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. 2023 Jan 18;13(2):194. doi: 10.3390/biom13020194

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© 2023 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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Representation of the molecular activation mechanism of intrinsic and extrinsic pathways of programmed cell death. Both intrinsic and extrinsic pathways depend on specific signals to initiate an energy-dependent cascade of molecular events, thereby activating initiator caspases which leads to the activation of executioner caspase-3.TNF (Tumor necrosis factor), FASL (FS-7-associated surface antigen ligand), TRAIL (Targeting TNF-related apoptosis-inducing ligand), TNFR1 (Tumor necrosis factor receptor 1), DRS (Death receptors), DISC (death-inducing signaling complex), BID (BH3 interacting-domain), MCL (myeloid leukemia cell differentiation protein), ER (Endoplasmic reticulum), BAX (Bcl-2-associated X protein), BAK (B-cell lymphoma 2 killer), SMAC (Second mitochondria-derived activator of caspase), XIAP (X-linked inhibitor of apoptosis protein), MOMP (mitochondrial outer membrane permeabilization), and APAF (Apoptotic protease activating factor). (Adapted from “Apoptosis Extrinsic and Intrinsic Pathways” by BioRender.com. (https://app.biorender.com/biorender-templates by BioRender.com, access on 30 November 2022).