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Human Polyclonal SLC39A4 Primary Antibody for IHC - ABIN967274
Küry, Dréno, Bézieau, Giraudet, Kharfi, Kamoun, Moisan: Identification of SLC39A4, a gene involved in acrodermatitis enteropathica. in Nature genetics 2002
Show all 3 Pubmed References
Human Polyclonal SLC39A4 Primary Antibody for IHC - ABIN967275
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
Show all 3 Pubmed References
Human Polyclonal SLC39A4 Primary Antibody for ELISA - ABIN450071
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
Cow (Bovine) Polyclonal SLC39A4 Primary Antibody for WB - ABIN2781713
Antala, Ovchinnikov, Kamisetty, Baker, Dempski: Computation and Functional Studies Provide a Model for the Structure of the Zinc Transporter hZIP4. in The Journal of biological chemistry 2015
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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 (show SPRN Antibodies) that silencing of zinc transporter ZIP4 resulted in increased bone tissue mineral density, and restoration of bone strength.
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 (show CREB1 Antibodies) and requires this transcription factor to increase miR (show MLXIP Antibodies)-373 expression through the regulation of its promoter.
While Zip4 was not found to be essential for proper glucose homeostasis and insulin (show INS Antibodies) secretion in vivo in mice, this study found that Zip4 mediates increases in cytoplasmic and granular zinc pools and stimulates glucose dependent insulin (show INS Antibodies) 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 (show PLAT Antibodies), 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
ZIP4 and ZIP5 (show SLC39A5 Antibodies) 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 (show KLF4 Antibodies) 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