Hepcidin antimicrobial peptide with ferroportin (FPN)

Hepcidin antimicrobial peptide with ferroportin (FPN)
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SLC40A1 solute carrier family 40 (iron-regulated transporter), member 1 Ferroportin-1, locus: 2q32 [§§] is mediated by the divalent metal transporter, DMT1 and the duodenal iron transporters divalent-metal transporter 1 (SLC11A1). Hemochromatosis genes encode molecules that regulate hepcidin synthesis described for C282Y mutations or TFR2 (transferrin receptor 2) of genes controlling iron metabolism, and two CYBRD1 gene mutations. Hepcidin antimicrobial peptide directly interacts with ferroportin (FPN) and modulates iron transport from macrophages and enterocytes to red blood cell precursors. Ferroportin-1 (SLC11A3) is involved in iron export from enterocytes in mammals, initiated by uptake of ferrous Fe(II) iron across the brush border membrane and localized to the basolateral membrane requires: a glycophosphosinositide-linked, CP gene found in ceruloplasmin and its homologue copper-containing iron oxidase known as (Heph) hephaestin. A mutation in the SLC40A1 genes (Ferroportin) secondary effects of the ‘erythropoietic regulator’ stimulating intestinal iron absorption from dietary sources, and point mutation in the L ferritin (FTL; 134790) in lens ferritin accumulation contributing to age-related cataract in situations that alter normal iron homeostasis of certain forms of “ferroportin disease” results from dominant negative effects either a regulatory function or as the necessary link in iron homeostasis in health and disease can be interpreted.

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4 Comments

  1. Posted March 2, 2011 at 9:38 pm | Permalink | Reply

    Hello – my child has a deletion from 2q32-2q33.1. I’m a curious parent – is this a reason to do a metabolic study or are there other iron related impacts you are aware of?

    • Posted March 5, 2011 at 10:18 pm | Permalink | Reply

      copper deficiency parallels the secondary effects of stimulating intestinal iron absorption from dietary sources. Abeta (APP) deposits in the cavity of the cell need to be degraded without causing secondary symptoms associated with Iron defiencie makeing GEPT, a combination of herbal extracts include vitamin D, genistein, and sesamin. Is the only workable way out of the bottle neck in medical literature from the iron,copper inbalances defecits if you read on to find out the pharmacology. http://wp.me/pex06-19I

    • Posted October 9, 2011 at 9:05 pm | Permalink | Reply

      Data has led researchers to suggest therapeutics that could increase hepcidin levels or act as hepcidin agonists might help treat the abnormal iron absorption in individuals with β-thalassemia and related disorders.
      http://en.wikipedia.org/wiki/Hepcidin
      The LIF receptor heterodimer, containing defined regions of human chromosome 2q12.2 N-terminal deletions…
      and LIF can induce hepcidin expression mainly through the JAK/STAT pathways.
      http://www.ihop-net.org/UniPub/iHOP/pm/14631755.html?nr=8&pmid=19915946
      Oncostatin-M Homo sapiens
      http://www.ihop-net.org/UniPub/iHOP/gs/90769.html?ID=89455
      Hepcidin antimicrobial peptide with ferroportin (FPN)
      http://goo.gl/f4Fp7

    • Posted November 15, 2011 at 10:22 pm | Permalink | Reply

      Deferoxamine is used to treat acute iron poisoning, especially in small children. This agent is also frequently used to treat hemochromatosis, a disease of iron accumulation that can be either genetic or acquired. http://en.wikipedia.org/wiki/Deferoxamine

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