哺乳动物铁转运蛋白的结构和机制-猫眼课题宝

哺乳动物铁转运蛋白的结构和机制

批准号：

10183365

负责人：

Yaping Pan

金额：

$40.0万

依托单位：

BAYLOR COLLEGE OF MEDICINE

依托单位国家：

美国

项目类别：

财政年份：

2021

资助国家：

美国

项目状态：

未结题

起止时间：

2021-05-01 至 2025-04-30

来源：

https://reporter.nih.gov/project-details/10183365

关键词：

Affinity Binding Binding Sites Biological Assay Cells Complex Cryoelectron Microscopy Endocytosis Enzymes Fab Immunoglobulins Family Foundations Future Genus Tarsius Goals Hemochromatosis Hemoglobin Hereditary Disease Homeostasis Human Ion Transport Ions Iron Iron Metabolism Disorders Iron Overload Iron deficiency anemia Lipids Liver Mammals Maps Measures Mediating Metal Ion Binding Metals Molecular Conformation Monoclonal Antibodies Mutation Myoglobin Nutrient Oxidation-Reduction Regulation Resolution Role Side Site Solid Solvents Structure Symptoms Trace Elements Transition Elements antiporter extracellular hepcidin improved indexing inhibitor/antagonist iron deficiency member metal transporting protein 1 nanodisk peptide hormone reconstitution small molecule small molecule inhibitor solute therapeutic target three dimensional structure

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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.

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