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In conditions of low body iron, Fe 2+ is mobilized into circulation through two pathways: either directly exported through ferroportin-1 (FPN1) on the basal membrane, where it is oxidized to Fe 3+ by copper-containing iron oxidases, such as ceruloplasmin and hephaestin, or by FTN degradation via autophagy mediated by nuclear receptor coactivator 4 (NCOA4)

Gut microbiota and Parkinsons disease

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2007;Jan 15;109(2):412-421

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Taken together, these studies highlight the importance of better characterization and quantification of the involvement of mechanical and physical properties of the environment in which the cells reside, giving attentions not only on the mechanotransductive machinery involved, but also achieving a better control on this machinery through the passive function of the substrates and the active adaptation of the cells