 (show SLC39A14 Proteins) may take up increasing amounts of non-transferrin (show Tf Proteins) bound iron in these two mouse models of retinal iron accumulation.
Findings identify a reciprocal activation mechanism involving HIF-2alpha (show EPAS1 Proteins) and the zinc-ZIP8-MTF1 (show MTF1 Proteins) axis during osteoarthritis pathogenesis that amplifies catabolic signaling and cartilage destruction.
Data, including data from transgenic mice with high Slc39a8 gene copy number, suggest that early signs of cadmium poisoning (via oral exposure to cadmium chloride) are not exacerbated by increased expression of Slc39a8.
We ligated mouse ZIP14A, ZIP14B and ZIP8 cDNA coding regions into the Xenopus-specific vector pXFRM, transcribed these in vitro, and microinjected the capped RNAs into Xenopus oocytes. K(m) and V(max) values for Cd, Zn and Fe uptake were determined.
The knockdown of ZIP8, ZIP14 (show SLC39A14 Proteins) or DMT1 (show SLC11A2 Proteins) by siRNA transfection significantly reduced the uptake of Cd(2 (show CD2 Proteins)+) and Mn(2+) from the apical membrane.
Observations indicate that ZIP14 and ZIP8 are both broad-scope metal-ion transporters that can mediate the cellular uptake of nutritionally important metals as well as the toxic heavy metal cadmium.
Results show that ZIP8-mediated zinc transport plays an unappreciated critical role during in utero and neonatal growth, organ morphogenesis, and hematopoiesis.
Zinc transporters of the Slc30a/ZnT and Slc39a/Zip families play crucial roles in cell functions, mediating zinc influx to and efflux from the lumen of the secretory pathway, constitutively or in a cell-specific manner. (Review)
We show that-similar to ZIP4-the ZIP8 eight-transmembrane protein is largely internalized during Zn(2+) homeostasis, but moves predominantly to the cell surface membrane (trafficking) under conditions of Zn(2+) depletion.
These results indicate that the ZIP8 Ala391-to-Thr391 substitution has an effect on intracellular cadmium accumulation and cell toxicity, providing a potential mechanistic explanation for the association of this genetic variant with blood pressure.
We identified an association between Crohn's Disease and a missense variant encoding alanine or threonine at position 391 in the zinc transporter solute carrier (show SERTAD2 Proteins) family 39, member 8 protein (SLC39A8 alanine 391 threonine, rs13107325) and replicated the association with Crohn's Disease in 2 replication cohorts.
SLC39A8 SNP (rs13107325) was associated with NT-proBNP levels in patients with acute coronary syndrome (ACS (show PLA2G15 Proteins)). The SLC39A8 SNP was also associated with higher risk of cardiovascular death.
data provide evidence of positive selection on a schizophrenia risk SNP rs13107325 in the SLC39A8 gene, and we propose a hypothesis about the relationship among positive selection of host alleles, schizophrenia, hypertension, energy intake, and the unique history of Europeans.
The lead single nucleotide polymorphism (SNP) in the 4q24 locus was rs13107325 (P-value = 5.1 x 10(-11), beta = -0.77), located in an exon of SLC39A8, which encodes a protein involved in manganese and zinc transport.
Autosomal-recessive intellectual disability with cerebellar atrophy syndrome is caused by mutation of the manganese and zinc transporter gene SLC39A8.
Polymorphisms in SLC39A14 (show SLC39A14 Proteins) and SLC39A8 seemed to affect blood cadmium concentrations, for SLC39A14 (show SLC39A14 Proteins) this effect may occur via differential gene expression.
Data indicate that the average expression level of zinc transporter Zip2 was significantly higher and zinc transporters Zip6, Zip8 mRNA levels were significantly lower in short stature children than in health controls.
MicroRNA-488 regulates zinc transporter SLC39A8/ZIP8 during pathogenesis of osteoarthritis
The zinc transporter SLC39A8 (ZIP8) is a transcriptional target of NF-kappaB (show NFKB1 Proteins) and functions to negatively regulate proinflammatory responses through zinc-mediated down-modulation of IkappaB kinase (show CHUK Proteins) (IKK (show CHUK Proteins)) activity in vitro.
This gene encodes a member of the SLC39 family of solute-carrier genes, which show structural characteristics of zinc transporters. The encoded protein is glycosylated and found in the plasma membrane and mitochondria, and functions in the cellular import of zinc at the onset of inflammation. It is also thought to be the primary transporter of the toxic cation cadmium, which is found in cigarette smoke. Multiple transcript variants encoding different isoforms have been found for this gene. Additional alternatively spliced transcript variants of this gene have been described, but their full-length nature is not known.
, Zrt- and Irt-like protein 8
, solute carrier family 39 member 8
, zinc transporter ZIP8
, BCG induced integral membrane protein BIGM103
, BCG-induced integral membrane protein in monocyte clone 103 protein
, LIV-1 subfamily of ZIP zinc transporter 6
, solute carrier family 39 (metal ion transporter), member 8
, zrt- and Irt-like protein 8