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When cysteine residues in KEAP1 undergo redox oxidation, NRF2 interacts with the Cul3/RING-box protein complex, ultimately leading to NRF2 ubiquitination and subsequent degradation via proteasomes

This is suggestive of a prolonged formation of catechin via gut microbial degradation of procyanidins in the colon (Figure 3)

251,252,253 Thus, NAD(P) + /NAD(P)H acts as an important modulator of cellular energetic status, enabling the reset of redox rhythmic and transcriptional oscillations based on metabolic signals

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The consistent involvement of residues like VAL A:135 and ASN A:64 across multiple compounds suggests their critical role in the binding mechanism