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Lodish H, Berk A, Zipursky SL, et al. Molecular Cell Biology. 4th edition. New York: W. H. Freeman; 2000.

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Molecular Cell Biology. 4th edition.

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Figure 23-50. Current models of the intracellular pathways leading to cell death by apoptosis or to trophic factor–mediated cell survival in mammalian cells.
Figure 23-50. Current models of the intracellular pathways leading to cell death by apoptosis or to trophic factor–mediated cell survival in mammalian cells.

Figure 23-50Current models of the intracellular pathways leading to cell death by apoptosis or to trophic factor–mediated cell survival in mammalian cells

The details of these pathways in any given cell type are not yet known. (a) In the absence of a trophic factor. Bad, a soluble pro-apoptotic protein, binds to the anti-apoptotic proteins Bcl-2 and Bcl-xl, which are inserted into the mitochondrial membrane. Bad binding prevents the anti-apoptotic proteins from interacting with Bax, a membrane-bound pro-apoptotic protein. As a consequence, Bax forms homo-oligomeric channels in the membrane that mediate ion flux. Through an as-yet unknown mechanism, this leads to the release of cytochrome c from the space between the inner and outer mitochondrial membrane. Cytochrome c then binds to the adapter protein Apaf-1, which in turn promotes a caspase cascade leading to cell death. (b) In the presence of a trophic factor such as NGF. In some cells, binding of trophic factors stimulates PI-3 kinase activity, leading to activation of the downstream kinase Akt, which phosphorylates Bad. Phosphorylated Bad then forms a complex with the 14 - 3 - 3 protein. With Bad sequestered in the cytosol, the antiapoptotic Bcl-2/Bcl-xl proteins can inhibit the activity of Bax, thereby preventing the release of cytochrome c and activation of the caspase cascade. [Adapted from B. Pettman and C. E. Henderson, 1998, Neuron 20:633.]

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From: Section 23.8, Cell Death and Its Regulation

Copyright © 2000, W. H. Freeman and Company.

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