Figure 1. Schematic illustration of Dox-controlled FTH1 expression.

FTH1 expression was controlled by a tetracycline-responsive element (TRE). With Dox administration, the reverse tetracycline-controlled transactivator (rtTA), regulated by ubiquitin (Ubi), activated the TRE and switched “on” FTH1 expression. With Dox withdrawal, the TRE was not activated by rtTA, and FTH1 expression was switched “off.”