further:

-   changes in activity of the hepcidin gene in the liver have little effect on the size of the labile iron pool,

-   the rate of expression of HFE has a high control over the steady state level of hepcidin,

-   the strong effect of HFE is due to its interaction with TfR2 rather than TfR1,

-   the rate of liver iron export by ferroportin has a strong dependence on the expression of TfR1, TfR2 and HFE,

-   the rate of expression of hepcidin is approximately linear with the concentration of plasma iron within the physiological range.

The present model is the most detailed quantitative mechanistic model of cellular iron metabolism to date, allowing for a comprehensive description of its regulation. It can be used to elucidate the link from genotype to phenotype, as demonstrated here with hereditary haemochromatosis. The model provides the ability to investigate scenarios for which there are currently no experimental data available — thus making predictions about the system and aiding in experimental design.

Materials and Methods {#materials-and-methods .unnumbered}
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The model is constructed using ordinary differential equations (ODEs) to represent the rate of change of each chemical species. COPASI [@Hoops2006COPASIa] was used as the 