Structure and mechanism of mammalian ferroportin

项目总结： 铁转运蛋白是人类体内唯一的铁输出物。铁蛋白基因突变导致 血色沉着症。铁蛋白受一种多肽荷尔蒙海普西丁调节，这种激素是 在肝脏中产生，并通过诱导内吞作用抑制铁转运蛋白的活性 通过直接抑制铁孔蛋白的活性。FPN-海普西丁轴是一种潜在的治疗方法 血色素沉着症铁稳态正常化的靶点。然而，很少有 了解铁蛋白如何识别和转运铁，以及它如何与铁相互作用 海普西丁。在这项研究中，我将结合结构分析和功能分析来理解 原子分辨条件下铁在磷化铁中的迁移和抑制机理。

Project Summary: Ferroportin is the only iron exporter in humans. Mutations in ferroportin cause hemochromatosis. Ferrorpotin is regulated by a peptide hormone hepcidin, which is produced in the liver and inhibits the activity of ferrorportin by inducing endocytosis and by direct inhibition of ferroportin activity. The FPN-hepcidin axis is a potential therapeutic target for normalizing iron homeostasis in hemochromatosis. However, very little is known about how ferroportin recognizes and transport iron and how it interacts with hepcidin. In this study, I will combine structural and functional analyses to understand the mechanism of iron transport and inhibition in ferroportin at the atomic resolution.