Lecture 11 Flashcards
1
Q
Apoptosis
A
- Highly regulated, reproducible cell death
- Necrosis accidental, uncontrolled cell death and can cause inflammation
2
Q
Caspase
A
- Synthesized as inactivate procaspases
- Signals initiate caspase cleavage to form caspase dimers
- Caspase cleave target proteins to trigger apoptosis
- Initiator caspase(8, 9) cleaved and activated in response to apoptotic signals -> cleave and activate executioner caspase(3, 6, 7) -> cleave target proteins to initiate apoptosis
3
Q
Alter cell surface lipid composition
A
- Healthy cells have specific lipid makeup -> use flippase
- Apoptotic cells maintain balance -> active scramblase
4
Q
Extrinsic pathway
A
- Caspase 8 has DED -> FADD adaptor protein has death domain and DED
- Fas death receptor at plasma membrane has death domain
- Killer lymphocytes express cell surface Fas ligands
- DISC assembly -> releaes domain and activate new caspase 8 -> activation of executioner caspase 3 and 7
- Healthy cells express decoy receptors without death domain -> no apoptosis
5
Q
Intrinsic pathway
A
- Cytochrome c binds to Apaf1 -> exposes CARD domain and oligomerization domain on Apaf1
- Apaf1 oligomerize -> unexposed CARD recruit caspase 9 monomers to form apoptosome and activation of caspase 9 -> activates executioner caspase
- Cyt c in mitochondrial intermembrane space: apoptotic stimuli trigger Bak and Bax to promote MOMP
- Bcl2 and BclxL bind to Bak and Bax to prevent formation of channels -> block MOMP -> anti-apoptotic
- Bad binds to Bcl2 and BclxL -> promote MOMP -> pro-apoptotic
6
Q
Inhibitor of Apoptosis
A
- IAP block apoptosis from accidentally occurring
- XIAP can directly block initiator and executioner caspases
- XIAP is anti-apoptotic
- Anti-IAP released whhen MOMP triggered -> inhibit XIAP -> pro-apoptotic