Bone Morphogenetic Protein-6 Mutations Take Their Place in Iron Overload Diseases
- 1 March 2016
- journal article
- Published by Elsevier in Gastroenterology
- Vol. 150 (3) , 556-559
Abstract
No abstract availableThis publication has 26 references indexed in Scilit:
- Heterozygous Mutations in BMP6 Pro-peptide Lead to Inappropriate Hepcidin Synthesis and Moderate Iron Overload in HumansGastroenterology, 2016
- Perturbation of hepcidin expression by BMP type I receptor deletion induces iron overload in miceBlood, 2011
- Bone Morphogenetic Proteins: A critical reviewCellular Signalling, 2011
- BMP6 is a key endogenous regulator of hepcidin expression and iron metabolismNature Genetics, 2009
- Hemojuvelin regulates hepcidin expression via a selective subset of BMP ligands and receptors independently of neogeninBlood, 2008
- Modulation of bone morphogenetic protein signaling in vivo regulates systemic iron balanceJournal of Clinical Investigation, 2007
- A role of SMAD4 in iron metabolism through the positive regulation of hepcidin expressionCell Metabolism, 2005
- Hepcidin Regulates Cellular Iron Efflux by Binding to Ferroportin and Inducing Its InternalizationScience, 2004
- A New Mouse Liver-specific Gene, Encoding a Protein Homologous to Human Antimicrobial Peptide Hepcidin, Is Overexpressed during Iron OverloadJournal of Biological Chemistry, 2001
- Hepcidin, a Urinary Antimicrobial Peptide Synthesized in the LiverJournal of Biological Chemistry, 2001