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Foundations > Cell Death > Flashcards

Cell Death Flashcards

1
Q

Three types of cell death-

A

Apoptosis, autophagy, necrosis

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2
Q

Necrosis-

A

largely unregulated; cells “blow up”. Release of cytosolic contents triggers inflammation

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3
Q

largely unregulated; cells “blow up”. Release of cytosolic contents triggers inflammation is called:

A

Necrosis

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4
Q

Apoptosis-

A

highly regulated; “programmed cell death”, frequently accompanied by orderly disposal of cell bodies by phagocytosis (neutrophils and macrophages)

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5
Q

highly regulated; “programmed cell death”, frequently accompanied by orderly disposal of cell bodies by phagocytosis (neutrophils and macrophages) is called:

A

Apoptosis

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6
Q

Autophagy-

A

highly regulated; actually a cell survival pathway

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7
Q

highly regulated; actually a cell survival pathway is called:

A

Autophagy

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8
Q

Blebbing-

A

membrane contained buds formed on cells undergoing apoptosis

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9
Q

membrane contained buds formed on cells undergoing apoptosis are called:

A

Blebbing

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10
Q

Caspases-

A

proteases which hydrolyze a large number of proteins during apoptosis

- MSTI (a kinase)- chromatin condensation
- ICAD (an inhibitor of a DNase)- DNA cleavage
- lamins- nuclear envelope breakdown
- Rho kinase- actin cytoskeleton disruption
- Cell-cell and cell-ECM adhesion junctions- cell rounding and detachment
- golgi and ER proteins- fragmentation of organelles
- eIFs- translation arrest
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11
Q

proteases which hydrolyze a large number of proteins during apoptosis

- MSTI (a kinase)- chromatin condensation
- ICAD (an inhibitor of a DNase)- DNA cleavage
- lamins- nuclear envelope breakdown
- Rho kinase- actin cytoskeleton disruption
- Cell-cell and cell-ECM adhesion junctions- cell rounding and detachment
- golgi and ER proteins- fragmentation of organelles
- eIFs- translation arrest
A

Caspases

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12
Q

Initiator caspases-

A

9,2,8,10; activated by proteolysis, found in apoptosome, PIDDosome, DISCs

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13
Q

9,2,8,10; activated by proteolysis, found in apoptosome, PIDDosome, DISCs are called:

A

Initiator caspases

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14
Q

Effector caspases-

A

3,7,9 also synthesized in inactive form, activated by proteolysis

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15
Q

3,7,9 also synthesized in inactive form, activated by proteolysis are called:

A

Effector caspases

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16
Q

Caspase cascades-

A

the substrates of caspases include themselves; once they are proteolytically activated, a caspase can cleave and activate other caspases; thus initiator caspases can activate effector caspases resulting in a great amplification of protease activity

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17
Q

Extrinsic pathway for apoptosis-

A

ligands, receptors, caspase activation mediate this route; involves signaling molecules of the Tumor Necrosis Factor family, ligand binding form scaffolding for adaptor proteins like FADD which activate and complex with caspases forming DISCs and trigger apoptosis

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18
Q

ligands, receptors, caspase activation mediate this route; involves signaling molecules of the Tumor Necrosis Factor family, ligand binding form scaffolding for adaptor proteins like FADD which activate and complex with caspases forming DISCs and trigger apoptosis

A

Extrinsic pathway

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19
Q

Intrinsic pathway for apoptosis-

A

mitochondria, apoptosomes and associated proteins mediate this route; involves damage or stress transmitted to mitochondria resulting in outer membrane pore opening (MOMP) and release of cytochrome C which complexes with APAF-1 and caspase 9 to form the apoptosome

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20
Q

mitochondria, apoptosomes and associated proteins mediate this route; involves damage or stress transmitted to mitochondria resulting in outer membrane pore opening (MOMP) and release of cytochrome C which complexes with APAF-1 and caspase 9 to form the apoptosome

A

Intrinsic pathway

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21
Q

Coupling of extrinsic and intrinsic pathways-

A

the two pathways can “cross talk”

22
Q

Apoptosome-

A

cytochrome C, APAF-1, and caspase 9; complex for intrinsic pathway of apoptosis

23
Q

cytochrome C, APAF-1, and caspase 9; complex for intrinsic pathway of apoptosis is called an:

