KEAP1 is a pivotal sensor of oxidative stress. Under oxidative or electrophilic stress conditions, critical cysteine residues on KEAP1 become modified, leading to a conformational change that impedes its ability to target Nrf2 for degradation. As a result, Nrf2 translocates to the nucleus where it binds to antioxidant response elements (ARE) in the promoter regions of various genes. This process leads to the expression of a battery of cytoprotective genes involved in detoxification, antioxidant defenses, and maintenance of redox balance.
