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Blood, 1 November 2007, Vol. 110, No. 9, pp. 3436-3437. Prepublished online as a Blood First Edition Paper on July 20, 2007; DOI 10.1182/blood-2007-05-091108. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2007-05-091108v1 110/9/3436    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Truksa, J. Articles by Beutler, E. Search for Related Content PubMed PubMed Citation Articles by Truksa, J. Articles by Beutler, E. Related Collections Red Cells Brief Reports Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  RED CELLS Brief Report The distal location of the iron responsive region of the hepcidin promoter Jaroslav Truksa1, Pauline Lee1, Hongfan Peng1, Jonathan Flanagan2, and Ernest Beutler1 1 Department of Molecular and Experimental Medicine, Scripps Research Institute, La Jolla, CA; 2 Department of Hematology, St Jude Children's Research Hospital, Memphis, TN The response of hepcidin transcription to iron has been repeatedly documented in living mice, but it is difficult to demonstrate the response in ex vivo systems. We have hydrodynamically transfected mice with plasmid constructs composed of a murine hepcidin 1 promoter and fragments of the promoter fused to a firefly luciferase reporter. This method enabled us to quantitate the response of the hepcidin promoter to short-term feeding of a high-iron diet to mice that have been maintained on an iron-deficient diet. We show that the region of the promoter between 1.6 Kb and 1.8 Kb upstream from the start of translation is essential for the response to iron. The promoter region between –260 bp and –1.6 Kb is not essential for the iron responsiveness of hepcidin promoter. The iron-responsive region that we have mapped is the same region required for the in vitro response of HepG2 cells to stimulation with bone morphogenetic proteins and differs from the LPS/IL-6 responsive area. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: F. B. Sow, G. R. Alvarez, R. P. Gross, A. R. Satoskar, L. S. Schlesinger, B. S. Zwilling, and W. P. Lafuse Role of STAT1, NF-{kappa}B, and C/EBP{beta} in the macrophage transcriptional regulation of hepcidin by mycobacterial infection and IFN-{gamma} J. Leukoc. Biol., November 1, 2009; 86(5): 1247 - 1258. [Abstract] [Full Text] [PDF] G. Ramey, J.-C. Deschemin, and S. Vaulont Cross-talk between the mitogen activated protein kinase and bone morphogenetic protein/hemojuvelin pathways is required for the induction of hepcidin by holotransferrin in primary mouse hepatocytes Haematologica, June 1, 2009; 94(6): 765 - 772. [Abstract] [Full Text] [PDF] X. Du, E. She, T. Gelbart, J. Truksa, P. Lee, Y. Xia, K. Khovananth, S. Mudd, N. Mann, E. M. Y. Moresco, et al. The Serine Protease TMPRSS6 Is Required to Sense Iron Deficiency Science, May 23, 2008; 320(5879): 1088 - 1092. [Abstract] [Full Text] [PDF] Y. Xia, J. L. Babitt, Y. Sidis, R. T. Chung, and H. Y. Lin Hemojuvelin regulates hepcidin expression via a selective subset of BMP ligands and receptors independently of neogenin Blood, May 15, 2008; 111(10): 5195 - 5204. [Abstract] [Full Text] [PDF]

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