A

Apoptosome

24
Q

DISC-

A

Death Inducing Signaling Complex; composed of FADD and procaspase 8, component of extrinsic pathway of apoptosis

25
Q

Death Inducing Signaling Complex; composed of FADD and procaspase 8, component of extrinsic pathway of apoptosis is called a:

A

DISC

26
Q

Cyctochrome C-

A

part of apoptosome in intrinsic pathway of apoptosis

27
Q

APAF-1-

A

part of apoptosome in intrinsic pathway of apoptosis

28
Q

FADD-

A

part of DISC in extrinsic pathway of apoptosis

29
Q

MOMP-

A

membrane pore opening in outer mitochondrial membrane due to stress, releases cytochrome C for participation in apoptosome

30
Q

membrane pore opening in outer mitochondrial membrane due to stress, releases cytochrome C for participation in apoptosome is called:

A

MOMP

31
Q

Bcl-2 protein-

A

centrally important to regulation of apoptosis; inhibit Bax inhibiting formation of MOMP and suppressing apoptosis

32
Q

centrally important to regulation of apoptosis; inhibit Bax inhibiting formation of MOMP and suppressing apoptosis. this protein is called:

A

Bcl-2

33
Q

Bcl-xL-

A

inhibit MOMP, suppress apoptosis

34
Q

Bax-

A

promote MOMP; promote apoptosis. Activated by p53 (DNA damage).

35
Q

promote MOMP; promote apoptosis. Activated by p53 (DNA damage). This protein is called:

A

Bax

36
Q

Bak-

A

promote MOMP; promote apoptosis

37
Q

Bid, Bad, Puma, Noxa-

A

inhibit Bcl-2 and Bcl-xL and promote apoptosis

38
Q

p53’s role in apoptosis-

A

activated by Chk1/Chk2 when DNA damage is bad→ activates Bax→ promotes apoptosis and cell death

39
Q

IAPs-

A

inhibitor of apoptosis proteins (caspases), can be inhibited by proteins released by mitochondria after MOMP like Smac/Diablo resuming apoptosis

40
Q

inhibitors of apoptosis proteins (caspases), can be inhibited by proteins released by mitochondria after MOMP like Smac/Diablo resuming apoptosis:

A

IAPs

41
Q

Caspase 12-

A

activated by stress in the ER (excessive unfolded proteins) then activates caspase 9 and the rest of the caspase cascade

42
Q

Myc-

A

immediate early transcription factor produces after growth factor signaling; excessive production activates MAPK stress pathway which eventually activates p53→ cell cycle arrest (via upregulation of p21) or apoptosis (via upregulation of Bax)

43
Q

immediate early transcription factor produces after growth factor signaling; excessive production activates MAPK stress pathway which eventually activates p53→ cell cycle arrest (via upregulation of p21) or apoptosis (via upregulation of Bax)

A

Myc

44
Q

Two “survival pathways”-

A

increased production of Bcl2 to inhibit Bax, or post translational inhibition of pro-apoptotic proteins like Akt kinase

45
Q

mTor-

A

inhibits Beclin and Atg# from initiating autophagy, can itself be inhibited by ER stress and/or AMPK (DNA damage) to allow autophagy to destruct damaged cell

46
Q

inhibits Beclin and Atg# from initiating autophagy, can itself be inhibited by ER stress and/or AMPK (DNA damage) to allow autophagy to destruct damaged cell

A

mTor-

47
Q

Beclin 1-

A

pro-apoptotic protein combines with Atg#’s → autophagy; can be inhibited by Bcl-2 (another reason along with being pro-apoptotic that Bcl-2 is a cell survival and possibly oncogene factor)

48
Q

pro-apoptotic protein combines with Atg#’s → autophagy; can be inhibited by Bcl-2 (another reason along with being pro-apoptotic that Bcl-2 is a cell survival and possibly oncogene factor)

A

Beclin 1

49
Q

Atg#’s-

A

factors that combine with beclin-1 to induce autophagy

50
Q

factors that combine with beclin-1 to induce autophagy

A

Atg#’s

Foundations (17 decks)

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