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Reversible sequestration of active site cysteines in a 2Fe-2S-bridged dimer provides a mechanism for glutaredoxin 2 regulation in human mitochondria

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doi: 10.1007/bf01963567 15 GerverWJDe BruinRDelemarre v d WaalHAAldewereldBTheunissenPet al

To cope with the elevated oxidative stress they generate, cancer cells enhance their antioxidant capacity, largely through sustained activation of the transcription factor NRF2 often driven by mutations in its negative regulator KEAP1

The mechanisms are different and do not directly conflict, but absence of conflict is not the same as evidence of benefit