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
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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
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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
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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