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Cell Death Flashcards

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1
Q

What are the morphological characteristics of cell death?

A

Shrinkage
Membrane blebbing
Fragmentation
Nucleur condensation

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2
Q

How is apoptosis different from necrosis?

A

They are excreted so there is no inflammation

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3
Q

What gene is crucial for cell death in C.elegans?

A

CED3

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4
Q

Why is apotosis needed?

A

Proper embryonic development
For cells with sustained damage which cannot be repaired
Cells which have undergone senescence
It has outlived it’s usefulness
If it is required to maintain the normal physiological processes in an organism

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5
Q

How many cells die every second

A

One million cell die per second

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6
Q

Give 5 examples where apoptosis needs to occur to maintain the normal physiological processes of an organism

A

Shedding of the uterine lining
To remove mutations
The eye lens consists of apoptotic cells
Formation of the epidermis on the skin (protective dead skin layer)
Auto-reactive T cells which would kill healthy cells die before they reach the blood stream

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7
Q

What happens in Bax and Bak KO mice?

A

They cannot remove the skin between their paws

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8
Q

What happens to the brain of Caspase-9 KO mice?

A

They get an overgrowth of the brain

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9
Q

What is syndactyly?

A

Webbed feet and hands because the interdigital space fail to undergo apoptosis

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10
Q

What diseases are associated with too little apoptosis?

A

cancer
autoimmune diseases
viral infection

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11
Q

What diseases are associated with too much apoptosis?

A

Neurodegenerative diseases e.g. parkinsons
Viral infection e.g. HIV
Ischemic injury

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12
Q

What is ischemic injury?

A

Heart attack or strokes

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13
Q

How does apoptosis not induce inflammation?

A

The macrophages eat the dead cells

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14
Q

What are caspases?

A

Cysteine-dependent aspartate-directed phosphatases

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15
Q

Why are caspases so named?

A

The active site has a cysteine, which cleaves after aspartate residues

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16
Q

What are the two types of caspases?

A

Initiator

Executioner/ effector

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17
Q

What are the initiator caspases?

A

Caspases -8, -10, -9 and -2

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18
Q

What are the executioner caspases?

A

Caspase -3, -7 and -6

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19
Q

What is the function of initiator caspases?

A

They activate the executioner complexes through cleavage

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20
Q

What is the structure of initiator caspases?

A

they have a long prodomain that is important in their function

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21
Q

How are initiator caspases activated?

A

Autocatalytic processing triggered by co-factor binding and/ or oligomerisation

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22
Q

What is CAD?

A

caspase activated DNase

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23
Q

How does actin aid apoptosis induction?

A

cell rounding and shrinkage

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24
Q

How does acinus aid apoptosis induction?

