Two iron transport proteins, divalent metal transporter 1 (DMT1) and ferroportin 1
(FPN), are expressed in duodenal enterocytes [4, 5].
However, the iron from different states such as absorbed iron in duodenal enterocytes or stored within hepatocytes or recycled by macrophages; ultimately pass from cytoplasm of cells to the transferrin (Ganz et al., 2012), and iron efflux from cells is facilitated via a multipass transmembrane protein i.e., iron exporter ferroportin 1
(Donovan et al., 2005).
Theurl et al., "Expression of the duodenal iron transporters divalent-metal transporter 1 and ferroportin 1
in iron deficiency and iron overload," Gastroenterology, vol.
This association between the levels of lead and iron is likely due to their sharing of the same transporters, such as the divalent metal transporter 1 (DMT1) and ferroportin 1
Tfr2[beta] levels were evaluated, together with the main proteins involved in cellular iron traffic, namely, the iron deposit protein ferritin (Ft-L), the iron importer DMT1, and the iron exporter Ferroportin 1
Hepcidin is also considered as a master regulator in the management of cellular iron homeostasis by binding to iron exporter protein ferroportin 1
(Fpn1) in cell membranes and causing its subsequent internalization and lysosomal degradation .
In the cell, iron is reduced to the ferric form and exported to the blood by ferroportin 1
[solute carrier family 40 (iron-regulated transporter), member 1; SLC40A1, formerly FPN1] at the basolateral membrane.
pylori infection and resulted in the upregulation of the expression of various downstream iron absorption and efflux genes such as Ferroportin 1
, Divalent metal transporter 1, and Transferrin receptor 1 .
The identification of ferroportin 1
B may explain how high ferroportin expression is possible in duodenal epithelial and erythroid precursor cells during high intracellular iron levels.
Iron overloading and erythrophagocytosis increase ferroportin 1
(FPN1) expression in J774 macrophages.
Novel mutation in ferroportin 1
gene is associated with autosomal dominant iron overload.