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Question 1

Extrinsic pathway

Answer 1

activated by external signals
Signal cell’s molecules on outside (FAS ligand) binds to FAS receptor on target cell
Binding recruits pro caspase 8
Pro caspase 8 binds to FAS receptor and becomes caspase 8
Pro caspase 8, FAS ligand and FAS receptor form a complex called a DISC
DISC: death inducing signalling complex
DISC releases caspase 8, which activates executioner caspases 3,6 or 7

Question 2

intrinsic pathway

Answer 2

activated by intracellular signals
Requires mitochondria
In response to signal, cytochrome c released
Release is mediated by two mitochondrial membrane proteins: Bax or Bak
These proteins promote release of cytochrome c from inside of mitochondrion to cytoplasm
Cytochrome c recruits ApaF1, leads to formation of death complex
Death complex: apoptosome
Then initiator caspase comes in : caspase 9
When caspase 9 joins apoptosome, it becomes activated and activates executioner caspases 3,6 and 7

Question 3

BcI-2

Answer 3

binds to Bak preventing the release of cytochrome C (anti-apoptotic regulator)

Question 4

IAPs

Answer 4

bind to activated caspases and inhibit function

Question 5

Cyclin p53

Answer 5

activates apoptosis if there are genetic mutations in DNA after G1 phase and before S phase
P53 is activated via a process called phosphorylation
P53 binds to two apoptotic mediators: Puma and Noxa

Question 6

Puma and noxa

Answer 6

pro apoptotic mediators; promote release of cytochrome c from mitochondria

Question 7

SIPS

Answer 7

As we get older we accumulate more and more mutations from environments
We generate so many mutations over time that cells no longer viable

Question 8

Why do we die

Answer 8

Antagonistic pleiotropy theory
mutation accumulation theory
selection shadow following reproduction