Beyond the antioxidant switch
Figures and interactive outputs are conceptual illustrations, not experimental measurements.
Adjust the inputs and compare a brief response with a response that persists.
How effectively feedback, turnover and recovery bring signaling back toward baseline.
A brief stress pulse with effective feedback permits output to return toward baseline.
Select a component to inspect its role in control and recovery.
Reactive cysteine residues respond to oxidative and electrophilic cues. Their modification can reduce KEAP1-mediated NRF2 ubiquitination and stabilize NRF2.
Different defects can produce persistent output through different routes.
Loss-of-function changes or persistent modification can weaken KEAP1-mediated NRF2 repression after the original stress signal subsides.
Explore why peak activation alone can miss the cost of persistent signaling.
Prioritizes whether NRF2 is activated and how strongly targets are induced.
Tracks input history, output duration, termination and recovery of responsiveness.
Choose a perturbation and the measurement that would best separate the models.
Choose settings, then generate a matched experiment plan.
Apply the selected perturbation and sample before, during and after it. Generate a prediction to compare model-specific outcomes.
Prioritizes pathway activation and target induction during stress.
Predicts that decay and recovery may distinguish conditions with similar peak output.
Select a context to see how persistent NRF2 signaling may be interpreted.
A time-limited NRF2 response can induce antioxidant and detoxification programs. Efficient termination helps return the system toward a responsive baseline.
The redoxostat framework shifts attention from peak NRF2 activity alone to the full trajectory: sensing, response, termination and renewed competence.
Read the published review ↗