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anti-Human 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 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
Human Polyclonal HFE Primary Antibody for IHC, IHC (p) - ABIN4317233
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
Overall, this increased understanding of the role of HFE in the immune response sets the stage for better treatment and management of hereditary hemochromatosis and other iron-related diseases, as well as of the immune defects related to this condition.
Results show that cystic fibrosis (CF) patients who carry a HFE gene mutation, particularly the C282Y substitution, demonstrate accelerated lung function and worsening of disease suggesting that HFE C282Y mutation is associated with CF severity and progression.
This study showed that the Iron related hemochromatosis (HFE) gene mutations in Friedreich Ataxia patients.
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 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 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 [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 of HAMP gene (c.-25G>A)
GNPAT p.D519G is strongly associated with markedly increased iron stores in p.C282Y homozygotes after correction for age, iron-related variables, and alcohol consumption
HFE p.C282Y homozygosity is significantly associated with lymphocyte and basophil counts
TFR2 expression altered within 4h of HAMP treatment, while HFE expression altered later at 24h and 48h, suggesting that TFR2 may function prior to HFE in HAMP regulation.
Studied association of HFE mutations on iron status among Indian beta Thalassemia carriers . A total of 100 beta thalassemia traits (BTT) with 100 normal individuals were screened for the C282Y and H63D mutations using PCR-RFLP.
Homozygosity for the HFE C282Y mutation appeared to be a strong predictor of increased iron stores and was predominantly observed in whites. The findings are consistent with the HFE C282Y mutation providing a protective effect from iron deficiency. [Review]
The goal of this study was to evaluate the impact of EHR point-of-care tools on medical record documentation of genetic testing care processes for the common HFE mutations, a thrombophilia panel, and HLA-B27.
HFE mRNA was independently elevated by extracellular and intracellular iron-excess. Thus, it may be involved in sensing both, extracellular and intracellular iron.
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(-)/(-) and double Hfe(-)/(-)Hjv(-)/(-) mice exhibit comparable iron overload. Hfe and Hjv regulate hepcidin via the same pathway.
Results show that HFE requires HJV to activate downstream signal transduction pathways for hepcidin 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 expression via the BMP pathway: HFE interacts with ALK3 to stabilize ALK3 protein and increase ALK3 expression at the cell surface.
These results support in vivo studies which suggest that Hfe and Tfr2 can independently regulate hepcidin.
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.
Hfe(-/-) retinal pigment epithelial cells exhibited slower senescence rate and higher survivin expression than wild type cells. Hfe(-/-) cells migrated faster and showed greater glucose uptake and increased expression of GLUTs.
Findings suggest a novel role for Hfe and/or imbalanced iron homeostasis in the regulation of the inflammatory response in the lung and hereditary hemochromatosis.
Double mutant mice lacking functional Hfe or Tfr2 and Tmprss6 exhibited a severe iron deficiency microcytic anemia phenotype mimicking the phenotype of single mutant mice lacking functional Tmprss6 demonstrating that Hfe and Tfr2 are not substrates for Tmprss6.
Disruption of both Hfe and Tfr2 caused more severe hepatic iron overload with more advanced lipid peroxidation, inflammation, and portal fibrosis than was observed with the disruption of either gene alone.
the Hfe(-/-) mouse brain showed numerous significant changes in transcript levels although few of these related to proteins directly involved in iron homeostasis
Loss of central and peripheral CD8+ T-cell tolerance to HFE in mouse models of human familial hemochromatosis.
Hfe(-/-) mice show defective hepatic-intestinal iron and lipid signaling, which predispose them toward diet-induced hepatic lipotoxicity, accompanied by an accelerated progression of injury to fibrosis.
the HFE H63D mutant protein is associated with prolonged ER stress and chronically increased neuronal vulnerability.
neither genetic loss of Hfe nor hepatic Hfe overexpression modulated the hepcidin elevation and systemic iron deficiency of Tmprss6(-/-) mice
Hfe influences erythropoiesis by 2 distinct mechanisms: limiting hepcidin expression under conditions of simultaneous iron overload and stress erythropoiesis, and impairing transferrin-bound iron uptake by erythroid cells.
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