Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

z:Cell 300 > Lecture 22: Apoptosis > Flashcards

Lecture 22: Apoptosis Flashcards

(89 cards)

Start Studying
1
Q

Two main ways in which cells die/types of death:

A

-death by injurious events or toxic agents (necrosis)
-induced to commit suicide (apoptosis)

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

necrosis (def.) and happens in cells that are ______

A

-unnatural death
-damaged by injury (mechanical damage + exposure to toxic chemicals/viruses)

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

Necrosis steps

A

1) Damage by injury
2) Cell + its organelles swell -> ability of the plasma to control passage of ions + water is disrupted
3) Cell contents leak out
4) Inflammation of surrounding tissues

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

Apoptosis is ____ process that is intrinsic to ______

A

orderly
cell physiology

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

Characteristics of cells undergoing apoptosis

A

-shrinkage
- mitochondrial integrity is disrupted -> release of cytochrome C
-blebs on the surface
-chromatin in nuclei degraded
-break into small, membrane-wrapped fragments called apoptotic bodies
-phosphatidylserine (PS) exposed on cell surface

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

Purpose of apoptotic bodies (+ method)

A

limits inflammation; immune cells remove the bodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

purpose of apoptosis (aka _____)

A

-programmed cell death
-needed to remove unwanted tissues

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

apoptosis is the controlled _____

A

demolition of the cell

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

in healthy cells, PS is _____

A

on the inner leaflet of PM

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

What is the purpose of exposing PS in outer leaflet during apoptosis?

A

PS is bound by receptors on phagocytic cells (macrophages and dendritic cells) which engulf apoptotic bodies

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

necrosis typically involves a ____ and a necrotic cell can ____

A

-reversible injury
-recover

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

necrosis + apoptosis both involves ____ but apoptosis has smaller _____ for controlled destruction

A

membrane blebs

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

necrosis doesn’t _____ like apoptosis

A

break into apoptotic bodies

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

single dead cell = ______

A

many apoptotic bodies

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

epithelial cell vs apoptotic cell

A

epithelial cell are in contact with one another
apoptotic cell round up & withdraw connections

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

drug that induces apoptosis

A

Daunorubicin

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

Importance of Apoptosis

A
  1. Needed for proper development (fingers/toes needed the apoptosis of tissue between them, removal of embryonic tails)
  2. Needed to destroy cells that threaten organism (virus-infected cells, cell with DNA damage -> cancer)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

________ can kill virus-infected cells by inducing apoptosis. Some viruses _____

A

-Cytotoxic T lymphocytes (CTLs)
-counteract apoptosis

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

Damage to genome can cause cell to:

A

-Disrupt proper embryonic development leading to birth defects
-Become cancerous

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

Cells respond to DNA damage by _______, a potent inducer of _____.

A

-increasing their production of the transcription factor p53
-apoptosis

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

Mutations in ______ found in >50% of cancer cells

A

p53 gene

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

______ induces apoptosis in some types of cancer
cells

A

Radiation/chemotherapy

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

As immune response wanes, effector cells
must be _______

A

-removed to prevent them from attacking the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

______ induce apoptosis in other immune cells (and in themselves). Defects in the apoptotic machinery associated with _______

