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

apoptosis and necrosis