Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

MCM Final Exam > MCM Final - Cell Death and Adaptations > Flashcards

MCM Final - Cell Death and Adaptations Flashcards

(84 cards)

Start Studying
0
Q

apoptotic bodies

A

small, membrane-bound vesicles occur from membrane blebbing from cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

apoptosis

A

programmed cell death

no inflammation

cell shrinks, degrades, forms apoptotic bodies, induces membrane signaling (phosphatidylserine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

membrane signaling during apoptosis?

A

phosphatidylserine from inner leaflet to outer leaflet
-signals for phagocytes

no inflammation response**

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

necrosis

A

cell death due to trauma
-cells swells and ruptures

**leads to inflammation response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

when does apoptosis occur?

A

eliminate unwanted cells
-development loss of cells to form digits

quality control
-get rid of nonfunctional cells

homestasis of cell death and cell division important

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

caspase

A

protease during apoptosis

active site - cysteine - cleaves target aspartic acid

synthesized as zymogen (pro-caspase)
-activated by other caspases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

initiator caspases

A

cleave and activate downstream caspase

have CARD domain that assemble in activation complex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

executioner caspases

A

cleave and activate other caspases and target proteins

target proteins: nuclear lamins, endonuclease inhibiting enzyme, cytoskeleton, adhesion proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

endonuclease inhibiting enzyme

A

cleaved by executioner caspase in apoptosis

endonuclease is activated and can cleave DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Extrinsic Pathway

A

one type of apoptosis initiation

from an external signal

death receptor binds is activated

- recruits FADD
	- recruits initiator procaspases 8 and 10
		- DISC is formed
			- initiator caspases activate executioner
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

death receptor

A

of the tumor necrosis factor (TNF) family

homotrimer activated by homotrimer ligand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what happens during lymphocyte mediated cell death?

A

Fas death receptor activated by Fas ligand on lymphocyte
-juxtacrine signaling

Adaptor protein FADD recruited

- recruits procaspase 8 and 10
* *these two form the Death Inducing Signal Complex (DISC)

procaspases then activate executioner caspases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

DISC

A

death inducing signaling complex

association of FADD with initiator procaspases 8 and 10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

which caspases are involved in lymphocyte apoptosis (extrinsic)?

A

procaspases 8 and 10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Intrinsic Pathway

A

pathway of apoptosis
-result of injury (intracellular)

cytochrome c from mitochondria released into cytosol

- binds APAF-1 protease
	- oligomerizes into a heptamer called apoptosome
	- recruits initiator procaspase 9

caspase 9 recruits executioner caspases > apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Cytochrome C

A

released from the intermembrane space of mitochondria in response to high oxidative stress

binds APAF-1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

APAF-1

A

binds cytochrome C

apoptotic protease

oligomerizes into a heptamer called apoptosome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

apoptosome

A

oligermized (heptamer) APAF-1 that recruits initiator procaspase 9

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what procaspase is involved in the intrinsic pathway of apoptosis?

A

procaspase 9

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Bcl2 family of proteins

A

regulate apoptosis
-control release of cytochrome C

include pro-apoptotic BH123 and anti-apoptotic Bcl2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

BH123 proteins

A

pro-apoptotic

Bax and Bak

form oligomers in the membrane and form pores for leakage of cytochrome C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Bak

A

BH123 protein involved in apoptosis signaling
-bound to mito membrane

form oligomer (with Bax) that is a pore for cytochrome release)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Bax

A

involved in the BH123 protein release of cytochrome C into the cytoplasm

translocated to mitochondria from the cytosol and associates with Bak to form a cytochrome C leak pore

