FIGURE 1.

Overview of the Keap1–Nrf2 pathway.

Under homeostatic conditions, Nrf2, bound to a trimeric complex with Keap1 and Cullin3, is ubiquitinated and thence degraded by the 26S proteasome. During oxidative stress, the reactive cysteine residues in Keap1 bind to ROS or electrophilic toxins, causing a conformational change that impairs its ability to bind Nrf2. Nrf2 accumulates in the cytoplasm and then translocates into the nucleus where it activates the transcription of antioxidant-responsive genes. ARE, antioxidant response element; sMaf, small musculoaponeurotic fibrosarcoma. This figure was made in BioRender.com