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BMS 2 > Cell Death, Apop/Autophagy > Flashcards

Cell Death, Apop/Autophagy Flashcards

(60 cards)

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1
Q

apop definition

A

death by programmed cell death-death by suicide

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2
Q

autophagy defintion

A

catabolic process includeing digression of cells own component through lysosomes
-cell eats itself

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3
Q

Ncrosis definition

A

Premature death of cells death by external

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4
Q

Intracellualr=Apoptosis

A

very similar between different species-same things die

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5
Q

Apoptosis uses

A

tissue sculpting

Eliminate used T and B cells

Tissue hoeostatus

Eliminating damaged cells

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6
Q

Syndactiliy

A

no apoptosis between digits

-more severe form of webbing-no differentiation between fingers

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7
Q

caspase-9

A

apoptosis protein

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8
Q

morphological markers of apop

A

INTACT CELL MEMBRANES!!!!

large clear valcuoules on surface

look like splitting up into small circles (blebs)

loss of cell cell adhesion

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9
Q

PS flipping

A

marker of apoptosis

phosphotidyl serine (normally on cyto side-moves to other side_

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10
Q

Annexin 5

A

antibody to phosphotidyl serine

tell degree of apoptosis

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11
Q

TUNEL

A

label nicks that are in DNA of apoptotic cells

0added by terminal transferase-adds dUTP

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12
Q

TUNEL advantages/disadvantes

A

Highsenestity, fast, high reproductibility

No idea of number of strands breaks needed for detection-may miss early stages

  • nectrotic cells cause fale positive
  • detergent for permeablitizng cells-make fragile
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13
Q

Biomolecular diagnosis for apop

A

membrane intact, DNA ladering, PS flipping, TUNEl

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14
Q

DNA laddering

A

caspase degrades DNA-in little ladder rungs

-normal cell is just smear or 1 pand

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15
Q

caspase activation

A

at 33 kda

can rescue cells after capsize is activated
-remove noxious element

capspases must be cleaved to become activef

  • two proteolytic cleavages activate initiator
  • initator cleaves effector
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16
Q

cell extrinisic apoptotic pathway

A

proapoptotic ligand binds to death receptor and activates caspases

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17
Q

caspase facts

A

cleaved to become active

inititator caspse- 2,8,9, 10

effector (exectue) caspases-3, 6, 7

regulated post translationally (reapidly activated)

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18
Q

caspase cascade (with numbers)

A

pro-apop stimulus

2,8,9, 10

3,6,7

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19
Q

what does effector cleave? initiator?

A

initator cleaves effector

effector cleaves nuclear lamina, inhibitors of DNAases (DFF450), Actin

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20
Q

DFF45 inhibits

A

DFF40-normally exist as inert dimer
-DFF40 oligomerizes before cutting

begins cleaving

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21
Q

Intrinsic apop pathway proteins

A

BCL2 proteins
-pro-apoptotic- BAX and BAK
-Anti-BCl2, BCL-XL, MCL1
Regulators-DA

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22
Q

BCL

A

responsible for keeping integrity of mito membrane

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23
Q

Insrinsic apop pathway

A

LACK of survival signals/DNA damage
-activation of sensor proteins (BH3 only)
-these adhere to mito membrane and make leaky
-leakiness activates Bax/Bak channel
-leakage of city c and other proteins
-also bcl2 is antagonized by BH3 protein-plug up channel
-2, 8-10 get cleaved
-cleave 367
Apop

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24
Q

intrinsic app when cell viable

A

survival signal and growth factor
-produceds bcl2
bcl2 keeps integrity of protein

