In response to oxidative stress or exposure to toxic agents, Nrf2 is released from Keap1, translocates to the nucleus, and activates the expression of various cytoprotective genes. This process is often triggered by electrophilic chemicals or oxidative stress that modify cysteine residues on Keap1, disrupting its ability to bind Nrf2. Consequently, Nrf2 accumulates and translocates to the nucleus to initiate a protective genetic program.
