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MCM II > Lec 6 cell cycle, apop, cancer > Flashcards

Lec 6 cell cycle, apop, cancer Flashcards

1
Q

Cell cycle and its checkpoints

A
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2
Q

What happens at the restriction point (R)

A

if growth factors are limiting restriction occurs

2hours before

many diff growth factors

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3
Q

what happens at the G1 checkpoint?

A

timing sim to restrcition point (2 hr)

occurs in response to DNA damage

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4
Q

what is checked at the G2 checkpoint?

A

verify complete genomic duplication

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5
Q

what happens at the metaphase checkpoint

A

ensures chromosomes attached to mitotic spindle

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6
Q

explain the steps that drive cell proliferation

A
  • Myc-Transcription factor that drives cell prolif
  • Myc increases G1-cyclin-dependent kinases (CDK)
  • CDK phosphorylates retinoblastoma (Rb)
  • Phospho-Rb releases sequestered E2F
  • E2F- TF that drives cells from G1 to S phase
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7
Q

simplified cell proliferation cascade

A

Myc increases CDK which phosphorylates Rb which releases E2F which drives cells from G1 to S phase

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8
Q

E2F drives expression of what?

A

Cyclin E and Cyclin A

these activate CDK2

CDK2 hyper-phosphorylates Rb (inactive)

which activates E2F

allow transition pass G1 checkpoint

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9
Q

what does CDK need to be active?

A

Cyclin (cyclin-dependent kinase)

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10
Q

CDK activation

A

partially via binding of cyclin

full requires CDK- activating kinase (CAK)

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11
Q

CDK inhibition

A

inhibitors (WEE1/ P27) inhibit cyclin CDK complex

inactivates kinase activity

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12
Q

CDK-acitvating kinase (CAK) and the T-Loop

A
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13
Q

What cyclin and CDK are used in restriction point

A

Cyclin D with CDK 4/6

inhibited by CKI (WEE1/p27)

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14
Q

S phase CDK and cyclin type

A

Cyclin A with CDK2

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15
Q

CDK and Cyclin in M phase/G2 cp

A

Cyclin A/B with CDK1

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16
Q

What does WEE1 do in regulating CDK activity

What reverses it?

A
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17
Q

What are the CDK inhibitory proteins?

A

P27 chich binds to both Cdk and cyclin

regulates early in cell cycle events (RP and G1 CP)

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18
Q

how is cyclin regulated

A

cyclin turnover is regulated by signal-dependent protein degradation

Metaphase to Anaphase triggered by cyclin turnover

regulator (APC/C) cyclosome

which is a ubiquitin ligase family of enzymes

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19
Q

what happens in order to move into anaphase in the cell cycle?

A

Cyclin-S and Cylin-M must be down regulated

APC/C activated by Cdc20 (binding)

APC/C poly ubiquitinates S and M cyclin

which go to proteosome destruction

no cyclins=inactive Cdk (dephosph)

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20
Q

What are the ubiquitylation enzymes in APC/C regulation

A

E1 and E2

21
Q

P53 and the cell cycle

A
22
Q

P21 and the cell cylce

A

it is a cyclin-dependent kinase inhibitor (CKI)

usually CDK2

can do all cyclin/CDK complexes

23
Q

extrinsic pathway (apoptosis)

A
24
Q

Intrinsic pathway (apoptosis)

A
25
Q

Caspase activation

A

first procaspase which is activated by protease cleavage

form a large and small subunit (heterodime)

26
Q

BCL-2 family

A

Bax and Bak are pro-apoptotic

while Bcl-2 and Bcl-XL are anti-apoptotic

27
Q

Role of Bax

A
28
Q

Apaf1 and its role in the intrinsic pathway

A
29
Q

Factors that increase expression P53 BAX and BAK

A

tBid (caspase-8 activates Bid to tBId)

this is for BAX and BAK

DNA damage for P53

30
Q

What inhibits free cytochome C?

A

BCL-2

BCL-XL

31
Q

What inhibits Apaf1 binding to cytochrome C?

A

BCL-2

32
Q

proto-oncogene vs oncogene

A
33
Q

Retinoblastoma role with cancer

A

it is a tumor suppressor

sequester E2F and prevents to much cell division

34
Q

Hereditary retinoblastoma

A

mutation or deletion in one Rb1

if another mutation then no more sequester E2F

(common tumors in eyes)

35
Q

sporadic retinoblastoma

A

non-hereditary

needs both copies of Rb1 to be mutated

36
Q

metastasis suppressors

A

cell adhesion proteins

(prevent tumor cells from dispersing

block loss of contact inhibition

inhibit tumor metastasis

37
Q

affect of mutation on early and late stages of cancer

A
38
Q

The different hallmarks of cancer

A
39
Q

Viral oncogenes

A
  • virus infects host
  • viral genome integrates into host genome next to proto-oncogene
  • replicates with hosts proto-onco
  • proto-onc mutates to oncogene
  • infects normal cell making it tumor cell
40
Q

HPV

A

E6 binds p53 causes degredation

E7 binds Rb causes E2F to be unbound

41
Q

Chemo types

A
42
Q

Herceptin

A

binds HER2 receptor which doesnt allow dimerization

which leads to degredation or lysis

(breast cancer)

43
Q

Gleevec

A

chronic myelogenous leukemia

44
Q

Erbitux

A

cetuximab

binds ligand that binds EGFR receptor a TK

blocks action

glioblastoma

45
Q

HER2 to oncogene

A

Val switched to glutamine causes TK activity activated in absence of ligand

Breast Cancer

46
Q

EGF receptor to oncogene

A

EGFRvIII after deletion

TK activity is always active

glioblastoma

47
Q

ABL and BCR

A

by them selves fine but the fuse it goes into nucleus and acts as TF and cell cylce increase

Chronic Myelogenous leukemia

48
Q
A

MCM II (11 decks)

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