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BMS247 - Stem cells > The cell cycle II > Flashcards

The cell cycle II Flashcards

1
Q

What cyclin/CDK pairs controls G1?

A

Association of D-type cyclins (D1, D2 or D3) with CDK4 and CDK6

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2
Q

What cyclin/CDK pairs controls G1 after the R point?

A

E-type cyclins (E1 and E2) with CDK2

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3
Q

What does cyclin E/CDK2 mediate?

A

The phosphorylation of substrates required for ENTRY into the S phase

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4
Q

What cyclin/CDK pairs controls the beginning of S phase?

What mediates S phase later on?

A

A-type cyclins (A1 and A2) replace cyclin E in complex with CDK2

Cyclin A/Cdc2 later on in S phase

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5
Q

What is Cdc2 also known as?

A

CDK1

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6
Q

What cyclin/CDK pairs controls G2?

A

B-type cyclings with Cdc2 (CDK1)

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7
Q

What does cyclin B/Cdc2 trigger?

A

Mitosis

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8
Q

What is the G0 –> G1 transition mediated by?

A

Cyclin C/CDK3 complex

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9
Q

Describe the levels of cyclin E in G1

A

Low during most of G1

Rapid increase after the R point

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10
Q

When do cyclin A levels increase?

A

In concert with entrance to the S phase

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11
Q

What happens to cyclin B levels in the cell cycle?

A

Increases with anticipation into mitosis

Levels drop once mitosis has finished

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12
Q

How do cycling levels decrease?

A

Degradation of the protein by ubiquitination

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13
Q

What ensures that the cell cycle only occurs in one direction?

What is the exception to this?

A

Cyclins GRADUALLY accumulate and are RAPIDLY degraded

Cyclin D is the exception - levels don’t change during the cell cycle

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14
Q

How is cyclin D regulated?

A

By EXTRACELLULAR signals:

1) Growth factors
2) Integrin-mediated ECM attachment

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15
Q

What is the function of cyclin D?

A

To convey messages from the EXTRACELLULAR environment to the CELL CYCLE CLOCK

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16
Q

Where is the cell cycle clock present?

A

In the NUCLEUS

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17
Q

How does cyclin D achieve its function?

A

Cyclin D is synthesised in the cytoplasm and transported to the nucleus (where the cell cycle clock is present)

ONLY when the environment is right to undergo CELL PROLIFERATION

18
Q

How does cyclin D fluctuate?

A

NUCLEAR cyclin D fluctuates (but the amount of cyclin D in the cell doesn’t)

19
Q

What occurs in G1, before the R point?

A

Cells asses their environment and decide if the environment is right to divide or not

20
Q

What is the decision to divide or not in G1 taken by?

A

Controlling the activity of cyclin D

21
Q

What happens is cyclin D goes into the nucleus in G1?

A

It associates with CDK4/6 and triggers the cells THROUGH the R point

22
Q

What happens if cyclin D is not localised in the nucleus in G1?

When might this happen?

A

Cell cycle cannot proceed

In the ABSENCE of GF
When the cell is not attached to the ECM

23
Q

What is the only cyclin that is regulated by extracellular signals?

A

Cyclin D

24
Q

What are the cyclins NOT dependant on after the R point?

What are they dependant on instead?

A

NOT dependant on extracellular signals

Dependant on autonomous, intracellulr signals

25
Q

What do cyclin/CDKs activate?

Inhibit?

What does this ensure?

A

Active the formation of the complexes in the subsequent phases

Inhibit the complexes in the previous phase

Ensures that the cell cycle only occurs in 1 direction

26
Q

What activates cyclin A?

What does cyclin A do following this activation?

A

Activated during the G1/S phase by cyclin E/CDK2

Replaces cyclin E in the complex and leads to the inactivation of cyclin E

Cyclin A-CDK2 complex then ACTIVATES the cyclin B/Cdc2, which inactivates the synthesis of cyclin A

27
Q

What are CKIs?

A

CKD inhibitors

28
Q

How many CKIs are there?

A

7

29
Q

What are the 2 groups of CKIs?

What are the members of these groups?

A

1) CKIs that inhibit the cyclin D/CDK4/6 complex but has NO activity towards the other complexes

(4 x INK4 proteins)

2) CKIs that inhibit the other cyclin/CDK complexes (E,A, B) but has no activity towards cyclin D

(P57^Kip2, P27^Kip1 P21^Cip1)

30
Q

What does TGFb play a role in?

How?

A

The pathogenesis of many carcinomas

Plays a different role in the different stages of cancer:

Early stages - Arrests the growth of many cell types

Late stages - Contributes to tumour invasivness and metastasis

31
Q

What does TGFb control?

A
  • Cell growth
  • Cell differentiation
  • Apoptosis
  • Cellular homeostasis
32
Q

What is the process of TGFb superfamily signalling?

A

1) Ligand binds type II receptors
2) Recruits type I receptor which DIMERISES and activates type II
3) Type II phosphorylates type I and leads to the overall activation of the receptor
4) Activated receptor phosphorylates specifics receptor-regulated SMAD proteins (r-SMADs) , which recruits SMAD4 (coSMAD) to form a complex
5) This complex acts as a TF and translocates into the nucleus to regulate gene expression

33
Q

What are the genes that are controlled by the R-SMAD/coSMAD complex?

What does this cause?

A

CDI:

  • Strongly INCREASES levels of P15^INK4B
  • Causes the inhibition of cyclinD/CDK4/6
  • Cells don’t reach the R point
  • Cells don’t proliferate
  • Weakly induces p21^Cip1
34
Q

When is P21^Cip1 more strongly induced by TGFb signalling?

What does this cause? Why?

A

Upon DNA damage

Inhibition of most cyclin/CDK complexes - to HALT the cell cycle whilst repair takes place

35
Q

How do GF/mitogenic factors promote the advancement of the cell cycle?

Process?

A

They MUTE the action of CKI:

  • Bind to the receptors
  • Activate the P13 pathway
  • Leads to the activation of Akt (PKB)

1) Akt/PKB phosphorylates p21^Cip in the NUCLEUS, causing its translocation to the cytoplasm
2) Akt/PKB phosphoylates p27^Kip in the CYTOSOL, PREVENTING the translocation to the nucleus
- p27 and p21 cannot function in the cytosol - cyclin-CDK complexes can trigger the progression of the cell cycle (not blocked)

36
Q

How can the effect of Akt/PKB be seen in the cell?

A

When they are stained with an antibody marker

37
Q

What is seen in constitutively active Akt/PKB?

A

Most p21^Cip is in the cytosol

No blockage of cyclin-CKD complexes

38
Q

What is seen in dominant-negative Akt/PKB?

A

Most p21^Cip in in the nucleus

Blocks cyclin-CDK complexes

39
Q

What is the difference between patients that have breast cancer that have P27^Kip in the nucleus or in BOTH the nucleus and the cytoplasm?

A

In the nucleus - Higher survival rate

In the nucleus and the cytoplasm - Lower survival rate

40
Q

In patients with breast cancer, what does Akt activation correlate with?

A

Cytoplasmic p27^Kip

No blockage of cell growth

41
Q

What can the localisation of p27^Kip be used as?

BUT, what doesnt this mean?

A

A prognostic marker to identify which kind or tumours are more likely to progress and become more aggressive

DOESN’T mean that cytoplasmic p27^Kip causes breast cancer

BMS247 - Stem cells (15 decks)

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