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The development of a peptide derived from the N-terminus of hBNIP3 has been shown to facilitate mitochondrial protection by competing with the BAX-activating domain of BNIP3 based on hotspot mimicry of key hydrophobic residues impeding the BAX-initiated point of no return and halting the signalling cascade that culminates in apoptosis and necrosis in human cells (Supplementary Fig

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