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BMS > Mechanisms of Cell Death: Apoptosis, Autophagy, and Necrosis > Flashcards

Mechanisms of Cell Death: Apoptosis, Autophagy, and Necrosis Flashcards

1
Q

Programmed cell death

-i.e. death by suicide

A

Apoptosis

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2
Q

Catabolic process involving the degradation of a cell’s own components through the lisosomal machinery

-i.e. Death by self-cannibalism

A

Autophagy

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3
Q

Defined as the premature death of cells by external factors

-i.e. Death by accident or murder

A

Necrosis

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4
Q

Most of what we know about apoptosis was discovered in

A

C. elegans

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5
Q

An integral part of both plan and animal tissue development

A

Apoptosis

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6
Q

In C. elegans, out of 1090 somatic cells, 131 of them underwent apoptosis. The different cells died at different times in

-remarkably accurate

A

Development

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7
Q

In normal development, apoptosis is required for

A

Tissue sculpting

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8
Q

Apoptosis is important in the immune system after infection for for eliminating used

A

T and B cells

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9
Q

A balance between proliferation and cell death is required to maintain

A

Tissue homeostasis

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10
Q

Crucial for eliminating cells that have been damaged by UV, radiation, chemical toxins, or viral infection

-i.e. it can prevent cancer

A

Apoptosis

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11
Q

An example of apoptosis function during tissue development is the development of the

A

Fingers and toes

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12
Q

Problems in apoptosis during finger and toe development results in

-2 or more fingers/toes are joined together

A

Syndactily

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13
Q

Lack of apoptosis during embryo development also disrupts

A

Normal brain development

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14
Q

Humans who are born with tails have deficiencies in

A

Apoptosis

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15
Q

What are five morphological markers of apoptosis?

A
  1. ) Electron dense nucleus
  2. ) Nuclear fragmentation
  3. ) Large, clear vacuoles
  4. ) Blebs at the surface
  5. ) Loss of cell adhesion
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16
Q

What is one very common biochemical marker of apoptosis?

A

Phosphatidylserine flipping from inner leaflet to outer leaflet

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17
Q

Phosphatidylserine flipping from inner leaflet to outer leaflet enables

A

Apoptotic cells to enter cell

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18
Q

Enables us to track nicks in DNA

A

Terminal Transferase dUTP Nick-End Labeling (TUNEL)

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19
Q

Used to add labeled dUTP to 3’ terminal end of the DNA fragments

A

Terminal Transferase

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20
Q

Highly sensitive and can detect fewer than 100 cells

-Fast: can be completed in 3 hours

A

TUNEL Assay

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21
Q

Has high reproducibility with good precision

A

TUNEL Assay

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22
Q

One of the disadvantages of TUNEL Assays are that we don’t know the minimum number of strand breaks necessary for detection. Thus we may miss the

A

Early stages of apoptosis

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23
Q

Designed to detect apoptotic cells that undergo extensive DNA degradation during the late stages of apoptosis

-Based on the ability of dUPT to label blunt ends of double-stranded DNA breaks independent of a template

A

Terminal Transferase dUTP Nick-End Labeling (TUNEL Assay)

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24
Q

Can generate false positives in a TUNEL assay

A

Necrotic cells

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25
Q

Another disadvantage of a TUNEL assay is that the detergent used to permeabilize cells can make them

A

Frgile

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26
Q

A distinctive feature of DNA degraded by caspase-activated DNAse (CAD)

A

DNA laddering

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27
Q

Cleaves genomic DNA at internucleosomal linker regions, resulting in DNA fragments that are multiples of 180-185 bps in length

A

Caspase-activated DNAse (CAD)

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28
Q

Must be cleaved to become active

A

Caspases

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29
Q

What are the two major apoptotic pathways?

A
  1. ) Cell-extrinsic pathway

2. ) Cell-intrinsic pathway

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30
Q

The key enzymes that give rise to all of the morphological and biochemical changes arising from apoptosis

A

Caspases

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31
Q

What are the two types of apoptotic caspases?

