Cell Death Flashcards

1
Q

Necrosis vs Apoptosis

A

Necrosis - involves a cellular response to injury that causes local inflammation and the bursting of the cell (pathological)
Apoptosis - cellular response to cellular stresses that cause the shrinkage of the cell to be taken up by phagocytes (physiological)

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2
Q

Six mechanisms of cell injury that would lead to cell death

A

ATP depletion, mitochondrial damage, accumulation of reactive oxygen species, influx of calcium, increased permeability of cellular membranes, accumulation of damaged DNA/misfolded proteins

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3
Q

Intrinsic pathway of apoptosis

A

DNA damaged, lack of O2 or other stress, increases mitochondrial permeability via Bcl2 effector activation. Cytochrome C is released to trigger activation of APAF-1 and initiator caspase 9. APAF-1 forms the apoptosome and pro-caspase 9 binds to this and autoactivates. Caspase 9 cleaves and activates caspase 3,6,7 (executioner caspases) and leads to cell death

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4
Q

Death receptors

A

Contain cytoplasmic death domain

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5
Q

Bcl family

A

Proteins that interact with the mitochondrial membrane and each other

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6
Q

Three types of Bcl-2 family proteins

A

Regulators, effectors, and sensors

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7
Q

Regulator Bcl-2 proteins

A

Bcl-2 or Bcl-X, maintain mitochondrial membrane permeability, anti-apoptotic

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8
Q

Effector Bcl-2 proteins

A

Bax or Bak, also known as BH123 proteins, form pores in the mitochondrial outer membrane, pro-apoptotic

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9
Q

Sensor Bcl-2 proteins

A

Bad, Bid, Bim, Puma, Noxa, also called BH3-only proteins, inhibit Bcl-2 and activate effectors, pro-apoptotic

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10
Q

Adaptors

A

APAF-1 (intrinsic) and FADD (extrinsic) both are pro-apoptotic

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11
Q

Caspases

A

Proteases that degrade cellular components

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12
Q

DNases

A

Digest genome

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13
Q

IAPs

A

Inhibitors of apoptosis

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14
Q

Anti-IAPs

A

Anti-inhibitors of apoptosis

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15
Q

Initiator caspases

A

Activate themselves and then activate effector or executioner caspases to start a signal cascade

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16
Q

Cellular stress (intrinsic)

A

Triggers activation of p53 or BH3-only proteins

17
Q

p53 (intrinsic)

A

Triggers the activation of BH3-only proteins

18
Q

BH3-only proteins

A

Inhibit Bcl-2 and activate BH123 proteins

19
Q

Bcl-2

A

Inhibits BH123 proteins from continuing apoptosis

20
Q

BH123 proteins

A

Activate anti-IAPs and trigger release of cytochrome c

21
Q

Cytochrome c

A

Activates APAF-1

22
Q

APAF-1

A

Activates caspase 9

23
Q

Caspase 9

A

Activate Caspases 3, 6, and 7

24
Q

Caspases 3, 6, 7

A

Activate various death substrates

25
Extrinsic pathway of apoptosis
Cell surface death receptor is bound by TNF family ligand, receptors cluster and bind FADD, pro-caspase 8 or 10 bind FADD and autoactivate. Caspase 8 or 10 cleave executioner caspases to cause cell death
26
Apoptosome
Made up of cytochrome c, APAF-1 and caspase 9
27
DISC
Death receptor, FADD, and caspase 8 or 10
28
Cellular stress (extrinsic)
Triggers activation of p53
29
p53 (extrinsic)
Activates death receptor/ligand complex
30
FADD
Activates caspases 8/10
31
Caspases 8/10
Activate caspases 3, 6, and 7
32
Apoptosis and health
Apoptosis is normal and helps maintain cellular functions. Any disorder in apoptosis will lead to cancer or other diseases.
33
Other types of cell death
Necroptosis, pyroptosis, and autophagy