Diagram showing how<unk>  controls ferroportin (FPN) levels which in turn control entry of iron into the circulation<unk>  is a regulator of iron metabolism. It inhibits iron transport by binding to the iron export channel ferroportin which is located in the basolateral plasma membrane of gut enterocytes and the plasma membrane of reticuloendothelial cells (macrophages), ultimately resulting in ferroportin breakdown in lysosomes. Inhibiting ferroportin prevents iron from being exported from the cell. In enterocytes, this prevents iron transmission into the hepatic portal system, thereby reducing dietary iron absorption. In macrophages, ferroportin inhibition causes iron sequestration within the cell. Increased<unk>  activity is partially responsible for reduced iron availability seen in anemia of chronic inflammation, such as kidney failure. Any one of several mutations in<unk>  result in juvenile hemochromatosis. The majority of juvenile hemochromatosis cases are due to mutations in hemojuvelin. Mutations in TMPRSS6 can cause anemia through dysregulation of<unk> .<unk>  has strong antimicrobial activity against Escherichia coli strain ML35P and Neisseria cinerea and weaker antimicrobial activity against Staphylococcus epidermidis, Staphylococcus aureus and Streptococcus agalactiae. It is also active against the fungus Candida albicans, but has no activity against Pseudomonas aeruginosa.
Hepcidin
Ferritin
Ovoferrin
Beta-2 transferrin
Thyroglobulin
Gamma globulin
Alpha-1 antitrypsin
Toxidrome