Brainscape's Knowledge GenomeTM

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


See full index

Cancer > Apoptosis > Flashcards

Apoptosis Flashcards

1
Q

Apoptosis

A

Programmed cell death

  • controlled disassembly of cellular contents without disruption
  • no inflammatory response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Why programmed cell death?

A
  • Harmful cells
  • Developmentally defective cells
  • Excess/unnecessary cells
  • Obsolete cells
  • Exploitation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Necrosis

A

-unregulated cell death associated with trauma, cellular disruption and an inflammatory response

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

Features of necrosis

A
  • plasma membrane becomes permeable
  • cell swelling and rupture of cellular membranes
  • release of proteases leading to autodigestion and dissolution of the cell
  • localised inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Apoptosis phases

A
  • latent phase

- execution phase

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

Apoptosis latent phase

A

-death pathways are activated, but cells appear morphologically the same

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

Apoptosis execution phase

A

-loss of microvilli and intercellular junctions
-cell shrinkage
-loss of plasma membrane asymmetry (phosphatidylserine lipid appears in outer leaflet)
-chromatin and nuclear condensation
-DNA fragmentation
-formation of membrane blebs
-fragmentation into membrane-enclosed apoptotic bodies
PLASMA MEMBRANE REMAINS INTACT=NO INFLAMMATION

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

DNA modification in apoptosis

A

/

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

Apoptosis-like PCD

A
  • some, but not all, features of apoptosis

- display of phagocytic recognition molecules before plasma membrane lysis

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

Necrosis-like PCD

A
  • variable features of apoptosis before cell lysis

- ‘aborted apoptosis’

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

Apoptotic cell death mechanism

A
  • The executioners (Caspases)
  • Initiating the death programme (death receptors, mitochondria)
  • The Bcl-2 family
  • Stopping the death programme
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Caspases

A

Cysteine-dependent aspartate-directed proteases

  • executioners of apoptosis
  • activated by proteolysis
  • cascade of activation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Initiator caspases

A

-trigger apoptosis by cleaving and activating

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

Effector caspases

A
  • carry out the apoptotic programme
  • cleave and inactive proteins or complexes (eg: nuclear lamins leading to nuclear breakdown)
  • activate enzymes (including proteins kinases, nucleases eg: CAD) by direct cleavage, or cleavage of inhibitory molecules
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Caspase maturation

A

-cleavage of the inactive procaspase precursor is followed by folding of 2 large and 2 small chains to form an active L2S2 heterotetramer

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

Caspase cascades

A
  • amplification
  • divergent responses
  • regulation
17
Q

Caspase activation mechanisms

A
  • death by design (receptor-mediated pathways)

- death by default (mitochondrial death pathway)

18
Q

Death receptors

A

-secreted or transmembrane ligands (trimeric)

19
Q

Adaptor proteins in receptor-mediated apoptosis

A

/

20
Q

Signalling through death receptors

A

/

21
Q

Initiator procaspase 8 oligomerisation results in cleavage and activation

A

/

22
Q

Death receptor activation of caspase 8 is inhibited by FLIP

A
  • competes for binding to receptor tails/FADD via DED domains
  • incorporates into receptor-procaspase complexes and interferes with transcleavage
23
Q

Caspase 8 activation of downstream effector caspases

A

/

24
Q

Mitochondrial regulation of apoptosis

A
  • cellular stresses activate (eg: lack of or overstimulation by growth factors, DNA damage (p53), ROS)
  • loss of mitochondrial membrane potential
  • release of cytochrome c
  • release of other apoptosis-inducing factors
  • formation of the apoptosome complex
25
Q

The apoptosome

A

/

26
Q

Apoptosis energy requirement

A
  • the apoptosome requires ATP

- energy levels in the cell may determine whether death is by necrosis or apoptosis

27
Q

Bid links receptor and mitochondrial death pathways

A

/

28
Q

Bcl-2 family proteins as the modulators of apoptosis

A

/

29
Q

Anti-apoptotic Bcl-2 family proteins

A

Bcl-2
Bcl-xL
MITOCHONDRIAL

30
Q

Pro-apoptotic Bcl-2 family proteins

A 
Bid
Bad
Bax
Bak
MOVE BETWEEN CYTOSOL AND MITOCHONDRIA
31
Q

PI3’-Kinase signalling pathway in cell cycle and apoptosis regulation

A

/

32
Q

PKB/Akt inducing cell survival by blocking apoptosis

A
  • phosphorylates and inactivates Bad
  • phosphorylates and inactivates caspase 9
  • inactivates FOXO transcription factors (FOXOs promote expression of apoptosis-promoting genes)
  • Other eg: stimulates ribosome production and protein synthesis
33
Q

BH3 heterodimerisation

A

/

34
Q

PTEN (lipid phosphatase) counteracts PI3’-K signalling

A

/

35
Q

Inhibitor of Apoptosis Proteins (IAPs) regulate apoptosis

A

EXTRINSIC PATHWAY

  • bind to procaspases and prevent activation
  • bind to active caspases and inhibit their activity
36
Q

Cytoprotective/anti-apoptotic pathways

A
  • INTRINSIC PATHWAY: Bcl-2, Bcl-xL
  • EXTRINSIC PATHWAY: FLIP, IAPs
  • GROWTH FACTOR PATHWAYS via PI3’-K and PKB/Akt
37
Q

How can cancer cells avoid apoptosis?

A

/

38
Q

Apoptosis therapeutic uses

A
  • For harmful (oncogenic) cells eg: cells with viral infection, DNA damage
  • Chemotherapeutic killing of tumour cells eg: Dexamethasone stimulates DNA cleavage

Cancer (15 decks)

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