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Cell proliferation, senescence and death > 7. Apoptosis > Flashcards

7. Apoptosis Flashcards

1
Q

Phosphatidyl serine

A

Increase of outwards-facing PS in plasma membrane are a indicator of apoptosis as well.

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2
Q

BH3-only proteins

A

Pro-apoptotic proteins eg. Bad, Bim, Bid, Puma, Noxa.

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3
Q

Caspase 3 cleavage

A

Catalyzed by caspase 9, facilitated by apoptosome assembly.

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4
Q

Granzyme B

A

Protease capable of truncating Bid, causing it to inhibit Bcl2 proteins.

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5
Q

BH123

A

Bax, Bak

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6
Q

Caspase cascade

A

Initiator caspases cleaves executioner caspases that cleaves cytosolic proteins and nuclear lamins.

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7
Q

Ced-3

A

Caspase. Cleaves after aspartic acid residues.

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8
Q

Bcl-xl, Bik function regulation

A

Bcl-xl sequesters Apaf-1 on the mitochondric surface. Bik binds and displaces Apaf-1, releasing it to form the apoptosome.

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9
Q

Bcl2 regulation

A

Bax, Bak (BH123 induces intrinsic apoptosis. Are inhibited by Bcl-2 proteins. BH3-only proteins inhibits Bcl2 proteins.

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10
Q

Asaptor proteins

A

Mediates dimerization of initiator caspases, which facilitates cleavage in trans of the inactive monomers.

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11
Q

Binding of cyt c to Apaf-1 results in…

A

ADP exchange for dATP and following oligomerization.

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12
Q

CARD domains

A

Dimerization domains found on eg. Apaf-1 and caspase 9.

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13
Q

What does cell do without trophic factors?

A

Undergo apoptosis.

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14
Q

p53 regulation of Bax and Bak function

A

Presumes to help Bax and Bak into an active conformation. Induces expression of Fas and Bax. (and IFGBP-3)

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15
Q

Death domain

A

Oligomerization domain between Fas death receptor, FADD adaptor protein and procaspase 8 or 10.

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16
Q

Apoptosome consists of

A

Apaf-1, Cyt C and caspase 9

17
Q

BH3 only

A

Bim, Bik, Bid, Puma, Noxa, Bad

18
Q

Bcl-2 proteins

A

Anti-apoptotic proteins. Eg. Bcl2, Bcl-Xl. Have BH4, 3, 2 and 1.

19
Q

Bax, Bak function

A

Bax and Bak make up the channel through which Cyt C is releases. Gets sequestered and inhibited by Bax or Bak.

20
Q

Procaspase activation

A

Caspases are activated by cleavage of the inactive procaspase into the active caspase.

21
Q

Initiator caspases

A

Caspase 8,9

22
Q

Bcl2 proteins

A

Family consist of Bcl2, BH123 and BH3-only proteins.

23
Q

Apoptosis characteristics

A

Individual cells, decreased cell volume, condensed chromatin. No inflammation

24
Q

Necrosis characteristics

A

Multiple cells, increased cell volume, inflammatory resonse.

25
Q

TUNEL

A

dUTP nick end labeling: labels bare DNA ends - sign of apoptosis

26
Q

Two major types of cell death

A

Apoptosis and necrosis

27
Q

Diablo/SMAC

A

Released from mitochondrion with Cyt C. Inhibits IAPs

28
Q

Bcl2 proteins (subgroup)

A

Bcl2, Bcl-Xl

29
Q

IAPs

A

Inhibitor of apoptosis proteins. Presumely binds active caspase as eg. XIAP, blocking caspase function

30
Q

Cyt C release

A

Release of Cyt C from mitochondria are a sign of apoptosis.

31
Q

3 strategies to avoid apoptosis:

A

Increased production of Bcl2 protein, inactivation of BH3-only Bcl2 proteins by active Akt, inactivation of anti-IAPs with MAPK-mediated phosphorylation

32
Q

Fas ligand

A

Binds Fas death receptor. Induces apoptosis in target cell.

33
Q

DNA fragmentation

A

In apoptosis, DNA fragments, creating af DNA ladder cause of fragmenting of linker regions between nucleosomes.

34
Q

Executioner caspases

A

Caspase 3,6,7

35
Q

Extrinsic pathway activation

A

Through cell death receptors. Binding induces DISC formation in which procaspase 8 is cleaved into caspase 8, initiating apoptosis.

36
Q

FADD

A

Fas-associated protein with death domain.

37
Q

Two ways Death receptor can induce apoptosis

A

Direct cleavage of procaspase 3 by caspase 8 or truncation of Bid, causing release of Cyt C.

38
Q

Roles of apoptosis

A

Morphogenesis, synaptogenesis, tissue turnover, removal of stressed cells

39
Q

BH123

A

Pro-apoptotic proteins. Eg. Bax, Bak.

Cell proliferation, senescence and death (3 decks)

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