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Human HFE2 ELISA Kit für Sandwich ELISA - ABIN415112
Rumjon, Sarafidis, Brincat, Musto, Malyszko, Bansal, Macdougall: Serum hemojuvelin and hepcidin levels in chronic kidney disease. in American journal of nephrology 2012
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Mouse (Murine) HFE2 ELISA Kit für Sandwich ELISA - ABIN415800
Krijt, Frýdlová, Kukačková, Fujikura, Přikryl, Vokurka, Nečas: Effect of iron overload and iron deficiency on liver hemojuvelin protein. in PLoS ONE 2012
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A novel homozygous mutation in HJV gene identified in an Arab patient with juvenile hemochromatosis (zeige HFE ELISA Kits) and hepatocellular carcinoma.
study shows that patients with CRA had high expression of BMP6 (zeige BMP6 ELISA Kits) and hepcidin (zeige HAMP ELISA Kits) and low expression of s-HJV. BMP6 (zeige BMP6 ELISA Kits) was found to be negatively correlated with s-HJV; both regulate hepcidin (zeige HAMP ELISA Kits) expression and play important roles in the development of anemia.
HJV levels are low in NAFLD (zeige TSC2 ELISA Kits) and even lower in iron overloaded NAFLD (zeige TSC2 ELISA Kits).
Data show that transmembrane serine protease (zeige F2 ELISA Kits) TMPRSS6 (zeige TMPRSS6 ELISA Kits) cleaves both the heterodimeric and the full-length mutant hemojuvelin (m-HJV).
Hereditary haemochromatosis caused by homozygous HJV mutation evolved through paternal disomy.
The study demonstrates that the two upstream open reading frames (with 28 and 19 codons) present in the 5' UTR (zeige UTS2R ELISA Kits) of the human HJV mRNA have the ability to significantly decrease translational efficiency under normal conditions.
Case Reports: juvenile hemochromatosis (zeige HFE ELISA Kits) associated with simple heterozygosity for novel HJV mutations and unknown genetic factors.
suggesting that the homozygous mutation p.C321X in HJV is causative in the patient with hemochromatosis (zeige HFE ELISA Kits)
In dialysis patients, hemojuvelin levels are significantly increased but obesity does not have an additional impact.
Membrane bound hemojuvelin (HJV) is associated with decreasing total kidney iron, secreting hepcidin (zeige HAMP ELISA Kits), and promoting the degradation of ferroportin (zeige SLC40A1 ELISA Kits) during acute kidney injury, whereas soluble HJV does the opposite.
The results provide support for the interaction between TMPRSS6 (zeige TMPRSS6 ELISA Kits) and hemojuvelin in vivo; they also suggest that hemojuvelin could be cleaved by another as yet unknown protease in the absence of functional TMPRSS6 (zeige TMPRSS6 ELISA Kits).
Hjv (--) and Hfe (zeige HFE ELISA Kits) (C282YC282Y) transgenic mice displayed enhanced colonization of deep tissues by Yersinia pseudotuberculosis following oral inoculation, recapitulating enhanced susceptibility of humans with hemochromatosis (zeige HFE ELISA Kits) to disseminated infection with enteropathogenic Yersinia.
The data demonstrate that endothelial cells are the predominant source of BMP6 (zeige BMP6 ELISA Kits) in the liver and support a model in which endothelial cells BMP6 (zeige BMP6 ELISA Kits) has paracrine actions on hepatocyte hemojuvelin to regulate hepcidin (zeige HAMP ELISA Kits) transcription and maintain systemic iron homeostasis.
The minor variant of the HJV polymorphic site rs16827043 is a significant factor associated with hypertension among 50 year-old individuals compared with the AA genotype carriers. For the other polymorphic variant rs7536827, association with hypertension was found only among normal or slightly overweight A-allele carriers. In conclusion, HJV genetic variants were associated with essential hypertension in Finnish subjects.
Results indicate that an efficient induction of hepcidin (zeige HAMP ELISA Kits) expression by hemojuvelin (HJV) requires its interaction with neogenin (zeige NEO1 ELISA Kits).
Single Hjv(-)/(-) and double Hfe (zeige HFE ELISA Kits)(-)/(-)Hjv(-)/(-) mice exhibit comparable iron overload. Hfe (zeige HFE ELISA Kits) and Hjv regulate hepcidin (zeige HAMP ELISA Kits) via the same pathway.
Results show that HFE (zeige HFE ELISA Kits) may depend on HJV for hepcidin (zeige HAMP ELISA Kits) regulation. Residual hepcidin (zeige HAMP ELISA Kits) in the absence of HFE (zeige HFE ELISA Kits) suggests either the presence of an unknown regulator synergistic with HJV or that HJV is sufficient to maintain basal levels of hepcidin (zeige HAMP ELISA Kits).
Parenchymal hepatic iron overload does not suffice to trigger progression of liver steatosis to steatohepatitis or fibrosis in Hjv knockout C57BL/6 mice.
Hjv is not required for sensing of body iron levels and merely functions as an enhancer for iron signaling to hepcidin (zeige HAMP ELISA Kits).
Deletion of Hjv in mice leads to abnormal retinal angiogenesis/vasculogenesis, with proliferation of new, leaky blood vessels in the vitreous.
The product of this gene is involved in iron metabolism. It may be a component of the signaling pathway which activates hepcidin or it may act as a modulator of hepcidin expression. It could also represent the cellular receptor for hepcidin. Alternatively spliced transcript variants encoding different isoforms have been identified for this gene. Defects in this gene are the cause of hemochromatosis type 2A, also called juvenile hemochromatosis (JH). JH is an early-onset autosomal recessive disorder due to severe iron overload resulting in hypogonadotrophic hypogonadism, hepatic fibrosis or cirrhosis and cardiomyopathy, occurring typically before age of 30.
RGM domain family member C
, hemochromatosis type 2 protein
, repulsive guidance molecule c
, hemochromatosis type 2 (juvenile)
, hemochromatosis type 2 protein homolog
, repulsive guidance molecule C
, hemochromatosis type 2 (juvenile) (human homolog)
, RGM-like protein