A
  1. ) Initiator (apical) caspases (#’s 2, 8, 9, and 10)

2. ) Effector (executioner) caspases (#’s 3, 6, and 7)

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32
Q

Regulated at a post-translational level, ensuring that they can be rapidly activated

A

Caspases

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33
Q

What are the steps of the caspase cascade?

A

Pro-apoptotic stimulus —> initiator caspases —> effector caspases —> apoptosis

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34
Q

Initiator caspase is activated by

A

2 proteolytic cleavages

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35
Q

Initiator caspase then cleaves and activates

A

Effector caspase

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36
Q

Cleaves nuclear lamins, inhibitors of DNAases, and Actin

A

Effector Caspases

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37
Q

The intrinsic apoptosis pathway is also known as the

A

Mitochondrial mediated pathway

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38
Q

The extrinsic apoptosis pathway is also known as the

A

Death receptor mediated pathway

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39
Q

Family of proteins that regulates the integrity of the mitochondrial membrane

A

BCL2

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40
Q

What are the two pro-apoptotic BCL2 proteins?

A

BAX and BAK

41
Q

What are the three anti-apoptotic BCL2 proteins?

A

BCL2, BCL-XL, and MCL1

42
Q

The regulators/sensors of the intrinsic pathway are “BH3-only proteins” and include

A

BAD, BID, and PUMA

43
Q

Characterized by permeabilisation of the mitochondria and release of cytochrome c into the cytoplasm

A

Intrinsic apoptotic pathway

44
Q

Forms a multi-protein complex known as the ‘apoptosome’ and initiates activation of the caspase cascade through caspase 9

A

Cytochrome C

45
Q

Cytochrome C activates

-activates caspase 9

A

Apoptotic protease activating factor 1 (APAF1)

46
Q

Antagonism of BCL2 causes the activation of the BAX/BAK channel which causes the mitochondria to release

A

Cytochrome C

47
Q

Responsive to DNA damage by UV radiation

-one of the most studied genes of all time

48
Q

Can activate DNA repair proteins, arrest cell at G1/S checkpoint, and initiate apoptosis

49
Q

p53 is a transcription factor that regulates

A

Cell cycle and apoptosis

50
Q

Acts as a ubiquitin ligase and covalently attaches ubiquitin to p53, thus marking it for degredation

51
Q

Also transports p53 from nucleus to cytosol

52
Q

The critical event leading to the activation of p53 is

A

Phorphorylation of its N-terminus

53
Q

The protein kinases known to target this transcriptional activation domain of p53 can be broken down into what two groups?

A
  1. ) Members of MAPK family

2. ) Checkpoint kinases

54
Q

Oncogenes also stimulate p53 activation, mediated by the protein

55
Q

Contains many pro-apoptotic proteins such as cytochrome C

A

Mitochondria

56
Q

Can be release from the mitochondria in response to pro-apoptotic signals

A

Cytochrome C

57
Q

Translocate to the mitochondrial membrane and stimulate the formation of pores allowing Cytochrome c to leak out

-normally found in the cytosol

A

Pro-apoptotic molecules (i.e. Bad, Bax, Bid)

58
Q

Interacts with APAF-1 to form the apoptosome

A

Cytochrome C

59
Q

Interaction between cytochrome C and APAF-1 activate

-promotes caspase cascade

60
Q

Promote apoptosis by tying up Bcl2 and freeing Bax/Bak

A

Bid and Bad

61
Q

Binds Bax/Bak and prevents pore formation

-anti-apoptotic

62
Q

Promote pore formation, release of cytochrome C and APAF1, and initiation of apoptosis

A

Bax and Bak

63
Q

Results from a chromosomal translocation between the 14th and 18th chromosomes, which places the BCL-2 gene next to the IgG heavy chain locus

A

Follicular Lymphoma

64
Q

The fusion gene of BCL-2 and IgG heavy chain leads to

A

High expression of BCL-2

65
Q

High expression of BCL-2 then results in a decreased propensity of cells for undergoing

