Apoptosis is the process of programmed cell death. During apoptosis, a cell initiates intracellular signaling in response to a strong stress or other cue. Death via apoptosis is characterized by many phenotypic changes in a cell, including cell shrinking, nuclear and chromosomal fragmentation, and PARP cleavage. Apoptosis is critical for proper embryonic development, immune system function, and hormone-dependent atrophy. Many of the most widely used cancer therapeutics activate apoptotic machinery to kill cancer cells. Alternately, inhibitors of apoptosis may also have therapeutic value in preventing unregulated apoptosis in HIV or neurodegenerative diseases (Alzheimer’s, Parkinson’s, Huntington’s).

There are two known apoptosis signal transduction pathways – the mitochondrial, or intrinsic pathway, and the death receptor, or extrinsic pathway. Apoptosis via the intrinsic pathway occurs when apoptotic stimuli trigger release of mitochondrial intermembrane proteins and SMAC in to the cytosol. These proteins ultimately coordinate to activate caspases which facilitate the process of programmed cell death. Conversely, apoptosis via the extrinsic pathway, as the name implies, relies on signals from outside of the cell. Specifically, death receptors on the surface of cells engage with their cognate ligands and this interaction leads to activation of signal transduction pathways that can activate caspases directly or indirectly through the Bcl-2 family of proteins.


1. Ouyang, L. et al., Cell Proliferat. 2012; 45(6): 487-498.

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