标题
Molecular basis of HFE-hemochromatosis
作者
关键词
-
出版物
Frontiers in Pharmacology
Volume 5, Issue -, Pages -
出版商
Frontiers Media SA
发表日期
2014-03-11
DOI
10.3389/fphar.2014.00042
参考文献
相关参考文献
注意:仅列出部分参考文献,下载原文获取全部文献信息。- Transgenic HFE-dependent induction of hepcidin in mice does not require transferrin receptor-2
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- Smad6 and Smad7 are co-regulated with hepcidin in mouse models of iron overload
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- The hemochromatosis proteins HFE, TfR2, and HJV form a membrane-associated protein complex for hepcidin regulation
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- Perturbation of hepcidin expression by BMP type I receptor deletion induces iron overload in mice
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- Hepcidin treatment in Hfe−/− mice diminishes plasma iron without affecting erythropoiesis
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- Combined deletion of Hfe and transferrin receptor 2 in mice leads to marked dysregulation of hepcidin and iron overload
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- Lack of the bone morphogenetic protein BMP6 induces massive iron overload
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- BMP6 is a key endogenous regulator of hepcidin expression and iron metabolism
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- Two BMP responsive elements, STAT, and bZIP/HNF4/COUP motifs of the hepcidin promoter are critical for BMP, SMAD1, and HJV responsiveness
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- Hfe Acts in Hepatocytes to Prevent Hemochromatosis
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- The Hereditary Hemochromatosis Protein, HFE, Inhibits Iron Uptake via Down-regulation of Zip14 in HepG2 Cells
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