apoptosis and necrosis

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Question Answer
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INTRISIC PATHWAY: recruitment of pro-caspase 9 that will activation effector caspases
Apoptotic bodies
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wrap in plasma membrane fragmentation
BCL-2 Family
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INTRISIC PATHWAY: anti-apoptosis that inhibits BAX and BAK (part of the BCL-2 family) that are pro-apoptosis. Form a chain that leads to the release of cytochrome c, that associates with proteins, forming the Apoptosome.
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bubble-like protrusions  deformations of plasma membrane (stage of apoptosis)
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protease that cause the rupture of lysosomal membrane of the release of lysosome contents
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major effector in the apoptotic program that orchestrate all the morphologic changes. They are post-translationally regulated  pro-caspase  ligation  active
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the content liberated from the lysosome that causes cell death
Cytochrome release
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due to the permeability of the mitochondrial membrane
Death Receptors
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when bound to death ligands, recruits adaptor proteins, aggregation of casapase 8, activation of caspase 3 and 7, caspase cascade  death
Intrinsic apoptosis pathways
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from within  extensive DNA damage in the nucleus
Extrinsic apoptosis pathways
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from exterior  withdrawal of growth or reception of death receptor
Programmed cell death
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cell intrinsic suicide pathways

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