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By selectively disrupting key antioxidant systemssuch as inhibiting glutathione synthesis with buthionine sulfoximine (BSO), blocking thioredoxin reductase with auranofin, or directly targeting NRF2therapies can push cancer cells beyond their limited oxidative buffering capacity

nanoBiT recruitment responses, FRET biosensor responses, and TR-FRET internalisation and recycling kinetic responses were expressed relative to individual well baselines

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