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BMS 2 > Cell Death, Apop/Autophagy > Flashcards

Cell Death, Apop/Autophagy Flashcards

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
Q

P53 has many mechanisms of anticancer function

A
  • activate dNA repair proteins mdm2
  • arrest growth by holding cell cycle at g1/s regulation pint
  • initate apop
26
Q

p53 in unstressed cells

A

-p53 is a tf

kept low concentrations by degradation

  • mdm2 adds ubi to p53
  • also moves p53 from nun to cyto
27
Q

mdm2

A

adds ubi to p53

moves p53 from nuc to cyto (but wants to be in nuc because it is a TF

28
Q

-53 activation

A 
phosphorylation of N terminal domain
-done by protein kinases
   -MAPK
   -Checkpoint kinases
Onco genes stimiulate p53 activation
-mediated by ARF
29
Q

Problem? what does p53/ mdm2 do

A

p53 gets activated

mdm2 is inhibited
no send p53 to sit and no ubi

30
Q

bcl2 proteins

A

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
Q

what does cut c interact with

A

apaf1-apotosome forms

apoptosomes activates caspase 9 (initiator)

32
Q

Bid and Bad function

A

promote apoptosis-te up bcl2 and free bax/bak

-may help open pore

33
Q

Bcl2 function

A

binds to bax and bak-prevents pore fomration-anti apoptotic

too much expression leads to cancer

34
Q

bax and bak function

A

promote pore formation-release to cyto c and APAF1 intimates apop

35
Q

little sentence thing

A

bad biddy frees up baxter bak and ties up bcl-2

36
Q

bcl2 and chacer

A

translation puts it in heavily promoted region-linked to cancers

37
Q

what triggers intrinsic pop pathway

A

triggered by p53 or response to dna damage

38
Q

conventioanl anti cancer therapies activate

A

intrinsic apop by means of p53

39
Q

p53 activates intrinsic pathway by

A

transcriptional upreg of BaK/baxter (bcl2 family proteins)

40
Q

Bax causes

A

release of city c from mito which bind to ADAPF1 to activate capsize 1

41
Q

Capase 9

A

activates cases 3,6,7 destroying critical components of cell

42
Q

which occurs more intrinsic /extrinisc

A

intrinsic (80%)

43
Q

death recepttors?

A

Dr4 and 5

44
Q

Apol2L/Trail

A

activate DR4 and DR5

45
Q

DR4/5

A

recruit FADD

46
Q

FADD recruits

A

initator caspase 8 and/or 10 to DISC

47
Q

DISC

A

death inducing signaling complex
-release case 8 and 10 into cytoplasm
0activte 367

48
Q

Extrinsic apop pathway

A

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
Q

Convergence of extrinsic and intrinsic pathways is at

A

caspases 3,6,7

50
Q

too much apop
vs
too little apop

A

cancer, auto immune disease
-cell survival proliferation

radion injury/isehmia/reperfusion
-cell death

51
Q

Autophagy function

A

recycle old things/things if don’t have enough energy

sekwester cellular organelle into cytoplasmic actuoles that fuse with lysosomes

52
Q

4 stages of autophagy

A

induciton, autophagosome, formation, atuophagosome lysosome fucntion, autophagosome breakdown

53
Q

Induction

A

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
Q

MTOR pathway

A

normaoxia-mTOR active
-phosphate on 4EBP

Hypoxia-4EBP1 not phosphorylated
-binds to ELF4E at CAP-decereased translation

55
Q

Autophagosome formation

A

mTOR deactivtion-gene product proteins particulpte in this process

formation of membrane around targeted portion of cell that need to be destroyed

56
Q

Autophagosome/lysosome fusion

A

lysosome releases contents into autophagosome

57
Q

autophagosome breakdown

A

autophagic body is broken down by degradative nature of lysosome

58
Q

necrosis

A

typically caused by factors external to cell

-always detrimental/irreversibel

59
Q

morphological features of necrosis

A

cell swelling, chrome digestion, disruption of PM

cell blows up-inflammation response
-usually late necrosis

60
Q

What do autophagy, apop, necrosis look like

A

auto=blebs

apop-chromasome condesnation

necrosis-just fucked

BMS 2 (41 decks)

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