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A hypothetical model of the central apoptotic pathway
A hypothetical model of the central apoptotic pathway. Initiation of apoptosis is held in check by survival signals received by cell surface receptors. Removal of the cell from its in vivo context or blockade of these survival signals allows induction of the apoptotic pathway, resulting in loss of mitochondrial outer membrane integrity and cytochrome c release. Cytosolic cytochrome c interacts with Apaf-1, which in the presence of ATP leads to caspase 9 processing and activation. This initiates a cascade of caspase activation, and ultimately in the characteristic morphologic changes of apoptosis. Bcl-2 and Bcl-xL reside in the mitochondrial outer membrane and can inhibit cytochrome c release. Other important apoptotic initiators include cell surface receptor-mediated cell death signals, DNA damage, cell cycle dysregulation, and metabolic alterations. Source: Apoptosis and Cancer, The Online Metabolic and Molecular Bases of Inherited Disease Citation: Valle D, Beaudet AL, Vogelstein B, Kinzler KW, Antonarakis SE, Ballabio A, Gibson K, Mitchell G. The Online Metabolic and Molecular Bases of Inherited Disease; 2014 Available at: Accessed: October 25, 2017 Copyright © 2017 McGraw-Hill Education. All rights reserved
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