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(HFE protein)
3,186 results
  • Ablation of Hepatocyte Smad1, Smad5, and Smad8 Causes Severe Tissue Iron Loading and Liver Fibrosis in Mice. [Journal Article]
    Hepatology 2019Wang CY, Xiao X, … Babitt JL
  • CONCLUSIONS: Hepatocyte Smad1/5/8 knockout mice are a model of hemochromatosis that encompasses liver injury and fibrosis seen in human disease. These mice reveal the redundant but critical role of SMAD8 in hepcidin and iron homeostasis regulation, establish a requirement for SMAD1/5/8 in hepcidin regulation by testosterone and EGF but not inflammation, and suggest a pathogenic role for both iron loading and SMAD1/5/8 deficiency in liver injury and fibrosis.
  • Diagnostic difficulties of primary hemochromatosis in a patient with posthemorrhagic anemia. [Journal Article]
    Ter Arkh 2019; 91(4):118-121Podzolkov VI, Pokrovskaya AE, … Oganesyan KA
  • Hereditary hemochromatosis (HH) is a disease with an autosomal recessive hereditary type, stipulated by the genetic defect that leads to a high intestinal absorption of iron and primary accumulation in the parenchymal cells of the liver and other organs. This is the most common hereditary disease among White population, the frequency is about 1 case per 250 people. The prevalence of HH is inhomog…
  • Prediction of features of the course of chronic hepatitis C using Bayesian networks. [Journal Article]
    Ter Arkh 2019; 91(2):32-39Samokhodskaya LM, Starostina EE, … Sadovnichii VA
  • CONCLUSIONS: In addition to traditional factors we have shown the contribution of the following mutations. Predicting EP1- liver cirrhosis - HFE H63D, C282Y, CYBA 242 C/T, AGT G-6G, ITGB31565 T/C gene mutations were significant. We also found a link between the rate of progression of liver fibrosis and gene polymorphisms of AGT G-6G, AGT M235T, FV 1691G/A, ITGB31565 T/C. Among the genetic factors associated with portal hypertension there are gene polymorphisms of PAI-I-675 5G/4G, FII 20210 G/A, CYBA 242 C/T, HFE H63D and Il-6 174GC. Cryoglobulins and cryoglobuliemic vasculitis (EP4) are associated with gene mutations MTHFR C677T, ATR A1166C and HFE H63D.The results obtained allow to detect the major pathophysiological and genetic factors which determine the status of the patient and the outcome of the disease, to clarify their contribution, and to reveal the significance of point mutations of genes that control the main routes of HCV course and progression.
  • Deregulation of Hepatic Mek1/2⁻Erk1/2 Signaling Module in Iron Overload Conditions. [Journal Article]
    Pharmaceuticals (Basel) 2019; 12(2)Tangudu NK, Buth N, … Spasić MV
  • The liver, through the production of iron hormone hepcidin, controls body iron levels. High liver iron levels and deregulated hepcidin expression are commonly observed in many liver diseases including highly prevalent genetic iron overload disorders. In spite of a number of breakthrough investigations into the signals that control hepcidin expression, little progress has been made towards investi…
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