Apoptosis Flashcards

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1
Q

what is apoptosis?

A

programmed cell death brought about by external or internal signals

needed for development into adult forms

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2
Q

characteristics of apoptosis

A
  • -cell shrinks
  • -loss of CAMS
  • -cytoskeleton collapses
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3
Q

cytochrome C

A

released from mito

marker for apoptosis

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4
Q

DNA cleavage in apoptosis

A

cleaved at linker DNA between nucleosomes by endonuclease

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5
Q

caspases

A

proteases that mediate an intracellular proteolytic cascade to cause apoptosis

cysteine in active site

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6
Q

caspases target

A

target proteins and cleave them where Asp acid residues occur

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7
Q

procaspases

A

caspases are first synthesized as these = inactive form

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8
Q

activation of procaspases

A

protease cleaves these

which transforms them into caspases

caspases then also activate procaspases

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9
Q

procaspase cleavage

A

are cleaved at a specific site to create and small and large subunit

which them form a heterodimer w/ a different cleaved procaspase = active caspase

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10
Q

2 major caspases

A

initiator caspase

executioner caspase

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11
Q

initiator caspase

A

–initiates death
–caspase -8 and -10
can self activate

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12
Q

executioner caspase

A

destroys targets to induce death
caspase -3

cleaves downstream proteins, inactive endonuclease, targeting cytoskeleton and CAMs

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13
Q

caspase cascade

A
  • -irreversible once started
  • -some caspases are needed for life and if gone, fetus will die
  • -machinery for apoptosis is always present
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14
Q

there are 2 pathways that depend on factors to induce apoptosis

A

extrinsic path

intrinsic path

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15
Q

mito dependence of the 2 pathways

A

extrinsic - mito independent

intrinsic - dependent

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16
Q

extrinsic pathway

A

death receptors

  • -survival factors are removed
  • -death signals bind
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17
Q

death receptor domains

A

3 domains

  1. extracell binding d
  2. TM d
  3. intracell death d

receptors are homotrimers - 3 proteins of tumor necrosis family

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18
Q

extrinsic pathway cascade

A
  • -Fas binds to Fas death receptor
  • -adaptor proteins recruited
  • -death domains come together to form DISC
  • -caspase -8 and -10 activated
  • -downstream executioner activated
19
Q

inhibitory proteins can stop the ____ pathway

A

extrinsic pathway

20
Q

recruited adaptor proteins - extrinsic pathway

A

FADD adaptor
procaspase -8 and -10

form trimers
bring death domains together = DISC

21
Q

DISC

A

death inducing signal complex

22
Q

inhibitory proteins

A
  • -are decoy receptors
  • -same as death receptors but no death domain so apoptosis is not induced
  • -also includes FLIP protein
23
Q

FLIP

A

–protein that resembles initiator procaspase but no proteolytic domain

–a competitive inhibitor to oppose procaspase -8 and -10 to prevent apoptosis

24
Q

both types of inhibitory proteins act like?

A

sponges to absorb the death signals to prevent the start of apoptosis

25
Q

intrinsic pathway

A

internal inducement of apoptosis
due to injury, DNA damage, lack of nutrients

mito dependent

26
Q

key event of intrinsic path

A

translocation of cytochrome C from intermediate space to cytosol

27
Q

release of cytochrome C

A
  • -binds to an adaptor protein Apaf1
  • -caspase -9 activated
  • -executioner caspase activated
28
Q

Apaf1

A

adaptor protein
forms apoptosome which activates caspase -9

which then activates downstream executioner caspase

29
Q

apoptosome

A

= Apaf1 + cytochrome C

30
Q

final step common to both pathways

A

activation of downstream executioner caspase

caspase -3

31
Q

Bcl2 protein family

A
  • -controls release of cytochrome C into cytosol

- -3 types of this: pro and anti apoptotic

32
Q

pro-apoptotic Bcl2

A

blocks release of cytochrome C

has 3 domains or 1
BH123 or BH3

33
Q

anti-apoptotic Bcl2

A

promotes release of cytochrome C

has 4 distinct domains
BH1234 which is also just called Bcl2

34
Q

BH123 activation

A
  • -pro apoptotic
  • -apoptosis is triggered
  • -this activates BH123
35
Q

BH123 function

A

forms aggregation in mito outer membrane

induces release of cytochrome C

thus inducing intrinsic pathway

36
Q

BH3

A

pro-apoptotic
located in cytosol
apoptotic signals activate it which causes it to translocate to mitochondria

37
Q

BH3 function

A

inhibits the anti-apoptotic Bcl2 proteins

thus allowing BH123 to do its function

38
Q

Bcl2

A

or BH1234
anti-apoptotic
includes Bcl2 & Bcl-XL

located on cytosolic side of outer mito memb.

39
Q

Bcl2 function

A

prevent apoptosis by binding to BH123

thus preventing aggregation

40
Q

IAPs

A

inhibitors of apoptosis

bind and inhibit caspases

some can add ubiquitin

these are necessary because some caspases are self-activating

41
Q

Anti-IAPs

A

when real apoptotic signals are received
–these will stop IAPs from inhibiting caspase activity

they release from mito

42
Q

excessive Bcl2 production

A
  • -related to lymphoma
  • -Bcl2 inhibits apoptosis
  • -if in excess cell can never die
43
Q

relate excessive Bcl2 protein and p53 mutations

A

in excess Bcl2 – cells will not die

thus cells w/ DNA damage will continue to live and divide

p53 gene stops cell cycles when DNA damage is detected

44
Q

excessive apoptosis is found in ?

A

heart attacks and stroke