apoptosis and necrosis

Apoptosome

INTRISIC PATHWAY: recruitment of pro-caspase 9 that will activation effector caspases

Apoptotic bodies

wrap in plasma membrane fragmentation

BCL-2 Family

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

bubble-like protrusions  deformations of plasma membrane (stage of apoptosis)

Calpain

protease that cause the rupture of lysosomal membrane of the release of lysosome contents

Caspases

major effector in the apoptotic program that orchestrate all the morphologic changes. They are post-translationally regulated  pro-caspase  ligation  active

Cathepsin

the content liberated from the lysosome that causes cell death

Cytochrome release

due to the permeability of the mitochondrial membrane

Death Receptors

when bound to death ligands, recruits adaptor proteins, aggregation of casapase 8, activation of caspase 3 and 7, caspase cascade  death

Intrinsic apoptosis pathways

from within  extensive DNA damage in the nucleus

Extrinsic apoptosis pathways

from exterior  withdrawal of growth or reception of death receptor

Programmed cell death

cell intrinsic suicide pathways