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Fas-induced apoptosis can be blocked by use of FLIPs ( FLICE-inhibitory proteins, which inhibit caspases-8 and-10 ), Bcl-2 ( which prevents cytochrome c release and the subsequent activation of caspase 9 ), and CrmA ( Cytokine response modifier A ).
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Fas-induced and apoptosis
* Cytotoxic T-cell activity: Fas-induced apoptosis and the perforin pathway are the two main mechanisms by which cytotoxic T lymphocytes induce cell death in cells expressing foreign antigens.
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Another extrinsic pathway for initiation identified in several toxin studies is an increase in calcium concentration within a cell caused by drug activity, which also can cause apoptosis via a calcium binding protease calpain.
A research done in 1999 exhibits how nitric oxide can both initiate and inhibit apoptosis due to the cellular variables.
Inhibition of apoptosis can result in a number of cancers, autoimmune diseases, inflammatory diseases, and viral infections.
These oncolytic properties provided a promising link between CDV and lymphoma apoptosis which can lead to development of alternative treatment methods for both canine lymphoma and human non-Hodgkin lymphoma.
Defects in the cell cycle are thought to be responsible for certain tumor cells resisting chemotherapy or radiation, so a virus that can induce apoptosis despite defects in the cell cycle is useful for cancer treatment.
To stimulate apoptosis, one can increase the number of death receptor ligands ( such as TNF or TRAIL ), antagonize the anti-apoptotic Bcl-2 pathway, or introduce Smac mimetics to inhibit the inhibitor ( IAPs ).
Many different methods can be used to stimulate apoptosis in various places along the death signaling pathway.
On the other hand, loss of control of cell death ( resulting in excess apoptosis ) can lead to neurodegenerative diseases, hematologic diseases, and tissue damage.
Viruses can trigger apoptosis of infected cells via a range of mechanisms including:
Most viruses encode proteins that can inhibit apoptosis.
These homologs can inhibit proapoptotic proteins such as BAX and BAK, which are essential for the activation of apoptosis.
Interestingly, viruses can remain intact from apoptosis particularly in the latter stages of infection.
Using these inhibitors it was discovered that cells can die while displaying a morphology similar to apoptosis without caspase activation.
A mild heat treatment combined with other stresses can cause cell death by apoptosis.
This in turn disrupts the metabolism of the cells so that cell death ( apoptosis ) can set in.
Errors in mitosis can either kill a cell through apoptosis or cause mutations that may lead to certain types of cancer.
Both internal and external signals can lead to the induction of apoptosis, or programmed cell death.
* It can initiate apoptosis, the programmed cell death, if DNA damage proves to be irreparable.
Deacetylase enzymes, such as Sirt1 and Sirt7, can deacetylate p53, leading to an inhibition of apoptosis.
While apoptosis often provides beneficial effects to the organism, necrosis is almost always detrimental and can be fatal.
Dendritic cells that are defective in apoptosis can lead to inappropriate systemic lymphocyte activation and consequent decline in self-tolerance.
* Pulsed dye laser treatment can be beneficial for keloids, and appears to induce keloid regression through suppression of keloid fibroblast proliferation, and induction of apoptosis and enzyme activity.
Upon release in close proximity to a cell slated for killing, perforin forms pores in the cell membrane of the target cell, creating an aqueous channel through which the granzymes and associated molecules can enter, inducing either apoptosis or osmotic cell lysis.
Antibodies that bind to antigens can be recognised by FcϒRIII ( CD16 ) receptors expressed on NK cells resulting in NK activation, release of cytolytic granules and consequent cell apoptosis
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After metamorphosis, these organs become redundant and will be reabsorbed by controlled cell death, called apoptosis.
Interestingly, these mice were found to be resistant to apoptosis mediated by CD95, TNFR, etc.
A discussion of every disease caused by modification of the various apoptotic pathways would be impractical, but the concept overlying each one is the same: the normal functioning of the pathway has been disrupted in such a way as to impair the ability of the cell to undergo normal apoptosis.
# HIV enzymes deactivate anti-apoptotic Bcl-2 This does not directly cause cell death, but primes the cell for apoptosis should the appropriate signal be received.
Apoptosis in some viruses is activated by extracellular stimuli, however, studies have demonstrated that the OROV infection causes apoptosis to be activated through intracellular stimuli and involves the mitochondria.
After metamorphosis, these organs become redundant and will be resorbed by controlled cell death, called apoptosis.
# If the damage cannot be repaired, the cell should initiate apoptosis ( programmed cell death ) to remove the threat it poses for the greater good of the organism.
The release of cytochrome-c from mitochondria to the cytosol, where it activates the caspase family of proteases is believed to be primary trigger leading to the onset of apoptosis.
In response to DNA damage ( including shortened telomeres ), cells either age or self-destruct ( apoptosis, programmed cell death ) if the damage cannot be easily repaired.
Following apoptosis, the dying cells need to be taken up into the surrounding tissues by macrophages in a process called efferocytosis.
Eventually, either sufficient damage will be done to the cell's chromosomes such that cell dies ( via programmed cell death, apoptosis ), or an additional mutation that activates telomerase will take place.
However, when glutamate molecules in the synaptic cleft cannot be degraded or reused, often due to dysfunction of the glutamate-glutamine cycle, the neuron becomes significantly overstimulated, leading to a neuronal cell death pathway known as apoptosis.
The autoimmune disease, type 1 diabetes can be caused by defective apoptosis, which leads to aberrant T cell AICD and defective peripheral tolerance.
Due to the fact that dendritic cells are the most important antigen presenting cells of the immune system, their activity must be tightly regulated by such mechanisms as apoptosis.
These receptors, which also respond to chemicals in cannabis, appear to be associated with apoptosis – programmed cell death – and may have a role in suppressing the overactive immune system and reducing inflammation by mopping up excess cells.
Activation of these genes can be due to many processes, but the main cellular " switch " to induce apoptosis is the p53 protein.
p53 is the " guardian of the genome ," which, during DNA and cell duplication, makes sure that the DNA is copied correctly and destroys the cell ( apoptosis ) if the DNA is mutated and can't be fixed.
The existence of donor stem cells in the recipient ’ s bone marrow causes donor reactive T cells to be considered self and undergo apoptosis.
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