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BS202 > 19.3 Programmed Cell Death > Flashcards

19.3 Programmed Cell Death Flashcards

1
Q

() balances cell proliferation and potentially dangerous cells (e.g. virus-infected cells, cells with damaged DNA/mutated DNA)

A

programmed cell death

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2
Q

3 main events in apoptosis:

A
  1. DNA fragmentation
  2. chromatin condensation
  3. fragmentation of nucleus
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3
Q

membrane-enclosed fragments that result from the apoptosis of cells

A

apoptotic bodies

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4
Q

how are cells that die by apoptosis rapidly removed from tissues

A

apoptotic bodies are efficiently recognized and phagocytosed by both macrophages and neighboring cells

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5
Q

apoptopic cells express () on their surface

A

‘eat me’ signals (e.g. phosphatidylserine)

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6
Q

apoptosis causes () to be expressed on the cell surface, where it is recognized by receptors expressed by phagocytic cells

A

phosphatidylserine

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7
Q

studies of () by Horvits and colleagues identified 3 genes with key roles in apoptosis:

A

C. elegans

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8
Q

studies of C. elegans by Horvits and colleagues identified 3 genes with key roles in apoptosis:

A
  1. Ced-3
  2. Ced-4
  3. Ced-9
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9
Q

(1) and (2) are genes that are required for developmental cell death

A

Ced-3 and Ced-4

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10
Q

Ced-9 serves as a () in apoptosis

A

negative regulator

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11
Q

Ced-3 was found to be the prototype of the ()

A

caspases (a family of proteases)

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12
Q

() was found to be the prototype of the caspases (a family of proteases)

A

Ced-3

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13
Q

called caspases due to the presence of (1) at their active sites and they cleave (2) in their substrate proteins

A
  1. cysteine (C) residues
  2. aspartic acid (Asp) residues
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14
Q

the () are the ultimate effectors/executioners of programmed cell death; they bring about apoptosis by cleaving more than 100 different target proteins

A

caspases

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15
Q

activation of an () starts a chain reaction of caspase activation leading to cell death

A

initiator caspase

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16
Q

main targets of caspases in apoptosis

A
  1. DNase inhibitor
  2. nuclear lamins
  3. cytoskeletal proteins
  4. Golgi matrix proteins
  5. scramblase
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17
Q

caspases targeting DNase inhibitor results in DNase activation, which in turn results in ()

A

nuclear DNA fragementation

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18
Q

caspases cleave nuclear lamins to result in ()

A

fragmentation of nucleus

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19
Q

caspases cleave cytoskeletal proteins to result in ()

A

cytoskeletal disruption, cell fragmentation, and PM blebbing (irregular bulging)

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20
Q

caspases cleave Golgi matrix proteins to result in ()

A

fragmentation of Golgi

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21
Q

caspases also cleave and activate a () that translocates phosphatidylserine to the outer leaflet of the PM

A

scramblase

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22
Q

higher eukaryotes have families of at least 7 caspases that are classified as either (1) or (2) caspases

A
  1. initiator
  2. effector
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23
Q

all caspases are synthesized as inactive precursors called ()

A

procaspases

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24
Q

procaspases are converted to the active form by () (catalyzed by other caspases)

A

proteolytic cleavage

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25
Q

() caspases are activated in response to various signals

A

initiator

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26
Q

() are cleaved and activated by initiator caspases and then act to digest cellular target proteins

A

effector caspases

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27
Q

Ced-9 was found to be closely related to a mammalian gene called (), an oncogene that contributed to the development of B-cell lymphomas

A

bcl-2

28
Q

instead of stimulating cell proliferation, bcl-2 was found to ()

A

inhibit apoptosis

29
Q

2 major classifications of Bcl-2 family members

A
  1. antiapoptotic regulatory proteins
  2. proapoptotic proteins
30
Q

proapoptotic proteins can be further divided into

A
  1. proapoptotic regulatory proteins
  2. proapoptotic effector proteins
31
Q

act to induce caspase activation and promote cell death

A

proapoptotic proteins

32
Q

inhibit proapoptotic effector proteins (e.g. Bcl-2) and are regulated by signals that induce cell death or survival

