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SFM Quiz 2 > Cell Cycle pt.4 > Flashcards

Cell Cycle pt.4 Flashcards

1
Q

Necrosis

A

uncontrolled cell death

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2
Q

Necrosis: cell membrane

A

swelling and rupture

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3
Q

Necrosis: cytoplasm

A

increased vacuolation, organelle degeneration, and mitochondrial swelling

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4
Q

Necrosis: nucleus

A

clumping and random degradation of nuclear chromatin and DNA (karyolysis)

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5
Q

Necrosis: cells involved

A

all cell types

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6
Q

Necrosis: inflammation

A

yes

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7
Q

Necrosis: features

A

failure of normal phys. pathways like homeostasis, ion transport, ATP depletion, ph balance

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8
Q

Necorsis: MOA

A

RIP1 and PARP-1 involved

stress/ca overload stimulates mitochondrial uncoupling as well as RIP3/RIP1 complex

this makes NADPH oxidase/increased O2 consumption

ROS are made as a result

ATP depletes and necrosis ensues

no caspases involved

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9
Q

Apoptosis

A

programed cell death

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10
Q

apoptosis: cell membrane

A

blebs and fragments into membrane bound apoptotic bodies

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11
Q

apoptosis: cytoplasm

A

fragmentation and shrinkage

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12
Q

apoptosis: nucleus

A

chromatin condensation and degradation by DNA cleavage leading to nuclear fragmentation

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13
Q

apoptosis: cells involved

A

hematopoietic cells and related (liquid tumors)

plays a role in solid tumors, which is most of cancers

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14
Q

apoptosis: inflammation

A

no

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15
Q

apoptosis: features

A

membrane loses asymmetry and PS is displayed

caspase/mitochondria dependent

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16
Q

apoptosis: MOA

A

fas ligand binds to receptor on surface
DISC is made with caspase 8
caspase 8 acts on caspase 3 to cause cell death

caspase 8 can also act on bid 
bid makes tbid 
tbid makes Bak 
Bak and Bax go to mito and cytochrome C
makes apoptosome with capsase 9 and activates caspase 3 to cause cell death

BH3 proteins actovate bax

Bcl2, Bclxl inhibit bak

DNA damage stimulates ATM which goes to nucleus and stimulates p53 which stimulates BH3 proteins

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17
Q

apoptosis: triggers

A 
DNA damage (membrane): trigger ATM, p53
Death receptor signaling (membrane): caspase 8 mediated 
cell membrane (membrane): sphingomyleniase turns it toc ceramide 
Mitochondrial damage (mitochondria): ceramide mediated
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18
Q

apoptosis: sensors

A

ATM
receptor
mitochondria

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19
Q

apoptosis: mediators

A 
p53
BCL2 (antiapoptotic) 
BH3 and Bax(pro apoptotic) 
cytochrome C
apoptotic protease activating factor 1
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20
Q

apoptosis: effectors

A

caspases

initiators: caspases 8, 9, 10
executioner: 3, 6, 7

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21
Q

apoptosis: pro/anti apoptotic mechanisms

A

Bax and Bak induce permeability by forming pores upon oligomerization

pro-apoptotic BH3 (bid, bim, bad, noxa, puma) activate bax /bak by binding anti-apoptotic Bcl2 proteins OR BH3 proteins can directly bind and activate bax/bak

22
Q

Autophagy

A

self eating/recycling
degrades long lived cells
mostly survival response to several stresses

23
Q

autophagy: cell membrane

A

membrane blebbing

24
Q

autophagy: cytoplasm

A

accumulation of 2 membrane autophagic vacuoles

25
autophagy: nucleus
partial chromatin condensation | no nuclear and DNA fragmentation
26
autophagy: cells involved
all cell types
27
autophagy: inflammation
no
28
autophagy: features
no caspases, increases lysosomal activity
29
autophagy: MOA
complex uses autophagy related genes (proteins) (ATG) coiled-coil myosin-like BCL2-interacting protein *(beclin-1)* *(Atg6)-initiation* of the formation of the autophagosome (nucleation) microtibile associated protein 1A/1B-light chain 3 (LC2) conjugation and elongation
30
More autophagy MOA
release of belcin from bcl2 forms class III PI3K that contributes to formation of nucleation complex two conjugation cascades, LC3-II and Atg5-12 cascades serve to elongate nucleation complex to generate the limiting membrane sole transmembrane Atg9 delivers addtiional membranes for limtiing membrane formation the limiting membrane sequesters cytosolic cargo and seals itslef to form an autosome fusion to lyosomes results in cargo degradation and nutrient release into cytosol
31
mitotic catastrophe
cell death that is caused by aberrant mitosis associated with deficiencies in cell cycle checkpoint
32
mitotic catastrophe: membrane
no change
33
mitotic catastrophe: cytoplasm
larger cytoplasm with the formation of giant cell
34
mitotic catastrophe: nucleus
micronucleation and multinucleation, nuclear fragmentation, premature chromosome condensation, formation of nuclear envelopes around clusters of missegregated chromosomes
35
mitotic catastrophe: cells involved
most dividing cells
36
mitotic catastrophe: inflammation
no
37
mitotic catastrophe: features
no caspase in the early stage, abnormal CDK1/cyclin B activation
38
mechanisms for the induction of the mitotic catastrophe
1. defects in cell cycle checkpoints 2. hyperamplification of centrosomes 3, caspase-2 activation during metaphase
39
defects in cell cycle chekpoints that trigger mitotic catastrophe
p53-G2 checkpoint PUB-related kinase (BUBR) spindle checkpoint increased expression of APC genes-spindle assembly
40
hyperamplification of centrosomes that trigger mitotic catastrophe
usually in subsequent cell cycle CDK2/cyclin E/A (S phase)
41
caspase-2 activation during metaphase that trigger mitotic catastrophe
delayed apoptosis
42
DNA damage at G2/M interferes with
p53
43
fate of cells with abberant mitosis
die without exiting mitosis-mitotic death proceed to G1 and continue division for amny cycles and then die-delayed cell death exit mitosis and undergo permanent G1 arrest-senescence
44
Senescence
permanent cell cycle arrest, reproductive death can be a replicative senescence related to telomere shortening antitransformation mechanism due to cellular damage
45
senescence: cell membrane
no change
46
senescence: cytoplasm
flattening and increased granularity
47
senescence: nucleus
distinct heterochromatic structure
48
senescence: cells involved
all types of cells
49
senescence: inflammation
yes but induced by secretory factors from the senscent cell
50
two pathways of senescence pathway
p53-p21 | p16-Rb

SFM Quiz 2 (25 decks)

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