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The product of HFE2 is involved in iron metabolism. Additionally we are shipping HFE2 Antibodies (97) and HFE2 Proteins (13) and many more products for this protein.
Showing 10 out of 33 products:
Human HFE2 ELISA Kit for 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
Show all 10 references for ABIN415112
Mouse (Murine) HFE2 ELISA Kit for 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
Show all 2 references for ABIN415800
study shows that patients with CRA had high expression of BMP6 (show BMP6 ELISA Kits) and hepcidin (show HAMP ELISA Kits) and low expression of s-HJV. BMP6 (show BMP6 ELISA Kits) was found to be negatively correlated with s-HJV; both regulate hepcidin (show HAMP ELISA Kits) expression and play important roles in the development of anemia.
HJV levels are low in NAFLD (show TSC2 ELISA Kits) and even lower in iron overloaded NAFLD (show TSC2 ELISA Kits).
Data show that transmembrane serine protease (show F2 ELISA Kits) TMPRSS6 (show 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 (show UTS2R ELISA Kits) of the human HJV mRNA have the ability to significantly decrease translational efficiency under normal conditions.
Case Reports: juvenile hemochromatosis (show 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 (show 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 (show HAMP ELISA Kits), and promoting the degradation of ferroportin (show SLC40A1 ELISA Kits) during acute kidney injury, whereas soluble HJV does the opposite.
Data show that Patients with iron-refractory iron-deficiency anemia with a mutation in the TMPRSS6 (show TMPRSS6 ELISA Kits) gene were found to have lower levels of circulating hemojuvelin than those in healthy patients.
Results indicate that an efficient induction of hepcidin (show HAMP ELISA Kits) expression by hemojuvelin (HJV) requires its interaction with neogenin (show NEO1 ELISA Kits).
Single Hjv(-)/(-) and double Hfe (show HFE ELISA Kits)(-)/(-)Hjv(-)/(-) mice exhibit comparable iron overload. Hfe (show HFE ELISA Kits) and Hjv regulate hepcidin (show HAMP ELISA Kits) via the same pathway.
Results show that HFE (show HFE ELISA Kits) may depend on HJV for hepcidin (show HAMP ELISA Kits) regulation. Residual hepcidin (show HAMP ELISA Kits) in the absence of HFE (show 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 (show 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 (show HAMP ELISA Kits).
Deletion of Hjv in mice leads to abnormal retinal angiogenesis/vasculogenesis, with proliferation of new, leaky blood vessels in the vitreous.
Loss of matriptase-2 (show TMPRSS6 ELISA Kits) increases bone morphogenetic protein-dependent signaling, while paradoxically decreasing liver hemojuvelin protein content.
Use of proteomic analysis enables identification of four disulfide linkages in hemojuvelin/repulsive guidance molecule C. This molecule is a single-chain HJV/RGMc isoform.
we conclude that TNF-alpha (show TNF ELISA Kits) suppresses Hemojuvelin(HJV) transcription possibly via a novel TNFRE within the HJV promoter
high levels of serum s-HJV in CDA I patients, suggesting that it may contribute to iron loading pathology in CDA I and eventually in other anemias with ineffective erythropoiesis.
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.
hemochromatosis type 2 (juvenile)
, RGM domain family member C
, hemochromatosis type 2 protein
, repulsive guidance molecule c
, hemochromatosis type 2 (juvenile) (human homolog)
, hemochromatosis type 2 protein homolog
, repulsive guidance molecule C