A

proapoptotic regulatory proteins

33
Q

downstream effectors that directly induce apoptosis

A

proapoptotic effector proteins

34
Q

activated proapoptotic regulatory proteins initiate apoptosis by 2 mechanisms:

A
  1. antagonize antiapoptotic regulatory proteins
  2. activate proapoptotic effector proteins
35
Q

in mammals, Bcl-2 family proteins act at the ()

A

mitochondria

36
Q

proapoptotic effector proteins (1) oligomerize to form pores in the outer mitochondrial membrane to release (2)

A
  1. Bax and Bak
  2. cytochrome c
37
Q

release of () triggers caspase activation

A

cytochrome c

38
Q

key initiator caspase in mammalian cells

A

caspase-9

39
Q

caspase-9 is activated by forming a complex with (1) in a multisubunit complex called (2)

A
  1. Apaf-1
  2. apoptosome
40
Q

pathways that regulate programmed cell death are either:

A
  1. intrinsic pathways
  2. extrinsic pathways
41
Q

programmed cell death regulatory pathways that are triggered by DNA damage and other cell stress

A

intrinsic pathways

42
Q

intrinsic pathways are triggered by (1) and other (2)

A
  1. DNA damage
  2. cell stresses
43
Q

the multiple signals that activate intrinsic apoptosis regulatory pathways converge on regulation of ()

A

proapoptotic regulatory Bcl-2 proteins

44
Q

programmed cell death regulatory pathways that are triggered by signals from other cells

A

extrinsic pathways

45
Q

extrinsic apoptosis regulatory pathways are activated by ()

A

signals from other cells

46
Q

give examples of intrinsic pathways that regulate apoptosis

A
  1. p53 pathway
  2. Akt/PI 3-kinase pathway
47
Q

transcription factor p53 mediates a major pathway that leads to cell cycle arrest in response to ()

A

DNA damage

48
Q

the Akt/PI 3-kinase pathway is an intrinsic pathway that regulates apoptosis; it responds to ()

A

growth factor deprivation

49
Q

(1) and (2) protein kinases (activated by DNA damage) phosphorylate and stabilize p53

A
  1. ATM
  2. Chk2
50
Q

induction of apoptosis due to increased p53 is due in part to the transcriptional activation of genes encoding () (proapoptotic regularory proteins)

A

PUMA and Noxa

51
Q

increased PUMA and Noxa lead to activation of ()

A

Bax and Bak

52
Q

most cells in higher animals are programmed to undergo apoptosis unless cell death is ()

A

actively supressed by survival signals from other cells (e.g. growth factors)

53
Q

a major pathway that promotes cell survival is initiated by (1) and results in the activation of (2)

A
  1. PI 3-kinase
  2. Akt
54
Q

how does Akt regulate proteins involved in apoptosis

A

Akt phosphorylates BH-3 proteins including Bad and FOXO transcription factors to inactivate them

55
Q

in absence of Akt, (1) promotes apoptosis and (2) stimulates transcription of another proapoptotic BH3-only protein called (3)

A
  1. Bad
  2. FOXO
  3. Bim
56
Q

example of extrinsic pathway that regulates programmed cell death

A

TNF-receptor signaling

57
Q

polypeptides in the () family bind to receptors and activate an initiator caspase

A

tumor necrosis factor

58
Q

polypeptides in the tumor necrosis factor family bind to receptors and activate an initiator caspase called ()

A

caspase-8

59
Q

caspase-8 cleaves and activates (1) and (2), which leads to the activation of (3)

A
  1. effector caspases
  2. Bid
  3. caspase-9
60
Q

() - provides a mechanism for the gradual turnover of the cell’s components through lysosomes

A

autophagy

61
Q

autophagy can lead to cell death by ()

A

degradation of essential cell components

62
Q

accidental cell death from acute injury; causes swelling and bursting of the cell

A

necrosis

63
Q

unlike apoptosis, autophagy does not require ()

A

caspases

64
Q

in necrosis, cell contents are released into extracellular space and cause ()

A

inflammation

65
Q

regulated necrotic cell death

A

necroptosis

BS202 (36 decks)

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