The hemochromatosis proteins HFE, TfR2, and HJV form a membrane-associated protein complex for hepcidin regulation (Q24338877)

homeostatic iron regulator

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Hemojuvelin BMP co-receptor

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Transferrin receptor 2

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Transgenic HFE-dependent induction of hepcidin in mice does not require transferrin receptor-2.

Matthias W Hentze

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Martina U Muckenthaler

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author name string

Flavia D'Alessio

series ordinal

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language of work or name

English

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publication date

November 2012

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published in

Journal of Hepatology

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volume

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issue

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page(s)

1052-60

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cites work

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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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Defective bone morphogenic protein signaling underlies hepcidin deficiency in HFE hereditary hemochromatosis

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Distribution of the iron-regulating protein hepcidin in the murine central nervous system.

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The hemochromatosis protein HFE competes with transferrin for binding to the transferrin receptor

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Mutational analysis of the transferrin receptor reveals overlapping HFE and transferrin binding sites

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Two to tango: regulation of Mammalian iron metabolism

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The transferrin receptor modulates Hfe-dependent regulation of hepcidin expression

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The serine protease matriptase-2 (TMPRSS6) inhibits hepcidin activation by cleaving membrane hemojuvelin

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Crystal structure of the hemochromatosis protein HFE and characterization of its interaction with transferrin receptor

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Structure of the human transferrin receptor-transferrin complex

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Disrupted hepcidin regulation in HFE-associated haemochromatosis and the liver as a regulator of body iron homoeostasis.

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The gene TFR2 is mutated in a new type of haemochromatosis mapping to 7q22.

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Constitutive hepcidin expression prevents iron overload in a mouse model of hemochromatosis

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Regulatory defects in liver and intestine implicate abnormal hepcidin and Cybrd1 expression in mouse hemochromatosis

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Mutations in HFE2 cause iron overload in chromosome 1q-linked juvenile hemochromatosis

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Bone morphogenetic protein signaling by hemojuvelin regulates hepcidin expression

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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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Bone morphogenetic protein signaling is impaired in an HFE knockout mouse model of hemochromatosis

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Iron-refractory iron deficiency anemia

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Mechanisms of HFE-induced regulation of iron homeostasis: Insights from the W81A HFE mutation

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The hemochromatosis gene product complexes with the transferrin receptor and lowers its affinity for ligand binding

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The hemochromatosis founder mutation in HLA-H disrupts beta2-microglobulin interaction and cell surface expression

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Comparison of the interactions of transferrin receptor and transferrin receptor 2 with transferrin and the hereditary hemochromatosis protein HFE

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Hereditary hemochromatosis protein, HFE, interaction with transferrin receptor 2 suggests a molecular mechanism for mammalian iron sensing

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A new mouse liver-specific gene, encoding a protein homologous to human antimicrobial peptide hepcidin, is overexpressed during iron overload

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Repulsive guidance molecule (RGMa), a DRAGON homologue, is a bone morphogenetic protein co-receptor

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HFE modulates transferrin receptor 2 levels in hepatoma cells via interactions that differ from transferrin receptor 1-HFE interactions.

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Expression of stimulator of Fe transport is not enhanced in Hfe knockout mice

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Hepcidin regulates cellular iron efflux by binding to ferroportin and inducing its internalization

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Molecular mechanisms of the defective hepcidin inhibition in TMPRSS6 mutations associated with iron-refractory iron deficiency anemia

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BMP/Smad signaling is not enhanced in Hfe-deficient mice despite increased Bmp6 expression.

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Hepcidin induction by transgenic overexpression of Hfe does not require the Hfe cytoplasmic tail, but does require hemojuvelin

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Identifiers

DOI

1 reference

Consolidated OpenCitations Corpus – April 2017

1 reference

Consolidated OpenCitations Corpus – April 2017

PubMed publication ID

22728873

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Consolidated OpenCitations Corpus – April 2017