Smad1/5 is required for erythropoietin-mediated suppression of hepcidin in mice-Reference-Cited by-同舟云学术

Smad1/5 is required for erythropoietin-mediated suppression of hepcidin in mice

Published:2017-07-06 Issue:1 Volume:130 Page:73-83
ISSN:0006-4971
Container-title:Blood
language:en
Short-container-title:

Author:

Wang Chia-Yu¹²,Core Amanda B.¹²,Canali Susanna¹²,Zumbrennen-Bullough Kimberly B.¹²,Ozer Sinan³,Umans Lieve⁴,Zwijsen An⁴,Babitt Jodie L.¹²

Affiliation:

1. Program in Anemia Signaling Research, Division of Nephrology, and

2. Program in Membrane Biology, Center for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA;

3. Center for Engineering in Medicine, Department of Surgery, Massachusetts General Hospital, Harvard Medical School, Shriners Hospitals for Children, Boston, MA; and

4. Laboratory of Developmental Signaling, VIB Center for the Biology of Disease, KU Leuven, Leuven, Belgium

Abstract

Key Points The presence of Smad1 or Smad5 in hepatocytes is sufficient to maintain iron homeostasis, whereas deficiency of both induces iron overload. Erythropoietin and erythroferrone fail to suppress hepcidin in mice with a conditional ablation of Smad1 and Smad5 in hepatocytes.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

Link

http://ashpublications.org/blood/article-pdf/130/1/73/1401901/blood759423.pdf

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