Cell Death Flashcards Preview

Foundations > Cell Death > Flashcards

Flashcards in Cell Death Deck (50):
1

Three types of cell death-

Apoptosis, autophagy, necrosis

2

Necrosis-

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

3

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

Necrosis

4

Apoptosis-

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

5

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

Apoptosis

6

Autophagy-

highly regulated; actually a cell survival pathway

7

highly regulated; actually a cell survival pathway is called:

Autophagy

8

Blebbing-

membrane contained buds formed on cells undergoing apoptosis

9

membrane contained buds formed on cells undergoing apoptosis are called:

Blebbing

10

Caspases-

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

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

12

Initiator caspases-

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

13

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

Initiator caspases

14

Effector caspases-

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

15

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

Effector caspases

16

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

17

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

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

Extrinsic pathway

19

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

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

Intrinsic pathway

21

Coupling of extrinsic and intrinsic pathways-

the two pathways can “cross talk”

22

Apoptosome-

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

23

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

Apoptosome

24

DISC-

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

25

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

DISC

26

Cyctochrome C-

part of apoptosome in intrinsic pathway of apoptosis

27

APAF-1-

part of apoptosome in intrinsic pathway of apoptosis

28

FADD-

part of DISC in extrinsic pathway of apoptosis

29

MOMP-

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

30

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

MOMP

31

Bcl-2 protein-

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

32

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

Bcl-2

33

Bcl-xL-

inhibit MOMP, suppress apoptosis

34

Bax-

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

35

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

Bax

36

Bak-

promote MOMP; promote apoptosis

37

Bid, Bad, Puma, Noxa-

inhibit Bcl-2 and Bcl-xL and promote apoptosis

38

p53’s role in apoptosis-

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

39

IAPs-

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

40

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

IAPs

41

Caspase 12-

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

42

Myc-

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

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

44

Two “survival pathways”-

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

45

mTor-

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

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-

47

Beclin 1-

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

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

49

Atg#’s-

factors that combine with beclin-1 to induce autophagy

50

factors that combine with beclin-1 to induce autophagy

Atg#'s