A

-Cytotoxic T lymphocytes
-autoimmune diseases (e.g. lupus erythematosus and rheumatoid arthritis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
DISC stands for ______
Death-Inducing Signaling Complex
26
Assembly of DISC involves _____
1) killer lymphocyte displays Fas ligand 2) target cell has Fas death receptor 3) Fas death receptor interacts with FADD adaptor protein via death domain (on both proteins) 4) FADD adaptor protein interacts with caspase 8 via death effector domain (on both proteins)
27
DISC = _______
FAS death receptor + FADD adaptor protein + caspase
28
FADD adaptor proteins have two domains (+ what they bind to)
-death domain (Fas death receptor) -death effector domain (initiator caspase)
29
initiator caspase proteins have two domains (+ what they bind to)
-adaptor binding domain -protease domain (has cleavage site)
30
apoptotic signal lead to the _____
dimerization, activation and cleavage of the inactive initiator caspase --> active initiator caspase
31
active caspase does what?
cleaves executioner caspase --> active caspase
32
Caspases stands for _____
Cysteinyl aspartyl proteinases
33
Caspases cleave after _______
aspartate residues in substrates
34
How different caspases in human cells?
15
35
Two main types of caspases
1) Initiator caspases 2) Executioner/effector caspases
36
Initiator caspases are _____
Caspases 8,9
37
Executioner/effector caspases are _____
Caspases 3,6,7
38
Role of Initiator caspases 8, 9
-activate executioner caspases and some Bcl-2 family members (Bid)
39
zymogen (def.)
inactive precursor of an enzyme
40
Activation of Initiator caspases 8,9 triggered by ______
oligomerization of the zymogen on adaptor or scaffold (eg. FADD-Fas associated death domain) followed by autocleavage
41
Executioner/effector capsases 3,6,7 function
-Cleave wide variety of substrates including proteins that confer structure to cells (cytoskeletal and nuclear proteins)
42
Executioner/effector caspases 3,6,7 are activated _____
by cleavage by caspases 8,9
43
Caspases can be activated by _______
to distinct apoptotic pathways
44
Two apoptotic pathways
-Intrinsic/Mitochondrial pathway -Extrinsic/Death receptor pathway
45
Intrinsic/Mitochondrial Pathway is activated by _______
-lack of survival factors -intracellular damage (oxidative or radiation damage)
46
Intrinsic/Mitochondrial Pathway: Survival factors for lymphocytes & neurons that prevent apoptosis)
-Interleukin-2 (IL-2) for lymphocytes -growth factors for neurons
47
Activation of Intrinsic/Mitochondrial Pathway leads to ______
activation of caspase-9
48
Intrinsic/Mitochondrial Pathway process involves ____
Bcl-2 family members
49
Intrinsic/Mitochondrial Pathway does not require _____
outside signal
50
neurons (and other cell types) undergo apoptosis when? why?
-absence of growth factors -to adjust number of nerve cells to size of target
51
_____ regulate apoptosis. They divided into _____
-Bcl-2 family members (20) -Bcl-2, Bax, BH3-only
52
Bcl-2 family members require _______ which is important for function and function as ______
-association with members -oligomers
53
Bcl-2 subgroup is _____
anti-apoptotic; inhibit Bax (mainly) and initiator caspases (eg. Bcl2, BclXl)
54
Bax subgroup is _____
pro-apoptotic; forms pores in mitochondrial membrane, activates initiator caspases (eg. Bax, Bak)
55
BH3-only subgroup is _____
primarily apoptotic initiators that function by inhibiting function of Bcl-2 members (mainly) + activating Bax --> tips balance of power to apoptosis (eg. Baf, Bim, Bid, Puma, Noxa)
56
anti-apoptotic Bcl2 protein had these domain: _______
BH4 BH3 BH1 BH2
57
pro-apoptotic Bax effector protein had these domains: _______
BH3 BH1 BH2
58
pro-apoptotic BH3 protein had these domains: _______
BH3
59
In healthy cells, ____ Bcl-2 protein is where?
anti-apoptotic in outer membrane of mitochondria (transmembrane protein)
60
Internal damage to the cell (ex. _____) leads to _____ production of _______ which does what?
-DNA damage -p53-dependent production of Bax (pro-apoptotic protein) which bind to mitochondria
61
Alteration of ratio of ________in mitochondrial membrane determines whether _____
-death promoting/death preventing Bcl-2 family members -cell lives or dies
62
Pro-apoptotic conditions cause ________
release of cytochrome c from mitochondria through aggregated Bax proteins that forms a pore in mitochondrial membrane
63
In healthy cells, cytochrome c is in ______ and _____=_____
-intermembrane space -Bcl2=Bax
64
Released cytochrome c binds to _____forming ______