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Bcl2 proteins

A

anti-apoptotic
-bind and inhibit pro-apoptotic proteins

on the surface of mitochondria
-Bcl2 and Bcl-XI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
BH3 only proteins
inhibit anti-apoptotic proteins enable aggregation of Bax and Bak (leak pore cytochome C) activated via signal transduction -MAPK and p53 Bid protein activated by caspase 8
25
Bid protein
link between the extrinsic and intrinsic pathways of apoptosis activated by caspase 8 -inhibits anti-apoptotic Bcl2 and stimulate pro-apoptotic BH123 proteins
26
Inhibitors of Apoptosis (IAP)
bind and inhibit caspases (or polyubiquitylate) inhibit apoptosis
27
Anti-IAPs
released from mitochondria during intrinsic pathway bind and inhibit IAPs - promoting apoptosis
28
survival factors
most cells need continuous signaling to avoid apoptosis ex./ neurons need neurotrophins
29
necrosis
releases intracellular components we can detect
30
ischemia
inhibition of blood supply decrease both metabolites and oxygen acute injury
31
myocardial infarction cell death?
necrosis of cardiac myocytes look for cardiac troponins and creatine kinase (CK-MB) in blood
32
apoptosis
clean cell death can either have too much or too little apoptosis
33
neurodegeneration
due to too much apoptosis neurons undergoing programmed cell deatah ex/glaucoma
34
glaucmoma
loss of visual bc apoptosis of retinal ganglion cells cause unknown
35
autoimmune disease
too little apoptosis autoimmune lymphoproliferative syndrome (ALPS) -mutation in Fas ligand -accumulation of autoreactive lymphocytes
36
cancer cells
resistance to apoptosis -due to mutations in apoptosis control genes ex/ Bcl2 (b cell lymphoma) proto-oncogene ex/ p53 tumor supressor
37
loss of p53
no cycle checkpoint for DNA damage -cells with damage proliferate cells escape apoptosis cells can resist chemo and radiation therapy
38
reversible cell injury
can be reversed if stimulus removed
39
irreversible cell injury
cell is committed to cell death
40
free radicals
unpaired electron and is highly reactive causes chain propagation > keeps reacting
41
reactive oxygen species
oxygen derived free radical normal mitochondria byproduct also from peroxisomes and lysosomes
42
reactive nitrogen species
NO is source of RNS | -signaling species in cell
43
lipid peroxidation
occurs at membranes synthesizes free radicals can become reactive peroxide (oxygen species + unsaturated FAs)
44
Fenton Reaction
Iron reacts with H2O2 to produce hydroxyl radicals source of ROS
45
UV light and radiation
have ionizing properties that can form ROS
46
oxidative stress
ROS and free radicals can lead to damage in the cell protein modification DNA lesion
47
necrosis and ROS?
acute irreversible damage
48
apoptosis and ROS?
chronic slow ROS damage
49
antioxidants
molecules that can scavange or inactivate ROS free unpaired electron ex/estrogens (conjugated ring structure)
50
catalase
H2O2 > H2O and O2 peroxisomal enzyme
51
superoxide dismutase (SOD)
cytosolic and mitochondrial convert superoxide to H2O2
52
glutathione peroxidase
break H2O2 down into OH- by oxidizing itself into a homodimer oxidized from GSSG reduced from GSH
53
GSSG
dimer - oxidized form of glutathione peroxidase
54
GSH
monomer reduced form **ratio of these can detect presence of oxidative stress**
55
ischemia
insufficient blood flow -no oxygen OR metabolic substrates halts both aerobic AND anaerobic metabolism
56
hypoxia
reduce in available oxygen only affects aerobic metabolism
57
anoxia
absence of oxygen
58
mechanism of hyopxia
less O2 to cell loss of aerobic metabolism > decrease ATP 1 sodium pump failure -cell swells 2 calcium pump failure -accumulate intracellular Ca2 (leads to activation of pathways) -can induce apoptosis -activates ATPases, endonuclease, proteases, phospholipases
59
mechanism of ischemia
same as hypoxia extra effect - no substrates for glycolysis in addition - accumulate lactic acid (changes pH)
60
Hif1
hypoxia-inducible factor-1 produced in response to hypoxia promotes angiogenesis (blood vessel formation)
61
Von Hippel Lindau
bonds to and degrades Hif-1 results in inhibition of angiogenesis
62
ischemia-reperfusion injury
return of blood flow to hypoxic tissue is even more damaging - generate even more ROS (more substrates ex/Iron) - induces inflammation
63
adaptation to stimulus
reversible change in a cell
64
hypertrophy
increase in cell size in non-dividing or senescent cells can be caused by functional demand or stimulation signals (growth factors)
65
hypertrophy heart
increase in protein synthesis of proteins allowing contraction of heart
66
hyperplasia
**occurs in dividing cells** increase in cell number not cancer ex/ endometrium of uterus - hyperplasia is normal however, some patients have too much hyperplasia -leads to dysfunction
67
glandular epithelial of breast
undergoing both hypertrophy and hyperplasia
68
agenesis
failure to form embryonic cell mass entire missing organ
69
aplasia
part of organ missing failure to differentiate into organ specific tissues
70
dysgenesis
missing tissue of an organ
71
hypoplasia
not growing to a full size
72
atrophy
decrease in cell size and number normal during development also pathological
73
involution
decrease in number of cell compared to the normal number non-pathological ex/ breast and uterus, thymus
74
metaplasia
substitution of one cell for another -reprogramming of stem cells due to environmental stimulus ex/ barrets esophagus - caused by regurgitation of acid from stomach
75
intracellular accumulations - categories?
endogenous exogenous
76
steatosis
accumulation of triglycerides in the cell
77
atherosclerosis
cholesterol accumulation in the cell
78
xanthoma
cholesterol accumulation in the cell
79
protein deposits
can be extracellular or intracellular
80
calcification
deposition of calcium phosphate usually associated with dying cells (necrosis) -intracellular calcium interacts with membrane phospholipids
81
cell starvation
will undergo autophagy - digest its own components - in autophagic vacuole
82
residual body
debris in a vacuole that we cannot digest in lysosome
83
lipofuscin
sign of free radical injury caused by lipid peroxidation

MCM Final Exam (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions