Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BIO230 - finals - section 2 > Lecture 11- Programmed cell death > Flashcards

Lecture 11- Programmed cell death Flashcards

1
Q

What is programmed cell death essential in?

A
  1. embryonic development
  2. metamorphosis
  3. immune system function
  4. cleanly removing excess, old, damaged, abnormal, or malfunctioning cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what does phosphorylated p53 bind to?

A

phosphorylated p53 is active and binds to the regulatory region of the p21gene. p21 mRNA is made and then the p21 protein (CDK inhibitor protein).
causes apoptosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

apoptosis

A

highly regulated, reproducible form of programmed cell death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

necrosis

A

accidental, uncontrolled cell death and can cause inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what does apoptosis do?

A

it carefully dismantles the cell and signals for its removal by engulment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what do changes in apoptosis include?

A
  1. cell shape changes and shrinkage
  2. cytoskeleton disassembly
  3. decreased cell adhesion
  4. DNA fragmentation
  5. surface lipid changes
  6. cell removal by engulfment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what protease triggers apoptosis?

A

caspase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

how are caspases synthesized?

A

as inactivae procaspases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

how are active caspase dimers formed ?

A

signals initiate caspase cleavage to form active caspase dimers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

caspase cascade

A

some caspases can cleave and activate other caspases to create and amplified caspase cascade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how do caspases trigger apoptosis?

A

they cleave specific target proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

which caspases are initiator caspases

A

caspase 8 and caspase 9

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

initiator caspases

A

cleaved and activated in response to apoptotic signals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

which caspases are executioner caspases

A

caspase 3, 6 and 7

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

executioner caspases

A

cleaved and activated by initiator caspases creating a caspase cascade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what do executioner caspases do?

A

the cleave and target proteins in the cell to initiate apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what does the caspase target to get cell shape change and shrinkage

A

cell-cell adhesion proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what does the caspase target to get DNA fragmentation

A

breakdown of nuclear lamins
activation of DNA endonucleases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what does the caspase target to get cytoskeleton disassembly

A

alter actin regulatng proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what does the caspase target to get surface lipid changes

A

lipid distibution proteins
1. flippase inactivation
2. scramblase activation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

how do executioner caspases indirectly cause DNA breakdown?

A

an inactive CAD is bound to the inhibitor of CAD
the executioner3 cascade cleaves inhibitor of CAD, activating CAD
active CAD causes cleavage of DNA between nucleosomes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what do healthy cells have

A

active flippase, inactive scramblase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what happens to flippase and scramblase in apoptotic cells

A
  1. caspase cleaves flippase to inactivate it
  2. caspase cleaves scramblase activating it (more lipids to outer layer)
24
Q

what pathways can apoptosis be triggered by?

A

extrinsic and intrinsic pathways

25
Q

extrinsic pathway

A

depends on cell surface receptors binding to an extracellular signal molecule to activate executionar caspases

26
Q

intrinsic pathway

A

depends on intracellular receptors - depends on cytochrome C

27
Q

components of extrinsic apoptosis pathway

A

caspase 8, FADD adaptor protein, Fas death receptor, killer lymphocytes

28
Q

domain in caspase 8

A

death effector domain

29
Q

domains in FADD adaptor protein

A

death effector domain and death domain

30
Q

domain in Fas death receptor

A

death domain

31
Q

what do killer lymphocytes express

A

cell surface Fas ligands

32
Q

DISC - death inducing signalling complex

A

killer lymphocyte with Fas ligand binds to the Fas receptor
the death domain in Fas receptor is activated
the death domain in Fas recptor binds and activates the death domain in FADD adaptor protein
the death effector protein in FADD is active and it binds to the death effector protein in caspase 8 activating it

33
Q

what can healthy cells express to evade extrinsic apoptosis pathway signals

A

decoy receptors

34
Q

what do decoy receptors lack

A

intracellular death domains

35
Q

how do decoy receptors help healthy cells to stay alive

A

When Fas ligand binds to decoy receptor, no DISC assembles, so apoptosis is not triggered

36
Q

what does intrinsic apoptosis pathway depend on

A

Apaf1 and cytochrome C

37
Q

how does intrinsic apoptosis work

A

cytochrome C binds to Apaf
this exposes the CARD domain and the oligomerization domain of Apaf1.

38
Q

what domains on Apaf1 are exposed when cytochrome C binds to it

A

CARD domain and oligomerization domain

39
Q

how does cytochrome C release activate the intrinsic apoptosis pathway ?

A
  1. cytochrome C is released from the intermembrane space
  2. it binds to Apaf 1, CARD domain and oligomerization domain are exposed
  3. oligomerization of Apaf1 takes place (apoptosome without caspase)
  4. there is recruitment of caspase 9 monomers to apoptosome and caspase 9 activation by dimerization
  5. cleavage and activation of executioner caspases by activated caspase 9 dimers
40
Q

what releases cytochrome C

A

mitochondrial outer membrane permeabilization
cyctochrome C cannot usually cross outer membrane

41
Q

how do channels in the outer mitochondrial membrane form

A

apoptotic stimuli trigger Bak and Bax proteins to form a channel in the outer mitochondrial membrane

42
Q

what do bak and bax channels promote

A

mitochondrial outer membrane permeabilization

43
Q

what bcl2 family members are similar to bac and bax

A

bcl2 and bcIxL

44
Q

Bcl2 and BclxL action

A

they bind bac and bax preventing them from forming channels
they block MOMP so they are considered anti-apoptotic proteins

45
Q

BcI1 family proteins that can promote MOMP

46
Q

explain the action of Bad

A

Bad binds to BcI2 and BcIxL
Bad promotes MOMP and is a pro-apoptotic protein

47
Q

IAPs

A

they are inhibitors of apoptosis

48
Q

IAP that can block both initiator and executioner caspases

49
Q

anti IAP proteins

A

usually in the mitochondrial intermembrane apce
they are released with cytochrome C when MOMP is triggered
they inhibit XIAP, allowing the caspase cascade to trigger apoptosis

50
Q

examples of anti IAP proteins

A

Omi and Smac

51
Q

Survival factors

A

Many cells will undergo apoptosis if they are not supplied with survival factors
cells that leave their correct environment are no longer protected by survival factors

52
Q

what limited availibility of survival factors do

A

regulate cell numbers

53
Q

cascade initiated by survival factors to activate anti apoptotic proteins

A

BcI2 transcription increases
BcI2 and BcIxL block Bak/Bax from forming a channel in the mitochondrial outer membrane
MOMP I blocked, apoptosis does not occur

54
Q

cascade initiated by survival factors to inactivate pro-apoptotic proteins

A

Akt kinas is activated and phosphorylated bad
BAD is inactive and cant bind to BcI2 and BcIxL
they bind Bax and Bax, MOMP not occurring, apoptosis does not proceed

55
Q

inappropraite cell death leading to disease

A
  1. cancer cells display properties that should makr them for apoptosis (changes to cell adhesion, DNA damage, survival outside their usually environment)
56
Q

how do cancer cells grow and proliferate

A

must escape apoptosis

BIO230 - finals - section 2 (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions