Energy Metabolism - Programmed Cell Death
9 important questions on Energy Metabolism - Programmed Cell Death
How does the extrinsic apoptosis pathway occur?
extracellular domain binding of ligands to death receptors of TNF superfamily
intracellular domain (death domain) to intracellular signalling pathways
intracellular recruitment of proteins into a death-inducing signalling complex (DISC)
activates initiator caspase: pro-caspase 8/10
activates downstream effector caspase 3/6/7 -> apoptosis
death receptor -> death domain -> DISC -> pro-caspase 8/10 -> caspase 3/6/7/ -> apoptosis
Which 6 receptor-independent stimuli result in mitochondrial permeabilization?
- radiation
- free radicals
- viral infections
- misfolded proteins
- cell damage/impaired cell functions
- serum/growth factor withdrawal
How does the intrinsic apoptosis caspase-INdependent pathway occur?
endonuclease G (endo G) and apoptosis inducing factor (AIF) are released -> both translocate to nucleus, promote DNA fragmentation -> results in programmed necrosis (caspase-independent, mito-dependent)
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How does the intrinsic apoptosis caspase-dependent pathway occur?
loss of transmembrane potential, arrest of bioenergetic function, release of pro-apoptotic proteins:
- Smac/DIABLO binds and inhibits IAPs (inhibitor of apoptosis proteins), permitting apoptotic progression
- Cyt c induces Apaf1 (apoptotic peptidase factor 1) oligomerization -> apoptosome formation -> activation /c/aspase 9 -> activation executioner caspases 3/7/6/9 -> nuclear defragmentation (apoptosis)
What is an apoptosome, and what does it consist of?
A large protein strucutre formed in the process of apoptosis. Wheel-like structure:
one wheel (pre-apoptosome) is formed by Cyt c and Apaf-1
procaspase 9 forms the hub, which connects two wheels.
What are 3 characteristics of apoptosis?
1: Inactivation of DNA repair enzymes.
2: Breakdown of structural nuclear proteins.
3: Fragmentation of DNA.
What is the permeability transition pore complex (PTPC) composed of? (5) What does it do?
1: voltage-dependent anion channel (VDAC)
2: adenine nucleotide translocase (ANT)
3: translocator protein (TSPO = PBR)
4: hexokinase II (HKII)
5: cyclophilin D (CYPD)
Regulates transport of ions and small metabolites in and out of mitochondria
Which 3 mechanisms cause mitochondrial outer membrane permeabilization (MOMP), resulting in mitochondrial permeability transition (MPT)?
1: Prolonged opening of PTPC, caused by high ROS, high Ca, pro-apoptotic proteins
2: channel formation by BAX and BAK. BAX + BID translocate to mitochondria upon activation and bind to sessile mitochondrial BAK, forms channels. Also promotes PTPC opening.
3: destabilization of mitochondrial lipdids by tBID
What is the cause of resistance to apoptosis, and what does it result in (4)?
Caused by deregulation of several master switch proteins: hypoxia inducible factor (HIF1), c-Myc and p53.
1: upregulation of pro-survival proteins
2: suppression of pro-apoptotic proteins
3: Silencing death receptors (Fas, TRAIL)
4: Hexokinase II (HKII) associates more tightly with VDAC, increasing resistance to MPT
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