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Following FOXO4 displacement, the released p53 undergoes nuclear export and mitochondrial translocation, activating the intrinsic apoptosis pathway via BAX upregulation and BCL-2 downregulation, culminating in caspase-3 cleavage and apoptotic cell death

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This article examines the structural modifications that distinguish the modified form from its parent peptide, reviews the published research on the AEDG sequence across its primary domains of investigation, and discusses the implications of enhanced metabolic stability for experimental design in cellular aging research

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