66
Q

Occurs in several cancers and is linked to poor disease outcome

A

Increased Bcl-2 protein expression

67
Q

Triggered by the p53 tumor-suppressor in

response to DNA damage and other types of severe cell stress

A

Intrinsic pathway

68
Q

Conventional anticancer therapies, such as chemotherapy, activate the intrinsic pathway via

69
Q

p53 activates the intrinsic pathway through transcriptional upregulation of pro-apoptotic members of the BCL2 family of proteins such as

A

PUMA and Bax

70
Q

The extrinsic apoptotic pathway is apoptosis via the pro-apoptotic receptors

A

DR4 and DR5 (Fas receptors)

71
Q

Activate the pro-apoptotic receptors DR4 and DR5

A

Endogenous Apo2L/TRAIL

72
Q

The activated pro-apoptotic receptors D4 and D5 then recruit

A

Fas-associated death domain (FADD)

73
Q

Recruits initiator caspase 8 and/or 10 to the death-inducing signaling complex (DISC)

74
Q

The DISC activates caspases 8 and 10 and releases them into the cytoplasm, where they activate

A

Caspases 3, 6, an 7

75
Q

Triggers apoptosis in response to the activation of pro-apoptotic receptors, such as DR4 and DR5, by specific pro-apoptotic ligands, such as Apo2L/TRAIL

A

Extrinsic apoptotic pathway

76
Q

The extrinsic apoptotic pathway stimulates apoptosis independently of

77
Q

Ligand-induced activation of DR4 and DR5 leads to the rapid assembly of the death-inducing signaling complex (DISC) and the recruitment of initiator caspases 8 and 10 through the adaptor

A

Fas-associate death domain (FADD)

78
Q

The extrinsic and intrinsic apoptosis pathways converge on

A

Caspases 3, 6, and 7

79
Q

Also, caspases 8 and 10 (extrinsic) activate Bid,which activates

A

Bax and Bak (intrinsic)

80
Q

Responsible for degrading cellular proteins and organelles and recycling them

-A survival pathway

81
Q

Autophagy is actually a response to

A

Cellular starvation

82
Q

Occurs in many disease states, including cancer, inflammatory bowel disease, and neurodegenerative disorders

A

Disregulation of Autophagy

83
Q

The sequestration of cellular organelles into cytoplasmic autophagic vacuoles (autophagosomes) that fuse with lysosomes and digest the enclosed material

84
Q

What are the four stages of autophagy?

A
  1. ) Induction
  2. ) Autophagosome formation
  3. ) Autophagosome-lysosome fusion
  4. ) Autophagosome breakdown
85
Q

A key regulator of autophagic induction is

-has an inhibitory affect

A

mTOR (mammalian target of rapamycin)

86
Q

A serine-theronine kinase

87
Q

Many of the genes that are upregulated in response to mTOR deactivation participate in

A

Autophagosome formation

88
Q

Involves formation of a membrane around a targeted portion of the cell

A

Autophagosome formation

89
Q

In autophagosome-lysosome fusion, the autophagosome fuses w/ the lysosome releasing its contents into the lysosome for

A

Degredation by proteases

90
Q

Inevitably breaks down the autophagosome

91
Q

Has contrasting roles during cancer development, progression, and treatment

92
Q

Typically caused by factors external to the cell or tissue, such as infection, toxins, or trauma

93
Q

Unlike apoptosis and autophagy, is almost always detrimental and can be fatal

94
Q

What are the five types of necrosis?

A
  1. ) Coagulation necrosis
  2. ) Liquefactive necrosis
  3. ) Enzymatic fat necrosis
  4. ) Caseous necrosis
  5. ) Gangrenous necrosis
95
Q

Cell destruction leading to escape of hydrolases

A

Liquefactive necrosis

96
Q

Typically begins with cell swelling, chromatin digestion, and disruption of the plasma and organelle membranes

97
Q

Charactrized by extensive DNA hydrolysis, vacuolation of the endoplasmic reticulum, organelle breakdown, and cell lysis

A

Late necrosis

98
Q

What is the cause of inflammation in necrosis?

A

Release of intracellular contents after plasma membrane rupture

BMS (62 decks)

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