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APOPTOSIS, an increase in permeabilization can be induced by Bax and Bac,…
APOPTOSIS
Bcl-2 family
pro-apoptotic
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BH3-only Bid, Bad, Bim, PUMA
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anti-apoptotic
Bcl-2
contains Bcl-2 homology domains through which they can interact with other Bcl-2 members negatively regulating
mitochondrial release of pro-apoptotic factors
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different pathways
extrinsic pathway activated by cell surface death receptor (TNFalpha, Fas, TRAIL)
lymphocytes recognize cells infected by a virus and induce the activation of their Fas death receptors that will recruit procaspase-8 and will interact with it through their shared DED domains
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cross-talk
caspase-8 can act on Bid (which belongs to the BH3-only family) cleaving it and resulting in tBid that will activate the intrinsic pathway
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caused by degradation of the cytoskeleton, are phagocytize by phagocytes
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the adaptor protein FADD needs to be recruited in order to create the complex DISC that will activate downstream events that will execute apoptosis
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