Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

SFM Quiz 2 > Cell Cycle pt.4 > Flashcards

Cell Cycle pt.4 Flashcards

1
Q

Necrosis

A

uncontrolled cell death

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

Necrosis: cell membrane

A

swelling and rupture

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

Necrosis: cytoplasm

A

increased vacuolation, organelle degeneration, and mitochondrial swelling

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

Necrosis: nucleus

A

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

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

Necrosis: cells involved

A

all cell types

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

Necrosis: inflammation

A

yes

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

Necrosis: features

A

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

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

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

Apoptosis

A

programed cell death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

apoptosis: cell membrane

A

blebs and fragments into membrane bound apoptotic bodies

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

apoptosis: cytoplasm

A

fragmentation and shrinkage

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

apoptosis: nucleus

A

chromatin condensation and degradation by DNA cleavage leading to nuclear fragmentation

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

apoptosis: cells involved

A

hematopoietic cells and related (liquid tumors)

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

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

apoptosis: inflammation

A

no

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

apoptosis: features

A

membrane loses asymmetry and PS is displayed

caspase/mitochondria dependent

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

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

apoptosis: sensors

A

ATM
receptor
mitochondria

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

apoptosis: mediators

A 
p53
BCL2 (antiapoptotic) 
BH3 and Bax(pro apoptotic) 
cytochrome C
apoptotic protease activating factor 1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

apoptosis: effectors

A

caspases

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

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

autophagy: nucleus

A

partial chromatin condensation

no nuclear and DNA fragmentation

26
Q

autophagy: cells involved

A

all cell types

27
Q

autophagy: inflammation

A

no

28
Q

autophagy: features

A

no caspases, increases lysosomal activity

29
Q

autophagy: MOA

A

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
Q

More autophagy MOA

A

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
Q

mitotic catastrophe

A

cell death that is caused by aberrant mitosis

associated with deficiencies in cell cycle checkpoint

32
Q

mitotic catastrophe: membrane

A

no change

33
Q

mitotic catastrophe: cytoplasm

A

larger cytoplasm with the formation of giant cell

34
Q

mitotic catastrophe: nucleus

A

micronucleation and multinucleation, nuclear fragmentation, premature chromosome condensation, formation of nuclear envelopes around clusters of missegregated chromosomes

35
Q

mitotic catastrophe: cells involved

A

most dividing cells

36
Q

mitotic catastrophe: inflammation

A

no

37
Q

mitotic catastrophe: features

A

no caspase in the early stage, abnormal CDK1/cyclin B activation

38
Q

mechanisms for the induction of the mitotic catastrophe

A
  1. defects in cell cycle checkpoints
  2. hyperamplification of centrosomes
    3, caspase-2 activation during metaphase
39
Q

defects in cell cycle chekpoints that trigger mitotic catastrophe

A

p53-G2 checkpoint
PUB-related kinase (BUBR) spindle checkpoint
increased expression of APC genes-spindle assembly

40
Q

hyperamplification of centrosomes that trigger mitotic catastrophe

A

usually in subsequent cell cycle CDK2/cyclin E/A (S phase)

41
Q

caspase-2 activation during metaphase that trigger mitotic catastrophe

A

delayed apoptosis

42
Q

DNA damage at G2/M interferes with

A

p53

43
Q

fate of cells with abberant mitosis

A

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
Q

Senescence

A

permanent cell cycle arrest, reproductive death

can be a replicative senescence related to telomere shortening

antitransformation mechanism due to cellular damage

45
Q

senescence: cell membrane

A

no change

46
Q

senescence: cytoplasm

A

flattening and increased granularity

47
Q

senescence: nucleus

A

distinct heterochromatic structure

48
Q

senescence: cells involved

A

all types of cells

49
Q

senescence: inflammation

A

yes but induced by secretory factors from the senscent cell

50
Q

two pathways of senescence pathway

A

p53-p21

p16-Rb

SFM Quiz 2 (25 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions