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Human Polyclonal SLC39A4 Primary Antibody for IHC - ABIN967275
Küry, Dréno, Bézieau, Giraudet, Kharfi, Kamoun, Moisan: Identification of SLC39A4, a gene involved in acrodermatitis enteropathica. in Nature genetics 2002
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Human Polyclonal SLC39A4 Primary Antibody for IHC - ABIN967274
Kim, Wang, Dufner-Beattie, Andrews, Eide, Petris: Zn2+-stimulated endocytosis of the mZIP4 zinc transporter regulates its location at the plasma membrane. in The Journal of biological chemistry 2004
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Cow (Bovine) Polyclonal SLC39A4 Primary Antibody for WB - ABIN2781713
Li, Zhang, Liu, Bharadwaj, Wang, Wang, Zhang, Liuzzi, Chang, Cousins, Fisher, Brunicardi, Logsdon, Chen, Yao: Aberrant expression of zinc transporter ZIP4 (SLC39A4) significantly contributes to human pancreatic cancer pathogenesis and progression. in Proceedings of the National Academy of Sciences of the United States of America 2007
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SLC39A4 is overexpressed in NSCLC and correlates with increased staging and diminished patient survival. Moreover, silencing of SLC39A4 induced an epithelial-like phenotype, decreased cancer stem cell marker expression, and increased cisplatin sensitivity.
The authors present the first report of SLC39A4 mutation in an acrodermatitis enteropathica family from the Middle East.
Results showed decreased expression of Zn uptake transporters ZIP2 and ZIP4 on mRNA and protein level correlating with SHANK3 expression levels, and found reduced levels of ZIP4 protein co-localizing with SHANK3 at the plasma membrane. ZIP4 exists in a complex with SHANK3. Further results confirmed a link between enterocytic SHANK3, ZIP2 and ZIP4.
Expression of zinc transporters ZIP4, ZIP14 and ZnT9 in hepatic carcinogenesis-An immunohistochemical study
exosomal ZIP4 promotes cancer growth and is a novel diagnostic biomarker for pancreatic cancer.
Structural insights of ZIP4 extracellular domain critical for optimal zinc transport have been uncovered.
ZIP4 regulates human epidermal homeostasis in patients with acrodermatitis enteropathica.
ZIP4 and intracellular zinc have essential roles in tumoral growth in oral squamous cell carcinoma
Case Report: heterozygote mutation in SLC39A4 resulting in acrodermatitis enteropathica.
Data sho that silencing of zinc transporter ZIP4 resulted in increased bone tissue mineral density, and restoration of bone strength.
Studied the zinc binding properties of the large intracellular loop of hZIP4.
The results described a previously uncharacterized role of ZIP4 in apoptosis resistance and elucidated a novel pathway through which ZIP4 regulates pancreatic cancer growth.
In glioma tumors, high ZIP4 expression was significantly associated with higher grade.
Developed is a structural model of ZIP4 by combining protein prediction methods with in situ experiments. Insight into the permeation pathway of ZIP4 is provided.
SLC39A4 mutations have roles in zinc deficiency
Both acrodermatitis mutations cause absence of the ZIP4 transporter cell surface expression and nearly absent zinc uptake.
ZIP4 activates the zinc-dependent transcription factor CREB and requires this transcription factor to increase miR-373 expression through the regulation of its promoter.
High ZIP4 expression is associated with glioma.
resulkts indicate ZIP4 is the only zinc transporter that is significantly up-regulated in pancreatic cancer and might be the major zinc transporter that plays an important role in pancreatic cancer growth
The results suggest that ZIP4 may be a tumor suppressor gene and down-regulation of ZIP4 may be a critical early event in the development of prostate carcinoma
While Zip4 was not found to be essential for proper glucose homeostasis and insulin secretion in vivo in mice, this study found that Zip4 mediates increases in cytoplasmic and granular zinc pools and stimulates glucose dependent insulin secretion in-vitro
These studies strongly suggest that wasting and lethality in acrodermatitis enteropathica patients reflects the loss-of-function of the intestine zinc transporter ZIP4, which leads to abnormal Paneth cell gene expression
Cell migration assays revealed that RNAi knockdown of Zip4 in Hepa cells depressed in vitro migration whereas forced over-expression in Hepa cells and MCF-7 cells enhanced in vitro migration
ZIP4 physically interacts with tPA, correlating with an increased intracellular zinc influx and lysosomal sequestration after excitotoxin stimulation. Changes in prosurvival signals support the idea that this sequestration results in neuroprotection.
results provide compelling evidence that ZIP4 is a zinc transporter that plays an important role in zinc homeostasis, a process that is defective in acrodermatitis enteropathica in humans
Zinc deficiency increased mZIP4 protein levels at the plasma membrane, and this was associated with increased zinc uptake.
ZIP4 and ZIP5 have roles in the adaptive response to dietary zinc in mice
that heterozygous mutations in the acrodermatitis gene Zip4 (Slc39a4) may be associated with a wider range of developmental defects than was previously appreciated, particularly when dietary zinc is limiting.
ZIP4 is induced by zinc deficiency in cultured mouse Hepa cells and is rapidly degraded in response to added zinc
The processing of ZIP4 may represent a significant regulatory mechanism controlling its function.
KLF4 is induced during zinc restriction and is a transcription factor involved in adaptive regulation of the zinc transporter ZIP4
This gene encodes a member of the zinc/iron-regulated transporter-like protein (ZIP) family. The transmembrane protein is required for zinc uptake in the intestine. Mutations in this gene result in acrodermatitis enteropathica, a rare inherited defect in the absorption of dietary zinc. Multiple transcript variants encoding different isoforms have been found for this gene.
solute carrier family 39 (zinc transporter), member 4
, zinc transporter ZIP4-like
, zinc transporter ZIP4
, zrt- and Irt-like protein 4
, solute carrier family 39 member 4
, solute carrier family 39, member 4
, activated in W/Wv mouse stomach 2