Fig. 9: The schematic depiction shows the mechanism underlying the regulatory effects of CERK-mediated C1P on NRF2 through binding to KEAP1.

Oxidative stress in the liver induces upregulated CERK expression, and CERK mediates the accumulation of C1P, which binds to the DGR region of KEAP1 and disrupts the binding of KEAP1 to NRF2. Then, NRF2 escapes KEAP1-mediated degradation and translocates to the nucleus, where it promotes the transcription of antioxidant genes.