Hemochromatosis Protein

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  Subject Areas on Research

  • An Hfe-dependent pathway mediates hyposideremia in response to lipopolysaccharide-induced inflammation in mice. 
  • Autosomal-dominant hemochromatosis is associated with a mutation in the ferroportin (SLC11A3) gene. 
  • Chronic hepcidin induction causes hyposideremia and alters the pattern of cellular iron accumulation in hemochromatotic mice. 
  • Comparison of the interactions of transferrin receptor and transferrin receptor 2 with transferrin and the hereditary hemochromatosis protein HFE. 
  • Constitutive hepcidin expression prevents iron overload in a mouse model of hemochromatosis. 
  • Contributions of beta2-microglobulin-dependent molecules and lymphocytes to iron regulation: insights from HfeRag1(-/-) and beta2mRag1(-/-) double knock-out mice. 
  • Expression of stimulator of Fe transport is not enhanced in Hfe knockout mice. 
  • Expression of the DMT1 (NRAMP2/DCT1) iron transporter in mice with genetic iron overload disorders. 
  • Genes that modify the hemochromatosis phenotype in mice. 
  • Haptoglobin modifies the hemochromatosis phenotype in mice. 
  • Hepatocyte-targeted HFE and TFR2 control hepcidin expression in mice. 
  • Hepcidin induction by transgenic overexpression of Hfe does not require the Hfe cytoplasmic tail, but does require hemojuvelin. 
  • Hepcidin, a candidate modifier of the hemochromatosis phenotype in mice. 
  • Hereditary hemochromatosis protein, HFE, interaction with transferrin receptor 2 suggests a molecular mechanism for mammalian iron sensing. 
  • Hereditary hemochromatosis: gene discovery and its implications for population-based screening. 
  • Hfe deficiency increases susceptibility to cardiotoxicity and exacerbates changes in iron metabolism induced by doxorubicin. 
  • Identification of the segments of the mouse transferrin receptor 1 required for mouse mammary tumor virus infection. 
  • Impact of gene patents and licensing practices on access to genetic testing for hereditary hemochromatosis. 
  • Iron and HFE or TfR1 mutations as comorbid factors for development and progression of chronic hepatitis C. 
  • Iron in skin of mice with three etiologies of systemic iron overload. 
  • Logistic regression models for polymorphic and antagonistic pleiotropic gene action on human aging and longevity. 
  • Lower serum hepcidin and greater parenchymal iron in nonalcoholic fatty liver disease patients with C282Y HFE mutations. 
  • Porphyria cutanea tarda, hepatitis C, and HFE gene mutations in North America. 
  • Regulation of iron absorption in Hfe mutant mice. 
  • Regulatory defects in liver and intestine implicate abnormal hepcidin and Cybrd1 expression in mouse hemochromatosis. 
  • Role of HFE gene mutations in liver diseases other than hereditary hemochromatosis. 
  • The C282Y mutation causing hereditary hemochromatosis does not produce a null allele. 
  • The transferrin receptor modulates Hfe-dependent regulation of hepcidin expression. 
  • Tmprss6 is a genetic modifier of the Hfe-hemochromatosis phenotype in mice.