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  • suppression
  • Here, we used a genetic approach to disengage HIF activation from EPO synthesis and found that HIF-mediated suppression of the hepcidin gene (Hamp1) required EPO induction. (jci.org)
  • 9 Indeed, patients with congenital dyserythropoietic anemia type I were found to express very high levels of serum GDF15, and this contributed to the inappropriate suppression of hepcidin with subsequent secondary overload. (haematologica.org)
  • promoter
  • To determine whether hepcidin interacts with Fpn, we generated a stable cell line (HEK293-Fpn) expressing mouse Fpn with a C-terminal green fluorescent protein (GFP) under the control of the ecdysone-inducible promoter. (sciencemag.org)
  • Time course analysis of the effect of a single EPO injection on hepcidin and BMP-SMAD target genes in WT and Erfe −/− mice and analysis of chromatin modifications at the hepcidin promoter locus 6 and 9 hours after EPO. (haematologica.org)
  • The heteromeric complexes translocate to the nucleus, where they bind directly or in complex with other transcription factors to promoter elements of target genes to regulate transcription. (els.net)
  • However, Smad4 DNA-binding activity and the binding of Smad4 to hepcidin promoter were attenuated. (hindawi.com)
  • novel
  • A novel hepcidin-like in turbot (Scophthalmus maximus L.) highly expressed after pathogen challenge but not after iron overload. (nih.gov)
  • MiR-485-3p-mediated repression of FPN may also offer a novel potential therapeutic mechanism for circumventing hepcidin-resistant mechanisms responsible for some iron overload diseases. (prolekare.cz)
  • molecular
  • Discoveries of the roles of ferroportin, hepcidin, lipocalin 2, and members of the six transmembrane epithelial antigen of the prostate (STEAP) and iron regulatory protein (IRP) families in cancer have provided specificity and molecular definition to the role of iron homeostasis in cancer growth and metastasis. (aacrjournals.org)
  • This connection between hepcidin and inflammatory pathways has provided a molecular explanation for the pathophysiology of the anemia of chronic disease, a common and heretofore poorly understood consequence of many common medical conditions, including cancer. (aacrjournals.org)