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The hemochromatosis proteins HFE, TfR2, and HJV form a membrane-associated protein complex for hepcidin regulation

Previously, this loss of activity had been determined to be due to a RhoA GTPase-dependent internalization which could be blocked by dominant-negative RhoA constructs and by genetic introduction of the exotoxin C3, a clostridial exotoxin that inactivates RhoA by ADP-ribosylation [1]