Skip Navigation
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

National Institute of Environmental Health Sciences

Use this QR code to view the newest version of this document
Use this QR code to view the newest version of this document

Your Environment. Your Health.

Publication Detail

Title: BMPER protein is a negative regulator of hepcidin and is up-regulated in hypotransferrinemic mice.

Authors: Patel, Neeta; Masaratana, Patarabutr; Diaz-Castro, Javier; Latunde-Dada, Gladys O; Qureshi, Aakafa; Lockyer, Pamela; Jacob, Molly; Arno, Matthew; Matak, Pavle; Mitry, Ragai R; Hughes, Robin D; Dhawan, Anil; Patterson, Cam; Simpson, Robert J; McKie, Andrew T

Published In J Biol Chem, (2012 Feb 03)

Abstract: The BMP/SMAD4 pathway has major effects on liver hepcidin levels. Bone morphogenetic protein-binding endothelial cell precursor-derived regulator (Bmper), a known regulator of BMP signaling, was found to be overexpressed at the mRNA and protein levels in liver of genetically hypotransferrinemic mice (Trf(hpx/hpx)). Soluble BMPER peptide inhibited BMP2- and BMP6-dependent hepcidin promoter activity in both HepG2 and HuH7 cells. These effects correlated with reduced cellular levels of pSMAD1/5/8. Addition of BMPER peptide to primary human hepatocytes abolished the BMP2-dependent increase in hepcidin mRNA, whereas injection of Bmper peptide into mice resulted in reduced liver hepcidin and increased serum iron levels. Thus Bmper may play an important role in suppressing hepcidin production in hypotransferrinemic mice.

PubMed ID: 22144676 Exiting the NIEHS site

MeSH Terms: No MeSH terms associated with this publication

Back
to Top