apoptosis and necrosis

 0    12 speciālā zīme    axelledieumegard
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sākt mācīties
INTRISIC PATHWAY: recruitment of pro-caspase 9 that will activation effector caspases
Apoptotic bodies
sākt mācīties
wrap in plasma membrane fragmentation
BCL-2 Family
sākt mācīties
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.
sākt mācīties
bubble-like protrusions  deformations of plasma membrane (stage of apoptosis)
sākt mācīties
protease that cause the rupture of lysosomal membrane of the release of lysosome contents
sākt mācīties
major effector in the apoptotic program that orchestrate all the morphologic changes. They are post-translationally regulated  pro-caspase  ligation  active
sākt mācīties
the content liberated from the lysosome that causes cell death
Cytochrome release
sākt mācīties
due to the permeability of the mitochondrial membrane
Death Receptors
sākt mācīties
when bound to death ligands, recruits adaptor proteins, aggregation of casapase 8, activation of caspase 3 and 7, caspase cascade  death
Intrinsic apoptosis pathways
sākt mācīties
from within  extensive DNA damage in the nucleus
Extrinsic apoptosis pathways
sākt mācīties
from exterior  withdrawal of growth or reception of death receptor
Programmed cell death
sākt mācīties
cell intrinsic suicide pathways

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