Apoptsis Flashcards

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1
Q

what happens during apoptosis?

A

cytoskeleton collapses, nuclear envelope disassembles
nuclear DNA breaks into fragments
phosphatidylserine on cell surface causes phagocytosis

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2
Q

how can apoptosis be triggered?

A

extrinsic pathway- death receptor activation

intrinsic pathway- internal trigger

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3
Q

what does an active caspase do?

A

invoke apoptosis, digest certain proteins

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4
Q

how does a caspase get activated?

A

apoptosis signals clusters inactive caspases. inactive procaspases get their prodomains cleaved. this cleaves executioner caspases then cleave other substrates

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5
Q

how does DNA get cleaved?

A

executioner caspase cleaves inhibitory CAD and then the now active CAD cleaved DNA

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6
Q

explain extrinsic pathway

A

receptors binds with fas ligand thats on a killer lymphocyte. FADD adaptor protein’s death doman binds to receptors death domain. caspase 8’s death effector domain binds to FADD’s death effector domain. receptor+FADD+caspase=DISC. procaspases cluster and cleave each other, activating the caspases

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7
Q

explain intrinsic pathway

A

cytochrome c released from intermembrane space in mitochondria and binds to Apaf 1. CARD domain on Apaf 1 bind on other Apaf 1s and form a wheel looking shit called apoptosome. procaspase 9’s CARD domain binds to apoptosome’s and clusters to cleave each other

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8
Q

how is a procaspase different from a caspase?

A

a procaspase turns into a caspase when they cluster and cleave each other

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9
Q

what regulates release of cytochrome c in the intrinsic pathway?

A

Bcl-2 family

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10
Q

what are the 3 categories of the Bcl-2 family?

A

anti-apoptotic Bcl-2
pro-apoptotic effector
pro-apoptotic BH3-only

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11
Q

what are Bcl-2 homology domains?

A

areas where proteins look similar

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12
Q

anti-apoptotic Bcl-2 has what BHs?

A

all 4, BH4/3/1/2

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13
Q

pro-apoptotic effector has what BHs?

A

BH3/1/2

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14
Q

pro-apoptotic BH3-only protein has what BHs?

A

BH3

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15
Q

what does pro-apoptotic effector do?

A

apoptotic stimulus causes them to aggregate and cluster to releases cytochrome c

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16
Q

what does the anti-apoptotic Bcl-2 do?

A

inhibit pro-apoptotic effector to stop release of cytochrome c

17
Q

what does pro-apoptotic BH3-only do?

A

inhibits anti-apoptotic Bcl-2 thats inhibits pro-apoptotic effector to stop release of cytochrome c (ALL IN ALL MOVES FORWARD WITH APOPTOSIS) and helps aggregate pro-apoptotic effector has what too

18
Q

what is IAP?

A

bind to activated caspase to block them when they are spontaneously activated, inhibitors of apoptosis

19
Q

what is anti-IAP?

A

gets released with cytochrome c to inhibit IAP to allow for apoptosis

20
Q

how do you regulate apoptosis?

A
  1. increased production of anti-apopototic bcl2 family protein
  2. inactivation of pro-apoptotic BH3-only protein
  3. inactivation of anti-IAPs
21
Q

how does increased production of anti-apopototic bcl2 family protein help regulate apoptosis?

A

survival factor and receptor activates transcription regulator to produce Bcl2 protein to block apoptosis

22
Q

how does inactivation of pro-apoptotic BH3-only protein block apoptosis?

A

survival factor binds to receptor which activates Akt kinase to take away Bcl2 inhibitor (Bad, BH3 only) through phosphorylation

23
Q

how does inactivation of anti-IAPs regulate apoptosis?

A

survival factor and receptor activates map kinase to phosphorylate Hid to inactive it. active Hid will inhibit IAPs.