A

Chromatin condensation

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25
How does ICAD and PARP aid apoptosis induction?
DNA fragmentation
26
How does Gelsolin, ROCK-1 and PAK-2 aid apoptosis induction?
Membrane blebbing
27
How does Xkr8 aid apoptosis induction?
Externalisation of phosphatidyl serine on the plasma membrane
28
What is ICAD?
It is cleaved by caspases to activate CAD
29
What is CADs function?
Cleaves DNA between two nucleosomes
30
What is PARPs function?
Modifies histones by catalysing the formation of ADP-ribose and by binding to the DNA strands
31
How does CAD normally exist in a cell?
As an inactive complex with ICAD
32
What inhibits PARPs function to fix DNA damage?
cleavage by caspase 3
33
What is the function of lamins?
Maintain the shape of the nucleus | Mediate interactions between chromatin and the nuclear membrane
34
What caspase degrades lamins?
Caspase 6
35
What does lamin cleavage induce?
chromatin condensation and nuclear fragmentation
36
What is the extrinsic apoptosis pathway?
Ligand binds to Death receptor -> FADD -> caspase 8 -> caspase-3 -> apoptosis
37
What is the intrinsic apoptosis pathway?
Drug -> Cytochrome C -> Aparf-1 -> caspase-9 -> caspase-3 -> Apoptosis
38
What does the ligand do to the death receptor?
Trimerisation and then polymerisation of the receptor
39
Why is the death receptor altered?
To increase the affinity of FADD to the receptor
40
What does FADD binding to the receptor cause?
Increased caspase-8 affinity to FADD
41
What ligand binds to the death receptor?
FAS
42
How is cytochrome C released?
By mitochondria using ATP
43
What does cytochrome C binding to aparf1 do?
Changes the shape to adapt to a quaternary structure
44
What does aparf1 binding to caspase-9 cause?
Apoptosome formation
45
What is the apoptosome?
7 components of aparf-1, caspase-9 and cytochrome c
46
What is the activation platform for caspase8 called?
death-inducing signalling complex (DISC)
47
What is DISC?
The death receptor and FADD
48
What is FADD?
An adaptor protein
49
What is the function of caspase-9?
To convert pro-caspase-3 to caspase-3
50
How does cytochrome C leave the mitochondria?
Through apoptosis-inducing signals which cause mitochondrial outer membrane permeabilisation and therefore cytochrome C can exit
51
What is BCL-2?
A pro-survival signal
52
What are BAK and BAX?
Pro-apoptotic signals
53
What is BCL-2 function?
To inhibit cytochrome C release by inhibiting Bax
54
what is Bax/Bak function?
to stimulate cytochrome C release
55
What is BID, BIM and BAD?
BH3-only proteins
56
What is the difference between Bcl-2 anti-apoptotic and pro-apoptotic proteins?
Pro-apoptotic proteins do not have a BH4 domain
57
What is the function of BAD?
Binds to Bcl-2 to inhibit the oligomerisation of Bcl-2
58
What is the function of BIM?
Too bind to BAX and inhibit oligomerisation of Bcl-2
59
How do Bax and Bak directly permeabilise the mitochondrial outer membrane?
They oligomerise -> make MOMP -> form proteinaceous chanels and lipid pores for cytochrome C to move through
60
What happens in B cell lymphoma?
BCL-2 of chromosome 18 translocates onto chromosome 14 | This enhances BCL-2 function
61
What is the function of Myc?
To increase proliferation and cause apoptosis
62
How do survival factors interact with Myc?
They inhibit their ability to cause apoptosis
63
What effect does the removal of p53 cause?
Inhibition of all apoptotic pathways since it controls the extrinsic and intrinsic pathway
64
As well as keeping cells alive, how else does apoptosis effect cancer cells?
Allows them to live in hypoxic and nutrient poor environments Promote metastasis
65
What is anoikis?
when our cells in the body detach from membranes and other cells to undergo apoptosis
66
What mechanisms do cancer cells induce to avoid apoptosis?
Mutation in death ligands or receptors some mutations of TP53 Expression of 'decoy' TRAIL receptors Loss of caspases Loss of pro-apoptotic Bcl-2 family members Upregulation of IAPs Upregulation of anti-apoptotic Bcl-2 family members
67
What are IAPs?
small proteins in the mitochondria
68
How can anti-apoptotic genes be altered?
Gene translocation Amplification Overexpression
69
How can pro-apoptotic genes be altered?
Genomic loss Silencing Mutation
70
Describe fragment based drug design
Identify chemical fragments that bind the protein of interest by NMR -> Low affinity -> Connect fragments together -> High affinity fragment -> drug
71
Name a BH3-mimic compound
Navitoclax
72
What is Navitoclax commonly used for?
Leukaemia to sensitise cells to apoptosis
73
Why isn't navitoclax used as openly anymore?
Due to off target toxicities
74
How does navitoclax work?
Target platelets and stop the differentiation of cells and cause them to die inhibits BCL-xL, Bcl-W and Bcl-2
75
What can venetoclax be used in combination for?
Increase BCL-2 priming Target resistance factors Mobilise tumour cells
76
How can venetoclax be used in combination to increase BCL-2 priming?
Add a priming agent, e.g. PI3Kdelta inhibitors, to BCL2 -> BCL-2 to bind to BIM -> Add venetoclax and BIM will bind to BAX and BAK -> Apoptosis
77
How can venetoclax be used in combination to target resistance factors?
Venetoclax will inhibit BCL-2 Add another agent e.g. JAK2 inhibitor, to block another anti-apoptotic enzyme -> Apoptosis
78
How can venetoclax be used in combination to mobilise tumour cells?
Add an mobilising agent, e.g. PI3Kdelta, to peripheral blood -> add venetoclax -> apoptosis
79
What is BH3 profiling?
Testing to see if patients cancer cells are 'primed to die' and therefore they will respond to drugs which induce mitochondrial apoptosis
80
How do you compete BH3 profiling?
Add BH3 peptide to cells, the more sensitive they are, the more primed to die they are Liquid or solid tumour sample -> single cancer cell suspension -> exposure to treatments -> Permeabilisation, staining and peptide exposure -> Analysis -> results
81
In terms of leukaemia, what do you measure when doing a BH3 profile?
The level of apoptosis and the release of cytochrome C

Cancer Biology (13 decks)

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