A chemical screen identifies small molecules that regulate hepcidin expression

• Published in: Blood cells, molecules, & diseases Vol. 53; no. 4; pp. 231 - 240
• Main Authors: Gaun, Vera, Patchen, Bonnie, Volovetz, Josephine, Zhen, Aileen W., Andreev, Aleksandr, Pollastri, Michael P., Fraenkel, Paula G.
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.12.2014
• Subjects: Bone Morphogenetic Proteins - genetics; Bone Morphogenetic Proteins - metabolism; Bone morphogenic protein; Cell Survival; Databases, Chemical; Drug Discovery; Gene Expression Regulation - drug effects; Genes, Reporter; Hemochromatosis; Hep G2 Cells; Hepcidins - agonists; Hepcidins - antagonists & inhibitors; Hepcidins - genetics; Hepcidins - metabolism; High-Throughput Screening Assays; Humans; Interleukin-6; Luciferases - genetics; Luciferases - metabolism; Plasmids - chemistry; Plasmids - metabolism; Promoter Regions, Genetic; Recombinant Fusion Proteins - genetics; Recombinant Fusion Proteins - metabolism; Signal Transduction; Smad Proteins - genetics; Smad Proteins - metabolism; Small Molecule Libraries - chemistry; Small Molecule Libraries - pharmacology; Stat3; STAT3 Transcription Factor - genetics; STAT3 Transcription Factor - metabolism; Thalassemia; Transfection; Stat3; Thalassemia; Hemochromatosis; Bone morphogenic protein; Interleukin-6

Hepcidin, a peptide hormone produced in the liver, decreases intestinal iron absorption and macrophage iron release via effects on ferroportin. Bone morphogenic protein and Stat3 signaling regulate Hepcidin's transcription. Hepcidin is a potential drug target for patients with iron overload syn...