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MCB > Cell Death and Autophagy > Flashcards

Cell Death and Autophagy Flashcards

1
Q

How does T300A mutation contribute to Crohn’s disease?

A
  • creates de novo caspase site
  • Activation of caspases leads to cleavage of ATG and defective autophagy so pathogens expand and disease progresses
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2
Q

What is the impact of Crohn’s disease linked mutations in ATG16L1 and NOD2 mutations?

A
  • No or abnormal antigen presentation
  • Failure of immune response
  • Chronic pathogenic infection which can contribute to CD
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3
Q

How can autophagy cause neurodegenerative disease?

A

Cellular accumulation of autophagosomes may process amyloid into toxic forms

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4
Q

How can autophagy help reduce neurodegenerative disease?

A
  • Breaks down abnormal proteins
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5
Q

What is the relationship between autophagy and stem cells?

A
  • As autophagy decreases stem cells become more quiescent
  • Activating autophagy can push back quiescence
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6
Q

Give 3 examples of what can cause apoptosis

A
  • Growth factor withdrawal
  • DNA damage
  • Anoikis
  • Mitochondrial damage
  • Cell surface death ligands
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7
Q

What kind of proteases are caspases?

A

Aspartate directed cysteine proteases

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8
Q

What is extrinstic apoptosis?

A

Death via death ligands which bind to death receptors

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9
Q

Once a death ligand interacts with a death receptor what happens?

A
  • DISC is formed
  • Adaptor recruited to death receptor and initiator caspase recruited
  • Effector caspase then recruited triggering enzyme cascades
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10
Q

How do adaptors and effectors of the extrinstic apoptosis pathway interact?

A
  • Death domains and death effector domains
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11
Q

Which caspase is recruited to DISC in extrinstic apoptosis?

A

Caspase-8

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12
Q

What inhibits the extrinstic apoptosis pathway and how?

A

FLIP mimicks caspase-8 and competes with it

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13
Q

How does apoptosis occur via the mitochondria?

A
  • BH3-only proteins activate Bax or Bak
  • Causes conformational changes
  • Produces pore in mitochondria, leaking proteins which signal for apoptosis
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14
Q

What is the most important protein released from mitochondria to trigger apoptosis?

A

Cytochrome c

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15
Q

What can block death via mitochondria?

A

Bcl-2 proteins

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16
Q

How can BH3-only proteins act as de-repessors?

A
  • Bind to Bcl-2 proteins and ‘take them out’ of the system
  • Produce a lower active threshold for Bak/Bax
17
Q

What happens to cytochrome c once it is released from mitochondria?

A
  • Associates with Apaf-1
  • dATP and pro-caspase 9 are then recruited to form the apoptosome
18
Q

What caspases does the apoptosome potently activate?

A

Caspase 3 and 7

19
Q

What links the extrinstic and intrinsic apoptosis pathways?

20
Q

What is bid a target of?

21
Q

How does Bid link the extrinstic and intrinsic apoptotic pathways?

A
  • Extrinstic pathway produces caspase 8 which will cleave Bid
  • Bid becomes truncated, moves to mitochondria and induces Bax/Bak conformational changes allowing for Cytochrome C to be released
22
Q

What happens to DNA when caspases are activated?

A
  • caspase activated DNase is activated
  • Causes nuclear lamina disassembly, chromatin condensation and peripheral chromatin redistribution
23
Q

Is necroptosis dependent on caspases?

24
Q

What are crucial proteins for necroptosis?

A
  • RIPK1
  • RIPK3
  • MLKL
25
Q

When does necroptosis occur?

A

When DISC complex activated caspase 8 is inhibited

26
Q

How does necroptosis occur?

A
  • Caspase 8 inhibition leads to activation of RIPK3 which activates MLKL
  • This oligomerises and forms pores at the plasma membrane
27
Q

What does RIPK3 also do?

A
  • Activates NLRP3 inflammasome
  • Can activate caspase 8
28
Q

What happens when inflammasome is activated?

A
  • Triggers caspase I and IL-1B maturation
29
Q

What makes up inflammasome?

A
  • NLRP3
  • ASC
  • Caspase 1
30
Q

What are the 2 steps in inflammasome activation?

A
  • Priming
  • Activation
31
Q

How does priming occur in atherosclerosis linked inflammasome activation?

A
  • NF-KB activated causing upregulated transcription of NLRP3 and PAMPs and DAMPs
32
Q

How does activation occur in atherosclerosis linked inflammasome activation?

A
  • ATP distrubed flow causes caspase 1 to cleave pro-IL-1beta activating it
  • Triggers inflammasome activation
33
Q

What type of proteins does pyroptosis involve?

A

Pore-forming proteins called Gasdermins

34
Q

How does pyropotosis occur?

A
  • Inflammsome causes cleavage and activation of GSDMD which forms plasma membrane pores
  • Lets water and salts in and cell bursts
35
Q

What drives ferroptosis?

A

Iron-dependent phospholipid peroxidation

36
Q

What is protective against ferroptosis?

A

Glutathione

37
Q

What is required for glutathione synthesis?

MCB (28 decks)

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