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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 Proteins (6) and many more products for this protein.
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Data suggest that most if not all tissues use ZIP8 and ZIP14A/ZIP14B (alternative splicing products) for Zn(2+) uptake, some tissues under basal conditions and others more so when inflammatory stressors are present (as in endotoxemia); collectively, this might lead to substantial alterations in plasma Zn(2+) levels due to Zn(2+) redistribution not just in liver but across many vital organs.
ZIP8 reclaims Mn from bile and regulates whole-body Mn homeostasis.
Intravitreal holo-transferrin (show Tf Antibodies) injection decreased Zip 14 (show SLC39A14 Antibodies) protein levels. These data indicate that Zip8 and Zip14 (show SLC39A14 Antibodies) may take up increasing amounts of non-transferrin (show Tf Antibodies) bound iron in these two mouse models of retinal iron accumulation.
Findings identify a reciprocal activation mechanism involving HIF-2alpha (show EPAS1 Antibodies) and the zinc-ZIP8-MTF1 (show MTF1 Antibodies) 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 Antibodies) or DMT1 (show SLC11A2 Antibodies) by siRNA transfection significantly reduced the uptake of Cd(2 (show CD2 Antibodies)+) 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)
The expression, localization, and function of ZIP8 and other divalent cation transporters within macrophages have important implications for TB prevention and dissemination and warrant further study. [review]
SLC39A8 deficiency can cause both a type II CDG and Leigh-like syndrome.
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 Antibodies) 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 Antibodies)). 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 Antibodies) and SLC39A8 seemed to affect blood cadmium concentrations, for SLC39A14 (show SLC39A14 Antibodies) 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.
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