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anti-Human HFE Antibodies:
anti-Rat (Rattus) HFE Antibodies:
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Human Monoclonal HFE Primary Antibody for ICC, ELISA - ABIN969192
Hosgood, Menashe, He, Chanock, Lan: PTEN identified as important risk factor of chronic obstructive pulmonary disease. in Respiratory medicine 2009
Show all 2 Pubmed References
Human Monoclonal HFE Primary Antibody for IF, ELISA - ABIN561252
Lenarduzzi, Hui, Yue, Ito, Shi, Williams, Bruce, Sakemura-Nakatsugawa, Xu, Schimmer, Liu: Hemochromatosis enhances tumor progression via upregulation of intracellular iron in head and neck cancer. in PLoS ONE 2013
Human Polyclonal HFE Primary Antibody for IF (p), IHC (p) - ABIN1714561
Rychtarcikova, Lettlova, Tomkova, Korenkova, Langerova, Simonova, Zjablovskaja, Alberich-Jorda, Neuzil, Truksa: Tumor-initiating cells of breast and prostate origin show alterations in the expression of genes related to iron metabolism. in Oncotarget 2016
p.Cys282Tyr homozygous women are diagnosed HFE Hemochromatosis at a later age than men, and thus corroborates the existence of a difference in the expression of this genotype between men and women. Nevertheless, these results do not confirm the protective effect typically attributed to pregnancy to explain the slower iron accumulation in women.
HFE could be a potential susceptibility gene for isolated recurrent aphthous oral ulcers
HFE mutation is associated with a lower level of aerobic capacity, even in the absence of iron accumulation.
Three single nucleotide polymorphisms associated with iron regulation were genotyped in multiple sclerosis : two in the human hereditary hemochromatosis protein gene HFE: rs1800562 (C282Y mutation) and rs1799945 (H63D mutation), as well as the rs1049296 SNP in the transferrin (show Tf Antibodies) gene (C2 mutation). We only observed a higher prevalence of TF-C2 in multiple sclerosis patients
The HFE gene including both coding and boundary intronic regions were sequenced and polymorphisms were identified in 304 Brazilian individuals, encompassing healthy individuals and patients exhibiting hereditary or acquired iron overload.
homozygosity for the HLA-A*03 allele significantly increases the risk of excessive iron loading in Norwegian p.C282Y homozygous male patients.
genetic association studies in cohort of infants in Spain: Data suggest that serum hepcidin (show HAMP Antibodies) levels increase in infants during first year of life and are positively associated with iron status only in infants with wild-type HFE gene (not in infants with genetic polymorphisms C282Y, H63D, and S65C).
HFE stability is pH-dependent.
Studies indicate that hemochromatosis protein (HFE) variants can positively influence the immune system and might even diminish the risk of developing diseases such as amyotrophic lateral sclerosis, Alzheimer's disease, Parkinson's disease, and atherosclerosis.
unreported iron metabolism-related genes in non-classic hereditary hemochromatosis patients that were predicted to be potentially pathogenic were three novel mutations in TFR2 (show TFR2 Antibodies) [two missense (p.Leu750Pro and p.Ala777Val) and one intronic splicing mutation (c.967-1G>C)], one missense mutation in HFE (p.Tyr230Cys), and one mutation in the 5'-UTR (show UTS2R Antibodies) of HAMP (show HAMP Antibodies) gene (c.-25G>A)
H67D mutation in HFE gene is associated with decreased susceptibility to manganese accumulation in the brain and neurotoxicity induced by inhaled manganese.
the aging HFE KO mouse on an SV129 genetic background has the potential to facilitate the investigation of cardiomyopathy induced by HFE gene mutations.
unlike homozygous Hfe deletion, heterozygous gene deletion disrupted glucose homeostasis but did not affect lipid metabolism or liver injury.
Single Hjv (show HFE2 Antibodies)(-)/(-) and double Hfe(-)/(-)Hjv (show HFE2 Antibodies)(-)/(-) mice exhibit comparable iron overload. Hfe and Hjv (show HFE2 Antibodies) regulate hepcidin (show HAMP Antibodies) via the same pathway.
Results show that HFE requires HJV (show HFE2 Antibodies) to activate downstream signal transduction pathways for hepcidin (show HAMP Antibodies) regulation.
Alterations in cholesterol metabolism associated with expression of H63D-HFE may contribute to the development of AD.
results provide evidence that HFE induces hepcidin (show HAMP Antibodies) expression via the BMP pathway: HFE interacts with ALK3 (show BMPR1A Antibodies) to stabilize ALK3 (show BMPR1A Antibodies) protein and increase ALK3 (show BMPR1A Antibodies) expression at the cell surface.
These results support in vivo studies which suggest that Hfe and Tfr2 (show TFR2 Antibodies) can independently regulate hepcidin (show HAMP Antibodies).
A mutation in the HFE gene is associated with altered brain iron profiles and increased oxidative stress in mice.
Hfe-knockout mice did not have higher brain iron levels than wildtype controls.
The protein encoded by this gene is a membrane protein that is similar to MHC class I-type proteins and associates with beta2-microglobulin (beta2M). It is thought that this protein functions to regulate iron absorption by regulating the interaction of the transferrin receptor with transferrin. The iron storage disorder, hereditary haemochromatosis, is a recessive genetic disorder that results from defects in this gene. At least nine alternatively spliced variants have been described for this gene. Additional variants have been found but their full-length nature has not been determined.
MHC class I-like protein HFE
, hereditary hemochromatosis protein
, hereditary hemochromatosis protein HLA-H
, high Fe
, hereditary hemochromatosis protein homolog
, hemochromatosis protein