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Apoptosis Video Demonstrates a model of a caspase cascade as it occurs in vivo. The Mechanisms of Apoptosis Archived 2018-03-09 at the Wayback Machine Kimball's Biology Pages. Simple explanation of the mechanisms of apoptosis triggered by internal signals (bcl-2), along the caspase-9, caspase-3 and caspase-7 pathway; and by external signals ...
Once activated, caspase-9 goes on to cleave caspase-3, -6, and -7, initiating the caspase cascade as they cleave several other cellular targets. [8] When caspase-9 is inactive, it exists in the cytosol as a zymogen, in its monomer form. [13] [20] It is then recruited and activated by the CARDs in apaf-1, recognizing the CARDs in caspase-9. [21]
Caspase-3 shares many of the typical characteristics common to all currently-known caspases. For example, its active site contains a cysteine residue (Cys-163) and histidine residue (His-121) that stabilize the peptide bond cleavage of a protein sequence to the carboxy-terminal side of an aspartic acid when it is part of a particular 4-amino acid sequence.
Apaf-1 is the protein that turns on caspase 9 by cleavage to begin the caspase cascade that leads to apoptosis. [77] Since a -/- mutation in the APAF-1 gene is embryonic lethal, a gene trap strategy was used in order to generate an APAF-1 -/- mouse. This assay is used to disrupt gene function by creating an intragenic gene fusion.
Caspase-1/Interleukin-1 converting enzyme (ICE) is an evolutionarily conserved enzyme that proteolytically cleaves other proteins, such as the precursors of the inflammatory cytokines interleukin 1β and interleukin 18 as well as the pyroptosis inducer Gasdermin D, into active mature peptides.
Once APO-1 aggregates within the cytosol, it recruits FADD, CAP3, and FLICE to the receptor, where FLICE is modified into several active subunits, which have the ability to cleave a variety of substrates. This proteolytic activity then results in a cascade of caspase activation, and ultimately cell death.
The precise mechanism for this reaction is still debated though work published by Guy Salvesen suggests that the apoptosome may induce caspase-9 dimerization and subsequent autocatalysis. [9] Activated caspase-9 stimulates the subsequent caspase cascade that commits the cell to apoptosis. [citation needed]
The caspase-dependent apoptosis cascade is initiated, causing cells to "commit suicide." If the cell dies through necrosis, it releases glutamate and toxic chemicals into the environment around it. Toxins poison nearby neurons, and glutamate can overexcite them. If and when the brain is reperfused, a number of factors lead to reperfusion injury.