The hemochromatosis protein HFE signals predominantly via the BMP type I receptor ALK3 in vivo

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11110%2F18%3A10393363" target="_blank" >RIV/00216208:11110/18:10393363 - isvavai.cz</a>

Result on the web

<a href="https://doi.org/10.1038/s42003-018-0071-1" target="_blank" >https://doi.org/10.1038/s42003-018-0071-1</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1038/s42003-018-0071-1" target="_blank" >10.1038/s42003-018-0071-1</a>

Result language

angličtina

Original language name

The hemochromatosis protein HFE signals predominantly via the BMP type I receptor ALK3 in vivo

Original language description

Mutations in HFE, the most common cause of hereditary hemochromatosis, lead to iron overload. The iron overload is characterized by increased iron uptake due to lower levels of the hepatic, iron regulatory hormone hepcidin. HFE was cloned 21 years ago, but the signaling pathway is still unknown. Because bone morphogenetic protein (BMP) signaling is impaired in patients with hereditary hemochromatosis, and the interaction of HFE and the BMP type I receptor ALK3 was suggested in vitro, in vivo experiments were performed. In vivo, hepatocyte-specific Alk3-deficient and control mice were injected with either AAV2/8-Hfe-Flag or PBS. HFE overexpression in control mice results in increased hepatic hepcidin levels, p-Smad1/5 levels, and iron deficiency anemia, whereas overexpression of HFE in hepatocytespecific Alk3-deficient mice results in no change in hepcidin, p-Smad1/5 levels, or blood parameters. These results indicate that HFE signals predominantly via ALK3 to induce hepcidin in vivo.

Czech name

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Czech description

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Type

J_imp - Article in a specialist periodical, which is included in the Web of Science database

CEP classification

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OECD FORD branch

30105 - Physiology (including cytology)

Project

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Continuities

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Publication year

2018

Confidentiality

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Name of the periodical

Communications Biology [online]

ISSN

2399-3642

e-ISSN

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Volume of the periodical

1

Issue of the periodical within the volume

June

Country of publishing house

GB - UNITED KINGDOM

Number of pages

7

Pages from-to

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UT code for WoS article

000461126500065

EID of the result in the Scopus database

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