Brainscape's Knowledge GenomeTM

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


See full index

Block II > Apoptosis > Flashcards

Apoptosis Flashcards

1
Q

What are the modes of cell death

A

Necrosis
Apoptosis
Autophagic cell death
Cornification

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

What are the types of apoptosis we care about today

A

Intrinsic
Extrinsic
There are 12 but we’re not doing them all. Thank god.

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

How is apoptosis pronounced

A

Trick question. No one cares. Don’t be pretentious

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

Why do cells undergo apoptosis

A

To allow for proper development - fingers and toes, nerve connections
Allow for tissues growth and regression in adults - remodeling, return to original size
Remove cells that threaten organism (DNA damage, viral infection, immune system homeostasis)

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

Morphologic changes of apoptotic cells

A

Cells shrink
Chromatin aggregates
Nuclear envelope breaks up
Blebbing of cell surface
Separation of cells into membrane-bound bodies
Engulfed by phagocytes/macrophages

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

Is there an immune response with apoptosis

A

No

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

How can apoptosis be seen with microscopy (what are the signs)

A

Relocalization of cytochrome c from mitochondria –> cytoplasm
Can fluorescently label phosphatidylserine (eat me signal)

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

How can apoptosis be seen with gel electrophoresis

A

DNA ladder of 180bp caused by internucleosomal DNA cleavage

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

How can apoptosis be seen using enzymatic assays

A

Caspase protease activity measured

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

What are the extracellular signals that induce apoptosis

A

Increase in bone morphogenic proteins (stimulate digit development)
T-cell clearance - death ligands
Lack of survival factors

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

What are intercellular signals that induce apoptosis

A

Increased levels of cellular oxidant
DNA damage –> increased levels of p53 protein

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

What do both apoptotic pathways result in (not the end result, a common step)

A

Activation of caspase cascade

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

What initiates the extrinsic pathway

A

Death receptors

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

How do cell death receptors contribute to apoptosis

A

Transmembrane proteins that bind death ligands (such as TNF)
Result in death-inducing signaling complex (DISC)
which includes death receptor, FADD protein, and initiator caspase

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

What are caspases

A

Proteases, synthesized as zymogens (inactive precursors), activated by proteolytic cleavage

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

What are the tyopes of caspases

A

Initiator
Executioner

17
Q

Initiator caspases:

A

Closely linked to apoptotic signal, cleave and activate executioner caspases

18
Q

Executioner caspases:

A

Cleaves proteins in cell (cytoskeletal, nuclear)

19
Q

Run down of the extrinsic pathway

A

Extracellular signal –>
Binds to death receptor –>
DISC formation –>
Procaspase cleaved to form active caspase –>
Caspase cascade –>
Executioner caspases activated –>
Destruction of cellular proteins

20
Q

Who initiates the intrinsic pathway

A

BcI-2 protein family

21
Q

What are the forms of the the Bcl-2 protein family & what do they do

A

Anti-apoptotic - prevent protein release from the mitochondria
Pro-apoptotic - enhance protein release from the mitochondria

22
Q

Who is in the ‘live’ Bcl-2 group

A

Bcl-2
Bcl-xL

l = live

23
Q

Who is in the die (Apoptosis Inducer) Bcl-2 group

A

Bax, Bak, Bad, Bid, Bim, Puma, Noxa
a & i = apoptosis and die

24
Q

How does Bcl-2 prevent apoptosis

A

anti-apoptotic Bcl-2 prevents oligomerization of pro-apoptotic Bcl-2 family proteins (Bax, Bak)

25
Q

How does Bcl-2 contribute to apoptosis

A

No longer inhibits Bax and Bak, Bax & Bak form complexes –> make holes in mitochondrial membrane –> allow proteins (cytochrome c) into cytoplasm

26
Q

What is the release of mitochondrial proteins into cytoplasm called

A

Mitochondrial outer membrane permeabilization (MOMP)

27
Q

What happens after holes are made in the mitochondrial membrane

A

Cytochrome c + Apaf1 forms the apoptosome complex

28
Q

What does the apoptosome complex do

A

Recruits and activates initiator caspase 9 –> caspase cascade initiated

29
Q

Run down of the intrinsic pathway

A

Triggered by DNA damage or increased oxidants –>
Bcl-2 forms complex that releases cytochrome from mitochondria into cytoplasm –>
Cytochrome c + apaf1 = apoptosome –>
Cleavage of initiator caspase-9 –>
Caspase cascade –>
Executioner caspases activated –>
Destruction of cellular proteins

30
Q

Can the apoptotic pathways cross-talk

A

Yes

31
Q

How does cross-talking between the pathways work

A

Initiator caspase from ext pathwat cleaves and activates Bax & Bak from int pathway –> amplification

32
Q

Too much cell death leads to…………….conditions

A

Degenerative

33
Q

Too little cell death (excessive survival) leads to…………….diseases

A

Proliferative

Block II (28 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions