Structure and mechanism of mammalian ferroportin

项目摘要： Ferroportin是人类唯一的铁输出者。铁转运蛋白的突变导致 血色病Ferrorpotin受肽激素hepcidin调节， 在肝脏中产生，并通过诱导内吞作用抑制铁蛋白的活性， 通过直接抑制膜铁转运蛋白活性。FPN-hepcidin轴是一种潜在的治疗药物， 用于使血色病中铁稳态正常化的靶点。然而，很少有 我们知道膜铁转运蛋白如何识别和转运铁，以及它如何与 铁调素在这项研究中，我将联合收割机的结构和功能分析相结合，以了解 在原子分辨率下探讨膜铁转运蛋白的铁转运和抑制机制。

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.