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25
P53 has many mechanisms of anticancer function
- activate dNA repair proteins mdm2 - arrest growth by holding cell cycle at g1/s regulation pint - initate apop
26
p53 in unstressed cells
-p53 is a tf kept low concentrations by degradation - mdm2 adds ubi to p53 - also moves p53 from nun to cyto
27
mdm2
adds ubi to p53 | moves p53 from nuc to cyto (but wants to be in nuc because it is a TF
28
-53 activation
``` phosphorylation of N terminal domain -done by protein kinases -MAPK -Checkpoint kinases Onco genes stimiulate p53 activation -mediated by ARF ```
29
Problem? what does p53/ mdm2 do
p53 gets activated | mdm2 is inhibited no send p53 to sit and no ubi
30
bcl2 proteins
has both pro and anti apop members BCL2-antiapop Bak/Bax/bad/bid?-pro apop-get signal from p53 or from dna damage -normally found in cytosol, translocate to mito membrane and simulate formation allowing cyto c to leak out BCL, BCLxl, MCL-apop
31
what does cut c interact with
apaf1-apotosome forms | apoptosomes activates caspase 9 (initiator)
32
Bid and Bad function
promote apoptosis-te up bcl2 and free bax/bak | -may help open pore
33
Bcl2 function
binds to bax and bak-prevents pore fomration-anti apoptotic too much expression leads to cancer
34
bax and bak function
promote pore formation-release to cyto c and APAF1 intimates apop
35
little sentence thing
bad biddy frees up baxter bak and ties up bcl-2
36
bcl2 and chacer
translation puts it in heavily promoted region-linked to cancers
37
what triggers intrinsic pop pathway
triggered by p53 or response to dna damage
38
conventioanl anti cancer therapies activate
intrinsic apop by means of p53
39
p53 activates intrinsic pathway by
transcriptional upreg of BaK/baxter (bcl2 family proteins)
40
Bax causes
release of city c from mito which bind to ADAPF1 to activate capsize 1
41
Capase 9
activates cases 3,6,7 destroying critical components of cell
42
which occurs more intrinsic /extrinisc
intrinsic (80%)
43
death recepttors?
Dr4 and 5
44
Apol2L/Trail
activate DR4 and DR5
45
DR4/5
recruit FADD
46
FADD recruits
initator caspase 8 and/or 10 to DISC
47
DISC
death inducing signaling complex -release case 8 and 10 into cytoplasm 0activte 367
48
Extrinsic apop pathway
Apo2l/trail bind to membrane death receptors DR4/5 FADD recruited and brings procaspases to DISC-where they are cleaved Activaes 8 and 10, which activates 3,6,7 independent of p53
49
Convergence of extrinsic and intrinsic pathways is at
caspases 3,6,7
50
too much apop vs too little apop
cancer, auto immune disease -cell survival proliferation radion injury/isehmia/reperfusion -cell death
51
Autophagy function
recycle old things/things if don't have enough energy sekwester cellular organelle into cytoplasmic actuoles that fuse with lysosomes
52
4 stages of autophagy
induciton, autophagosome, formation, atuophagosome lysosome fucntion, autophagosome breakdown
53
Induction
mTOR-serine threonine kinase nutrient rich-mTOR inhibits autophagy - starvation-mTOR inactivated - leads to dephospho rylation events resulting in transcriptional activation of autophagy related genes
54
MTOR pathway
normaoxia-mTOR active -phosphate on 4EBP Hypoxia-4EBP1 not phosphorylated -binds to ELF4E at CAP-decereased translation
55
Autophagosome formation
mTOR deactivtion-gene product proteins particulpte in this process formation of membrane around targeted portion of cell that need to be destroyed
56
Autophagosome/lysosome fusion
lysosome releases contents into autophagosome
57
autophagosome breakdown
autophagic body is broken down by degradative nature of lysosome
58
necrosis
typically caused by factors external to cell | -always detrimental/irreversibel
59
morphological features of necrosis
cell swelling, chrome digestion, disruption of PM cell blows up-inflammation response -usually late necrosis
60
What do autophagy, apop, necrosis look like
auto=blebs apop-chromasome condesnation necrosis-just fucked

BMS 2 (41 decks)

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