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BMSC339 > Lifengs Content > Flashcards

Lifengs Content Flashcards

1
Q

What is the role of G1-CdK in the cell cycle?

A

Phosphorylates Rb, activating E2F which starts the cell cycle

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2
Q

What does E2F activation lead to?

A

Transcription of genes needed in S-phase.

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3
Q

What is the role of G1/S-CdK in the cell cycle?

A

Phosphorylates the inhibitory p27 and promotes S-Cyclin expression.

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4
Q

What is the commitment step in the cell cycle?

A

The transition to S phase from G1 via G1/S-CdK activity is the commitment step. The cell is committing to DNA replication.

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5
Q

What is the role of S-CdK in the cell cycle?

A

Initiates DNA replication, produces DNA polymerase.

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6
Q

What is the role of M-CdK in the cell cycle?

A

Promotes events in mitosis like DNA condensation.

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7
Q

How does p53 regulate CdKs in response to DNA damage?

A

Turns on p21, inhibiting G1/S and S CdKs.

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8
Q

How does Myc regulate CdKs in response to mitogen activity?

A

Increases D cyclin expression, activating G1-CdK.

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9
Q

What happens when Myc is overexpressed?

A

Leads to uncontrolled cell growth, tumorigenesis.

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10
Q

What is the role of Nim1 in response to nutritional status?

A

Inhibits Wee1, promoting cell cycle progression.

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11
Q

What is Wee1?

A

Wee1 is a kinase that phosphorylates CdKs, inactivating them.

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12
Q

What role does CdK1 play in the nucleus?

A

Protects nucleus from fragmentation.

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13
Q

What is inhibited during nutritional starvation?

A

Nim1 inhibits Wee-1 in response to nutritional starvation, this promotes the cell cycle.

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14
Q

What inhibits Wee1 in a positive feedback loop?

A

Active M-CdK complexes.

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15
Q

What is the function of Cdc25?

A

Removes phosphorylation on CdKs.

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16
Q

What activates Cdc25 in a positive feedback loop?

A

Phosphorylation of M-CdKs.

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17
Q

What is PP2A-BB5?

A

A phosphatase that regulates CdKs.

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18
Q

What is the most important subunit in the PP2A-BB5 protein?

A

The B subunits, this subunit effects selectivity, localization, and enzyme regulation.

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19
Q

When is subunit B55 activity highest?

A

During G1/G2 phase.

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20
Q

What happens to subunit B55 during early M phase?

A

Its activity is Inhibited when M-CdK concentration rises

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21
Q

When is subunit B55 re-activated?

A

After cyclin degraded in anaphase.

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22
Q

What are CKIs?

A

CdK inhibitory proteins.

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23
Q

What phase do CKIs predominantly regulate?

A

G1/S passage.

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24
Q

What does P27 inhibit?

A

G1/S Cdks and SCdks.

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25
Q

What increases P21 expression?

A

DNA damage and subsequently p53

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26
Q

What controls P21 expression?

A

p53.

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27
Q

What is Ink4 and what does it do?

A

its a CKI that inhibits C1CdKs and acts as a tumor suppressor

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28
Q

What is APC/C?

A

A ubiquitin ligase that adds ubiquitin to M-cyclins and securin during anaphase and ensures that all centromeres are attached before mitosis begins.

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29
Q

What activates APC/C?

A

Binding of Cdc20, stimulated by MCdks activity, activates APC/C.

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30
Q

What role does APC/C play in anaphase?

A

Degrades M-cyclin, promotes anaphase, and ensures centromere attachment

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31
Q

What is the role of APC/C in anaphase?

A

What is the role of APC/C in anaphase?

32
Q

How is Cdc20 production stimulated?

A

By MCdks activity.

33
Q

How does the Cdc20-APC/C complex work?

A

Recruits E1, E2, and ubiquitin to form a polyubiquitin chain, this is then used on the m cyclins.

34
Q

What is the function of SCF in the cell cycle?

A

Ubiquitinates proteins, controlling G1/S cyclins.

35
Q

What regulates Rb activity in normal cells?

A

Phosphorylation level of G1 cyclins.

36
Q

How does Myc influence cell cycle progression?

A

Activates G1 cyclins, cdc25, and SCF subunits.

37
Q

What is the role of p53 in the cell cycle?

A

p53 arrests cell cycle for DNA repair

38
Q

What activates excessive proliferation signals like Myc?

A

mitogens binding to myc and actviating cascades

39
Q

How is p53 activated by DNA damage?

A

ATM and ATR activate Chk1/Chk2, phosphorylating p53.

40
Q

What role does Mdm2 play in p53 regulation?

A

Mdm2 decreases p53’s transcriptional activity

41
Q

How does p53 prevent cells from leaving G1?

A

Activates TFs like p21, arresting the cell cycle.

