Cell Death Flashcards Preview

Question 1

1

Three types of cell death-

Answer

Apoptosis, autophagy, necrosis

Question 2

2

Necrosis-

Answer

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

Question 3

3

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

Necrosis

Answer

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

Answer

highly regulated; actually a cell survival pathway

Answer

membrane contained buds formed on cells undergoing apoptosis

Answer

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

Answer

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

Answer

Initiator caspases

Answer

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

Answer

Effector caspases

Answer

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

Answer

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

Answer

Extrinsic pathway

Answer

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

Answer

Intrinsic pathway

Answer

the two pathways can “cross talk”

Answer

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

Answer

Apoptosome

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

Answer

part of apoptosome in intrinsic pathway of apoptosis

Answer

part of apoptosome in intrinsic pathway of apoptosis

Answer

part of DISC in extrinsic pathway of apoptosis

Answer

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

Answer

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

Answer

inhibit MOMP, suppress apoptosis

Answer

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

Answer

promote MOMP; promote apoptosis

Answer

inhibit Bcl-2 and Bcl-xL and promote apoptosis

Answer

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

Answer

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

Answer

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

Answer

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)

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

Answer

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

Answer

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)

Answer

factors that combine with beclin-1 to induce autophagy

Question 4

4

Apoptosis-

Question 5

5

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

Apoptosis

Question 6

6

Autophagy-

Question 7

7

highly regulated; actually a cell survival pathway is called:

Autophagy

Question 8

8

Blebbing-

Question 9

9

membrane contained buds formed on cells undergoing apoptosis are called:

Blebbing

Question 10

10

Caspases-

Question 11

11

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

Caspases

Question 12

12

Initiator caspases-

Question 13

13

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

Question 14

14

Effector caspases-

Question 15

15

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

Question 16

16

Caspase cascades-

Question 17

17

Extrinsic pathway for apoptosis-

Question 18

18

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

Question 19

19

Intrinsic pathway for apoptosis-

Question 20

20

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

Question 21

21

Coupling of extrinsic and intrinsic pathways-

Question 22

22

Apoptosome-

Question 23

23

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

Question 24

24

DISC-

Question 25

25

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

DISC

Question 26

26

Cyctochrome C-

Question 27

27

APAF-1-

Question 28

28

FADD-

Question 29

29

MOMP-

Question 30

30

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

MOMP

Question 31

31

Bcl-2 protein-

Question 32

32

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

Bcl-2

Question 33

33

Bcl-xL-

Question 34

34

Bax-

Question 35

35

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

Bax

Question 36

36

Bak-

Question 37

37

Bid, Bad, Puma, Noxa-

Question 38

38

p53’s role in apoptosis-

Question 39

39

IAPs-

Question 40

40

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

IAPs

Question 41

41

Caspase 12-

Question 42

42

Myc-

Question 43

43

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)

Myc

Question 44

44

Two “survival pathways”-

Question 45

45

mTor-

Question 46

46

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

mTor-

Question 47

47

Beclin 1-

Question 48

48

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)

Beclin 1

Question 49

49

Atg#’s-

Question 50

50

Cell Death Flashcards Preview

Foundations > Cell Death > Flashcards

Three types of cell death-

Apoptosis, autophagy, necrosis

Necrosis-

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

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

Necrosis

Apoptosis-

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

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

Apoptosis

Autophagy-

highly regulated; actually a cell survival pathway

highly regulated; actually a cell survival pathway is called:

Autophagy

Blebbing-

membrane contained buds formed on cells undergoing apoptosis

membrane contained buds formed on cells undergoing apoptosis are called:

Blebbing

Caspases-

Caspases

Initiator caspases-

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

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

Initiator caspases

Effector caspases-

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

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

Effector caspases

Caspase cascades-

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

Extrinsic pathway for apoptosis-

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

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

Extrinsic pathway

Intrinsic pathway for apoptosis-

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

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

Intrinsic pathway

Coupling of extrinsic and intrinsic pathways-

the two pathways can “cross talk”

Apoptosome-

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

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

Apoptosome

DISC-

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

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

DISC

Cyctochrome C-

part of apoptosome in intrinsic pathway of apoptosis

APAF-1-

part of apoptosome in intrinsic pathway of apoptosis

FADD-

part of DISC in extrinsic pathway of apoptosis

MOMP-

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

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

MOMP

Bcl-2 protein-

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

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

Bcl-2

Bcl-xL-

inhibit MOMP, suppress apoptosis

Bax-

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

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

Bax

Bak-

promote MOMP; promote apoptosis

Bid, Bad, Puma, Noxa-

inhibit Bcl-2 and Bcl-xL and promote apoptosis

p53’s role in apoptosis-

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

IAPs-

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

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

IAPs