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[19] [20] One of the damaging results of excess calcium in the cytosol is initiating apoptosis through cleaved caspase processing. [20] Another damaging result of excess calcium in the cytosol is the opening of the mitochondrial permeability transition pore, a pore in the membranes of mitochondria that opens when the organelles absorb too much ...
Unlike necrosis, apoptosis produces cell fragments called apoptotic bodies that phagocytes are able to engulf and remove before the contents of the cell can spill out onto surrounding cells and cause damage to them. [5] Because apoptosis cannot stop once it has begun, it is a highly regulated process.
The mitochondrial apoptosis-induced channel (or MAC), is an early marker of the onset of apoptosis. [2] [3] This ion channel is formed on the outer mitochondrial membrane in response to certain apoptotic stimuli. [4] MAC activity is detected by patch clamping mitochondria from apoptotic cells at the time of cytochrome c release. [5]
Cellular hypertrophy is an increase in cell size and volume. If enough cells of an organ hypertrophy the whole organ will increase in size. Hypertrophy may involve an increase in intracellular protein as well as cytosol (intracellular fluid) and other cytoplasmic components.
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.
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.
These budding fragments were termed "apoptotic bodies," thus coining the name "apoptosis" to describe this form of cell death. The authors of these studies, most likely unfamiliar with older publications on chromatolysis, were essentially describing apoptosis as a process identical to chromatolysis. [2]