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Because apoptosis cannot stop once it has begun, it is a highly regulated process. Apoptosis can be initiated through one of two pathways. In the intrinsic pathway the cell kills itself because it senses cell stress, while in the extrinsic pathway the cell kills itself because of signals from other cells.
Overview of signal transduction pathways involved in apoptosis. Cell death is the event of a biological cell ceasing to carry out its functions. This may be the result of the natural process of old cells dying and being replaced by new ones, as in programmed cell death, or may result from factors such as diseases, localized injury, or the death of the organism of which the cells are part.
Programmed cell death (PCD; sometimes referred to as cellular suicide [1]) is the death of a cell as a result of events inside of a cell, such as apoptosis or autophagy. [2] [3] PCD is carried out in a biological process, which usually confers advantage during an organism's lifecycle.
Cells with a defective G 2-M checkpoint will undergo apoptosis or death after cell division if they enter the M phase before repairing their DNA. [1] The defining biochemical feature of this checkpoint is the activation of M-phase cyclin-CDK complexes, which phosphorylate proteins that promote spindle assembly and bring the cell to metaphase. [2]
The presence or absence of particular apoptotic event(s), including DNA fragmentation, depends on the "time window" at which the kinetic process of apoptosis is being investigated. Often this may complicate identification of apoptotic cells if cell populations are analyzed only at a single time point e.g. after induction of apoptosis.
Cell damage (also known as cell injury) is a variety of changes of stress that a cell suffers due to external as well as internal environmental changes. Amongst other causes, this can be due to physical, chemical, infectious, biological, nutritional or immunological factors.
[6] [7] It was the first apoptosis regulator identified in any organism. [ 8 ] Bcl-2 derives its name from B-cell lymphoma 2 , as it is the second member of a range of proteins initially described in chromosomal translocations involving chromosomes 14 and 18 in follicular lymphomas .
Firstly, to bring multiple procaspase-9 molecules close together for cleavage. And secondly, to raise the threshold for apoptosis, therefore nonspecific leakage of cytochrome c would not result in apoptosis. [7] Once the apoptosome was established as the procaspase-9 activator, mutations within this pathway became an important research area.