HFE interacts with the BMP type I receptor ALK3 to regulate hepcidin expression

Author:

Wu Xing-gang1,Wang Yang1,Wu Qian2,Cheng Wai-Hang1,Liu Wenjing1,Zhao Yueshui1,Mayeur Claire3,Schmidt Paul J.4,Yu Paul B.5,Wang Fudi2,Xia Yin16

Affiliation:

1. Key Laboratory for Regenerative Medicine, Ministry of Education, School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, China;

2. Department of Nutrition, Center for Nutrition and Health, Institute of Nutrition and Food Safety, School of Public Health, School of Medicine, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Zhejiang University, Hangzhou, Zhejiang, China;

3. Anesthesia Center for Critical Care Research, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital,

4. Department of Pathology, Boston Children's Hospital, and

5. Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, Boston, MA; and

6. School of Biomedical Sciences Core Laboratory, The Chinese University of Hong Kong Shenzhen Research Institute, Shenzhen, China

Abstract

Key Points HFE increases Smad1/5/8 phosphorylation and hepcidin expression, and inhibition of BMP signaling abolishes HFE-induced hepcidin expression. HFE interacts with ALK3, inhibits ALK3 ubiquitination-proteasomal degradation, and increases ALK3 cell-surface expression.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

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