Background：

Substrate-specific adapter of a BCR E3 ubiquitin ligase complex that regulates the response to oxidative stress by targeting NFE2L2/NRF2 for ubiquitination. KEAP1 acts as a key sensor of oxidative and electrophilic stress: in normal conditions， the BCR(KEAP1) complex mediates ubiquitination and degradation of NFE2L2/NRF2， a transcription factor regulating expression of many cytoprotective genes. In response to oxidative stress， different electrophile metabolites trigger non-enzymatic covalent modifications of highly reactive cysteine residues in KEAP1， leading to inactivate the ubiquitin ligase activity of the BCR(KEAP1) complex， promoting NFE2L2/NRF2 nuclear accumulation and expression of phase II detoxifying enzymes. In response to selective autophagy， KEAP1 is sequestered in inclusion bodies following its interaction with SQSTM1/p62， leading to inactivation of the BCR(KEAP1) complex and activation of NFE2L2/NRF2. The BCR(KEAP1) complex also mediates ubiquitination of SQSTM1/p62， increasing