Apoptosis is defined as a process of programmed cell death. It is of importance not only in the body’s defense against diseases but also plays a crucial role in embryonic development. Apoptosis is one of the mechanisms that control cell proliferation and thereby restrict the development of cancerous cells.
In this context the p53 gene is of importance as a tumor-suppressor in apoptosis. The gene-product of p53 is the p53 protein accumulates due to DNA damage and triggers apoptosis. Hence, p53 can be used as a marker in apoptosis assays. In virus infections proteins like p53 are often inhibited and the apoptotic process is being stopped. For this reason virus infections have received much attention recently as possible causal events in the development of cancer.
The apoptotic process stops replication of the cell by cell cycle arrest, thereby inhibiting the possible development of a tumor. Because apoptosis is an intercellular process other cells are not harmed. This is in contrast to necrosis, where cells are damaged by traumatic external events. Contrary to apoptosis this external event can lead to the release of cellular components that are toxic to surrounding cells. The necrotic cell send inhibiting signals to cells of the immune system which leads stops these cells from removing the debris made up of chemical compounds of dead cells. The accumulation of these toxic chemicals can in some case spread through the circulatory system and cause systemic failure and ultimately death.
Within the cells that undergo apoptosis the mitochondria are central for the regulation and progression of the apoptotic event. Several mitochondrial and cytosolic proteins, including Cytochrome C and caspases interact and lead to the formation of a complex denominated the apoptosome that triggers the programmed cell death.