Sorry about taking so long to respond, as I was out of town last week for some vacation and a conference. Apoptosis is initiated by the some signalling pathway in the cell recieving a signal that the cell should die. Examples of this include the binding of the protein FasL to the the protein Fas (the cell that has the Fas dies), the protein tumor necrosis factor (TNF) binding to the TNF receptor (this _sometimes_ results in cell death, but can also result in cell growth!), and the detection of large amounts of DNA damage. After the signal for cell death is detected, the actual initiating event that results in cell death is the activating of a series of proteases called, I believe, caspases (Proteases are enzymes that degrade other proteins.). These proteases begin degrading other proteins that are critical for the cell's survival and activate other proteins that further degrade the cell. For example, a classic symptom of apoptosis is the cell's DNA being cut into small pieces.
Some of the these pathways appear to always result in cell death. An example of this is the Fas protein. If a cell expresses Fas and FasL binds to Fas, that cell will die. This signalling pathway is extremely to various organs in the body, such as the brain and eye, to prevent immune responces in these organs that would result in inflammation and consequent severe damage to the organ. The TNF pathway is extremely interesting, since binding of TNF to a cell can result in either cell death, growth or differentiation. The apparent reason for this is that after a cell binds TNF and perceives this signal, the signal is integrated with other signalling pathways before the cell decides wether to live or die. In contrast, the Fas pathway is directly connected to the caspaces and their does not appear to be any pathways that can stop cell death. (In 10 years, however, this last statment may prove to be false once we know a lot more about this how signalling works.) |