-Apaf-1 (Apoptotic protease activating factor) and procaspase 9 -the apoptosome
65
Apaf-1 functions as a ________ and causes recruitment and activation of ________ which then _____
-scaffold for oligomerization of procaspase 9 -caspase 9 -cleaves and activates the effector caspase 3>>downstream events leading to apoptosis
66
Anti-apoptotic Bcl2 proteins maintain ______ and prevent ______
-mitochondrial integrity by preventing aggregation of Bax proteins in membrane -cytochrome c release
67
intrinsic pathway: apoptotic stimulus -> ____
-activated BH3-only protein (Bid/Bad) --> -inactivated anti-apoptotic Bcl2 protein & activated Bax protein forms pores in mitochondrial membrane -cytochrome C release through pore
68
Some viral proteins (like RV capsid) do what to Bax?
interact with Bax and block it’s pore function thereby blocking release of cytochrome c >> blocks apoptosis of virus-infected cell
69
Extrinsic/Death Receptor Pathway is activated by _______
ligand-induced aggregation of receptors (tumor-necrosis receptor family, Fas) on cell surface
70
Activation of Extrinsic/Death receptor pathway leads to ________
clustering of caspase-8 (or -10) zymogens followed by autocatalysis and activation
71
Death Receptor Pathway has signaling through _______
“death receptors” including Fas (CD95), TNFR & others
72
Death Receptor Pathway: Ligands initiate signaling via _______
receptor oligomerization, recruitment of adaptor proteins and activation of caspases
73
Death Receptor Pathway steps
1. FasL (ligand on lymphocyte/T cells) binding induces Fas oligomerization 2. Recruits pro-caspase 8 via the adapter protein FADD to form the death inducing signaling complex (DISC). 3. Pro-caspase 8 then oligomerizes and is activated via autoproteolysis. 4. Activated caspase 8 (initiator caspase) stimulates apoptosis via two parallel cascades
74
Activated caspase 8 (initiator caspase) stimulates apoptosis via two parallel cascades:
A. Directly cleaves and activates caspase-3. B. Activates mitochondrial (Stress) pathway by cleaving Bid (Bcl-2 family)
75
mitochondrial (Stress) pathway
-cleaves Bid (Bcl-2 family) -truncated Bid (tBid) is then myristoylated and translocates to mitochondria -induces cytochrome c release, which activates caspases 9 and then 3. -activated effector caspases (3, 6 and 7) cleave cytoskeletal, nuclear proteins and activate nucleases that destroy chromatin.
76
When cytotoxic T cells recognize (bind to) their target, they ______.
produce more FasL at their surface
77
Intersection of Extrinsic and Intrinsic pathways via _____
Bid (BH3-only protein)
78
Apoptosis can be induced experimentally by ______
the microinjection of cyto-c into cytoplasm adding ant-Fas antibody >> clustering of Fas
79
Regulators of Intrinsic & Extrinsic pathways
Intrinsic: BH3, BCl-2, Bax Extrinsic: Death receptors
80
Scaffolds of Intrinsic & Extrinsic pathways
Intrinsic: Apaf-1 Extrinsic: FADD
81
Initiators of Intrinsic & Extrinsic pathways
Intrinsic: caspase-9 Extrinsic: caspase-8
82
Effectors of Intrinsic & Extrinsic pathways
Intrinsic + Extrinsic : caspase 3,6,7
83
Apoptotic pathways are often _____ in cancer cells by ______
-impaired -increasing the transcription and production of anti-apoptotic Bcl2 protein or -inactivating pro-apoptotic BH3-only protein (Bad)
84
Cancer cells have a lot of this protein?
Bcl2 proteins
85
BH3-only protein (Bad) normally does this to promote apoptosis? but when phosphorylated by ____ it does this?
-binds to Bcl2 protein keeping it inactivate -active Akt kinase (PKB) -releases active Bcl2 which blocks apoptosis
86
Survival of cells often requires _____ and/or _____. Without signal, _____blocks protective effects of Bcl-2/Bcl-XL ---> _____
-continuous stimulation from other cells -adhesion to the surface on which they are growing -Bad -stops preventing apoptosis >> apoptosis
87
In the presence of trophic/growth factors, signal transduction pathway leads to ______which inhibits ________(by _____) >>>Apoptosis is _____
-activation of protein kinase B (PKB) = Akt -the function of the pro-Apoptotic protein Bad -phosphorylation -blocked and cell survived
88
Growth/Trophic factors can induce _____
inactivation of pro-Apoptotic regulators
89
Possible cancer treatments
1) PI-3 kinase inhibitors (PI-3 activates PKB which inactivates Bad to release anti-apoptotic Bcl2 protein >> constitutively activate PKB mutant rescues cell) 2) Bcl-2 inhibitors (Bcl2 is anti-apoptotic -> inhibitor leads to apoptosis)

z:Cell 300 (17 decks)

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