Table 2.

List of nontrivial Maximal Common Transition (MCT) sets.

MCT Set	Contained Transitions	Biological Interpretation
$m_1$	$t_0$, $t_1$, $t_2$, $t_3$, $t_4$, $t_5$, $t_6$, $t_7$, $t_8$, $t_9$, $t_{10}$, $t_{13}$, $t_{14}$, $t_{16}$, $t_{17}$, $t_{54}$	Iron ion Fe${}^{3+}$ is reduced to ion Fe II by Dcytb and then is exported to enterocytes (to LIP) by DMT1. Hepcidin binds to Fpn and leads to degradation and internalization of Fpn. What results in prevention of iron release from enterocytes and macrophages.
$m_2$	$t_{66}$, $t_{67}$, $t_{68}$, $t_{69}$, $t_{70}$, $t_{71}$, $t_{72}$, $t_{73}$	Expression of hepcidin by HJV-BMP6-SMAD4 pathway.
$m_3$	$t_{23}$, $t_{25}$, $t_{27}$, $t_{28}$	Iron in enterocytes is absorbed by Ft and is also exported by Fpn to blood circulation.
$m_4$	$t_{57}$, $t_{58}$, $t_{59}$, $t_{60}$	Expression of hepcidin by cytokines IL-6 (JAK-STAT3 pathway) and IL-1$\beta$.
$m_5$	$t_{77}$, $t_{78}$, $t_{79}$, $t_{80}$	Low iron level activates furin which release HJV from membrane via proteolytic reaction. Soluble HJV blocks BMPRs and inhibits expression of hepcidin by inhibition of HJV-BMP6-SMAD4 pathway.
$m_6$	$t_{86}$, $t_{87}$, $t_{88}$, $t_{89}$	Vitamin A deficiency and iron deficiency impair of erythropoiesis, which results in increased phagocytosis of malformed and undifferential erythrocytes. This mechanism in consequence leads to accumulation of iron in spleen and to decrease of Hamp mRNA level.
$m_7$	$t_{35}$, $t_{36}$, $t_{37}$	Low iron level leads to degradation of FBXL5, which results in increase of IRP2. IRP2 play the same role as IRP1, leads to increase of TfR1 and DMT1 and to decrease of Ft and Fpn.
$m_8$	$t_{12}$, $t_{19}$	Hepcidin leads to degradation and internalization Fpn, which results in down-regulation of DMT1 and leads to decrease of iron absorption.
$m_9$	$t_{20}$, $t_{21}$	Iron is engaged in Fenton reaction, which leads to increase of oxidative stress via ROS.
$m_{10}$	$t_{29}$, $t_{32}$	Iron absorption by mammals via endocytosis. To be precise, iron ion Fe${}^{3+}$ binds to transferrin (Tf) and next binds to transferrin receptor protein 1 (TfR1), which results in iron absorption.
$m_{11}$	$t_{33}$, $t_{48}$	Formation of holo-IRP1 (IRP/IRE mechanisms) in case of increase of iron concentration.
$m_{12}$	$t_{34}$, $t_{39}$	Formation of apo-IRP1 (IRP/IRE mechanisms) in case of decrease of iron concentration.
$m_{13}$	$t_{40}$, $t_{44}$	apo-IRP1 binds to IRE in 3′UTR region of TfR1, which leads to increase of TfR1.
$m_{14}$	$t_{41}$, $t_{45}$	apo-IRP1 binds to IRE in 3′UTR region of DMT1, which leads to increase of DMT1.
$m_{15}$	$t_{42}$, $t_{46}$	apo-IRP1 binds to IRE in 5′UTR region of Ft, which leads to decrease of Ft.
$m_{16}$	$t_{43}$, $t_{47}$	apo-IRP1 binds to IRE in 5′UTR region of Fpn, which leads to decrease of Fpn.
$m_{17}$	$t_{61}$, $t_{64}$	In case of iron overload or iron normal status Tf bind to TfR1, which prevents HFE binding. Free HFE leads to increase of hepcidin expression.
$m_{18}$	$t_{62}$, $t_{63}$	In case of iron deficiency HFE binds to TfR1, which lead to decrease of hepcidin expression (and in consequence to increase of iron concentration).
$m_{19}$	$t_{74}$, $t_{75}$	BMP6 induces SMAD7, which negative regulates of hepcidin.
$m_{20}$	$t_{84}$, $t_{85}$	Low iron level and vitamin A deficiency lead to decrease of BMP6, which results in inhibition of HJV-BMP6-SMAD4 pathway.