Figure 5.
Figure 5. Phenotypes of crosses between Tmprss6 knockout mouse and other models of iron disorders. Tmprss6−/− mice with an iron-deficient phenotype (left) have been crossed with different models of iron overload (middle). The phenotype of the double knockout mice is shown. Double Tmprss6-Bmp6 and Tmprss6-Hjv knockout (top) develop iron overload. Crossing Tmprss6−/− with both Hfe−/− and TFr2−/− (middle) leads to iron-deficient double knockout mice. Loss of Tmprss6 activity in beta-thalassemia mice (bottom) reduces iron overload and improves anemia (see “Lessons from animal models of TMPRSS6 inactivation” for details).

Phenotypes of crosses between Tmprss6 knockout mouse and other models of iron disorders.Tmprss6−/− mice with an iron-deficient phenotype (left) have been crossed with different models of iron overload (middle). The phenotype of the double knockout mice is shown. Double Tmprss6-Bmp6 and Tmprss6-Hjv knockout (top) develop iron overload. Crossing Tmprss6−/− with both Hfe−/− and TFr2−/− (middle) leads to iron-deficient double knockout mice. Loss of Tmprss6 activity in beta-thalassemia mice (bottom) reduces iron overload and improves anemia (see “Lessons from animal models of TMPRSS6 inactivation” for details).

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