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There are three different ways that a cell can start the process of apoptosis. The first is to trigger it by sending internal signals through the mitochondrial pathway. The second way is through external signals through the death receptor pathway. Finally, the cell can trigger apoptosis through an inducing factor. [http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/A/Apoptosis.html] | There are three different ways that a cell can start the process of apoptosis. The first is to trigger it by sending internal signals through the mitochondrial pathway. The second way is through external signals through the death receptor pathway. Finally, the cell can trigger apoptosis through an inducing factor. [http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/A/Apoptosis.html] | ||
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In a healthy cell, the outer membranes of its mitochondria display the protein Bcl-2 on their surface. | |||
Internal damage to the cell (e.g., from reactive oxygen species) causes | |||
Bcl-2 to activate a related protein, Bax, which punches holes in the outer mitochondrial membrane, causing | |||
cytochrome c to leak out. | |||
The released cytochrome c binds to the protein Apaf-1 ("apoptotic protease activating factor-1"). | |||
Using the energy provided by ATP, | |||
these complexes aggregate to form apoptosomes. | |||
The apoptosomes bind to and activate caspase-9. | |||
Caspase-9 is one of a family of over a dozen caspases. They are all proteases. They get their name because they cleave proteins — mostly each other — at aspartic acid (Asp) residues). | |||
Caspase-9 cleaves and, in so doing, activates other caspases (caspase-3 and -7). | |||
The activation of these "executioner" caspases creates an expanding cascade of proteolytic activity (rather like that in blood clotting and complement activation) which leads to | |||
digestion of structural proteins in the cytoplasm, | |||
degradation of chromosomal DNA, and | |||
phagocytosis of the cell. | |||
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== Senesence Hormones == | == Senesence Hormones == |
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