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Model of BNIP3-induced cell death. Overexpression permits integration of BNIP3 into the outer mitochondrial membrane in an Ncyto-Cin orientation through its TM domain. BNIP3 then initiates permeability transition pore opening and Δψm suppression with increased ROS production in an undefined sequence, leading to cell death. Late DNA fragmentation and chromatin condensation are also induced as a consequence of BNIP3 integration via an unidentified pathway.
