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reported that activating ITGB4/BNIP3 could promote the phagocytosis of MHC-I by autophagosomes, thus promoting immune escape in PDAC [69]

Q., & Gu, J

It also comprises key residues that facilitate the GSH-based nucleophilic attack on the electrophilic substrate, leading to the formation of a thioether bond and the subsequent detoxification of the substrate