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While antioxidant response enzymes are well-characterized transcriptional targets of NRF2, it is recently becoming clear that NRF2 also supports cellular detoxification through metabolic rewiring to support the antioxidant systems

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Ferroptocide binds covalently to the active site cysteines 32 and 35 and the additional cysteine 73 of Trx1 [96] inhibiting its enzymatic function and the coordination of the FeS-cluster [13]