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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. Cell damage can be reversible or irreversible.
Phagocytosis of an otherwise-viable cell may occur because the cell is recognised as stressed, activated, senescent, damaged, pathogenic or non-self, or is misrecognised. Cells are phagocytosed as a result of: i) expressing eat-me signals on their surface, ii) losing don’t-eat-me signals, and/or iii) binding of opsonins. It is clear that ...
The second one is increase in sensitivity of damaged cells to these regulators, as it was demonstrated on the example of comuton. These effectors cause tissue-specific self-damage of homologous cells via disturbance of their ion homeostasis and energy-production processes. As a result, unspecific reaction to damage (CURD) is activated in the 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.
After DNA damage, cell cycle checkpoints are activated. Checkpoint activation pauses the cell cycle and gives the cell time to repair the damage before continuing to divide. DNA damage checkpoints occur at the G1/S and G2/M boundaries. An intra-S checkpoint also exists. Checkpoint activation is controlled by two master kinases, ATM and ATR.
Coagulative necrosis is a type of accidental cell death typically caused by ischemia or infarction. In coagulative necrosis, the architectures of dead tissue are preserved for at least a couple of days. [1] It is believed that the injury denatures structural proteins as well as lysosomal enzymes, thus blocking the proteolysis of the damaged cells.
Damage-associated molecular patterns (DAMPs) [1] are molecules within cells that are a component of the innate immune response released from damaged or dying cells due to trauma or an infection by a pathogen. [2]
Long-term live cell imaging (12h) of multinucleated mouse pre-Adipocyte trying to undergo mitosis. Due to the excess of genetic material the cell fails to replicate and dies by apoptosis. Label-free live cell imaging, time-lapse microscopy, flow fluorocytometry, and transmission electron microscopy can be used to compare apoptotic and necrotic ...