Cell Death Flashcards

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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
Q

Extrinsic pathway of apoptosis

A

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
Q

Apoptosome

A

Made up of cytochrome c, APAF-1 and caspase 9

27
Q

DISC

A

Death receptor, FADD, and caspase 8 or 10

28
Q

Cellular stress (extrinsic)

A

Triggers activation of p53

29
Q

p53 (extrinsic)

A

Activates death receptor/ligand complex

30
Q

FADD

A

Activates caspases 8/10

31
Q

Caspases 8/10

A

Activate caspases 3, 6, and 7

32
Q

Apoptosis and health

A

Apoptosis is normal and helps maintain cellular functions. Any disorder in apoptosis will lead to cancer or other diseases.

33
Q

Other types of cell death

A

Necroptosis, pyroptosis, and autophagy