42
Q

ATM is activated by ____ DNA breaks

A

Double Stranded

43
Q

ATR is activated by _ DNA Breaks

A

Single Strand

44
Q

What proteins do Chk1/Chk2 phosphorylate?

A

Mdm2 and subsequently p53

45
Q

What prevents MCdk activation after nuclear export?

A

14-3-3 protein holds it, arresting cell cycle.

46
Q

What does SCF ubiquitin ligase degrade?

A

It activates FBox proteins, ubiquitinates G1/S cyclins

47
Q
A
48
Q

What are the structural features of initiator caspases?

A

Inactive monomers with prodomain, large and small subunits.

49
Q

What activates executioner caspases?

A

Active initiator caspases cleave them.

50
Q

What do active executioner caspases cleave?

A

Nuclear lamin and cytosolic proteins.

51
Q

What initiates intrinsic apoptosis?

A

DNA damage leading to cytochrome c release.

52
Q

What forms the apoptosome?

A

7 Apaf1 molecules and cytochrome c.

53
Q

What is the role of cytochrome c in apoptosis?

A

it acts as an eat me signal and also binds to the card region of Apaf1

54
Q

What is the structure of active executioner caspases?

A

Heterotetramers with two large and small subunits.

55
Q

Heterotetramers with two large and small subunits. GARBAGE

A

Anti-apoptotic, bind to bak.

56
Q

What is the function of the apoptosome’s center?

A

CARD recruits and binds procaspase 9.

57
Q

What happens to cells not exposed to growth factors?

A

Enter quiescence (G0) via inhabition by p21

58
Q

What is the effect of Myc activation on the cell cycle?

A

Enhances expression of cyclin D, Cdc25, E2F

59
Q

How does mitogen/GF affect CdK regulation?

A

Increases D cyclin, G1-Cdk complexes expression

60
Q

What role does p53 play in apoptosis?

A

It localizes to the mitochondrial membrane, binds Bcl2, leading to Bax MOMP formation.

61
Q

What is the effect of Myc on apoptosis?

A

Myc activates p53 and Bim in response to excess growth factors, leading to apoptosis.

62
Q

How do extrinsic and intrinsic pathways crosstalk in apoptosis?

A

Bid initates crosstalk. Bid is activated into tBid, linking pathways and promoting cytochrome c release.

63
Q

What role do IAPs and anti-IAPs play in apoptosis regulation?

A

IAPs inhibit caspases; anti-IAPs bind IAPs, ensuring caspase functionality for apoptosis.

64
Q

How do growth factors influence apoptosis?

A

Growth factors inhibit apoptosis by activating PI3K-Akt pathway, phosphorylating/inactivating Bad.

65
Q

What triggers the intrinsic pathway of apoptosis?

A

DNA damage, leading to cytochrome c release via Bax and Bak proteins.

66
Q

How do Bcl2 proteins regulate apoptosis?

A

Bcl2 proteins inhibit Bax, preventing MOMP, thereby regulating apoptosis.

67
Q

What role do perforin and granzyme play in apoptosis?

A

Perforin creates channels; granzyme activates procaspases, leading to apoptosis.

68
Q

What triggers the intrinsic pathway of apoptosis

A

DNA damage leading to the activation of initiator caspase 9 via the apoptosome.

69
Q

How do initiator caspases lead to apoptosis in the intrinsic pathway

A

They cleave and activate executioner caspases

70
Q

How does Myc influence apoptosis when there is excessive growth stimulus?

A

Myc activates p53 and Bim, leading to apoptosis through various pathways including Mdm2 inhibiti

71
Q

How does p53 regulate apoptosis after DNA damage

A

It activates transcription factors for pro-apoptotic proteins like Bcl-2, Bax, and Apaf1, leading to mitochondrial membrane changes.

72
Q

How do growth factors regulate apoptosis

A

They stimulate cell proliferation, suppress apoptosis, and promote protein synthesis that inhibits apoptotic pathways.

73
Q

What are survival factors?

A

Factors required for cell survival that suppress apoptosis when bound to cell-surface receptors.

74
Q

What is the function of IAPs (Inhibitor of Apoptosis Proteins)?

A

They inactivate caspases through their BIR domains and serve as inhibitors against death-inducing stimuli.

75
Q

What initiates death ligand/death receptor mediated apoptosis?

A

The binding of death ligands (e.g., FasL) on cytotoxic T cells to death receptors (e.g., Fas/CD95) on target cells.

76
Q

How can apoptosis be inhibited in the death ligand/receptor pathways?

A

By decoy CD95 receptors and the protein FLIP, which blocks caspase 8 and 10 activation.

77
Q

How does Bad influence apoptosis in the absence of growth factors?

A

Unphosphorylated Bad complexes with Bcl-2, preventing it from inhibiting Bax, leading to MOMP.

BMSC339 (7 decks)

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