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PoM > MBC - Cell Replication > Flashcards

MBC - Cell Replication Flashcards

1
Q

Where do cells arise from?

A

Pre-existing cells

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2
Q

What are the three stages of the cell cycle?

A

Growth and chromosome replication
Chromosome separation
Cell division

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3
Q

In what scenarios will cells divide at different rates?

A 
Embryonic vs adult cell 
Complexity of system 
Necessity of replication 
State of differentiation 
Tumour cells
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4
Q

How does necessity for replication affect cell division?

A

E.g. intestinal epithelial cells replicate in 20 hours due high necessity, but hepatocytes replicate every year due to low necessity

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5
Q

How does state of differentiation affect cell division?

A

E.g. neurones and cardiac myocytes are specialised cells that don’t divide

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6
Q

How do tumour cells affect division?

A

Tumour cells undergo very quick and uncontrolled division

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7
Q

What is the correct order of phases for the cell cycle?

A

G1, S, G2, Mitosis, Cytokinesis

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8
Q

What phases are involved in interphase?

A

G1, S, G2

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9
Q

What is another name for G0?

A

Quiescent phase

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10
Q

What can a cell do before going to S phase from G1 at the cell checkpoint?

A

Either progress into S phase or withdrawn to G0.

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11
Q

Is the cell dormant in G0?

A

No - it is just not dividing

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12
Q

What decides the fate of cells in G1?

A

Cells in G1 need a stimulus to progress into S phase, without a stimulus the cells will withdraw into G0

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13
Q

How do cells in G0 go to S phase?

A

Cells need a stimulus which will take them back to G1 and then S phase afterwards.

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14
Q

What is the significance of the checkpoint before S phase?

A

The checkpoint allows the cell to see if the external environment is favourable:
Are there enough nutrients and growth factors?

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15
Q

If a cell is trying to enter mitosis from G2 but reversible DNA damage is detected at the checkpoint, what happens?

A

The cell will pause at the checkpoint and will attempt to repair DNA damage.

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16
Q

If DNA damage at a checkpoint is irreversible, what happens?

A

The cell will undergo apoptosis

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17
Q

How does the cell respond to growth factors in the external environment?

A

The cell has tyrosine kinase (growth factor) receptors which bind to external growth factors which are present in a favourable environment

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18
Q

What is the purpose of MAP kinases?

A

These are used in an intracellular signalling pathway to amplify the signal and increase protein synthesis/decrease protein degradation, causing cell growth.

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19
Q

What are examples of MAP kinases?

A

Ras

ERK

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20
Q

What is c-Myc?

A

Transcription factor - drives the production of specific genes.

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21
Q

What does c-Myc do?

A

Stimulates the expression of cell cycle genes which allow the cell to progress from G0 to G1

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22
Q

How and why does c-Myc concentration change?

A

It increases in response to growth factor addition to allow progression of the cell cycle

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23
Q

What is the relevance of c-Myc and cancer?

A

c-myc is an oncogene and is overexpressed in many tumours

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24
Q

What are cyclin dependent kinases?

A

Family of regulatory proteins essential for cell growth/division

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25
Q

Where are CDKs found?

A

Present in proliferating cells

26
Q

When do CDKs become active?

A

When bound to cyclin (+other factors)

27
Q

How does CDK concentration fluctuate?

A

It doesn’t

28
Q

What do CDKs phosphorylate?

A

The hydroxyl group on serine, tyrosine or threonine residues.

29
Q

Does cyclin concentration change in the cell?

A

Yes

30
Q

When does CDK activity peak?

A

When cyclin production peaks

31
Q

How does c-Myc affect entry into the cell cycle?

A

c-myc causes production of cyclin D, which then forms a CDK 4/6 complex with cyclin D for cell cycle entry

32
Q

Explain, using kinase 1 and kinase 2, the concept of protein kinase cascades?

A

Kinase 1 is off however phosphorylation turns it o, allowing the phosphorylation of kinase 2 and thus turning it on, this then repeats for many different proteins down a cascade.

33
Q

What does protein kinase cascading allow for?

A

Signal amplification
Diversification (multiple pathways can get involved)
Regulation of cell cycle progression

34
Q

What do phosphatases do?

A

Reverse the effects of phosphorylation thus turn off the kinases

35
Q

What are the 4 CDKs?

A

1,2,4,6

36
Q

What are the 4 Cyclins?

A

D,E,A,B

37
Q

How is CDK activity regulated?

A

CDKs require cyclin interaction and phosphorylation for activation

38
Q

How are cyclins expressed?

A

Transiently at specific points in the cell cycle, then they are degraded.

39
Q

What is the first step of active Cyclin-CDK complex formation?

A

Inactive CDK interacts with cyclin to form inactive complex.

40
Q

What is the second step of active Cyclin-CDK complex formation?

A

Inactive complex is then phosphorylated by protein kinase, adding a inhibitory and an activating phosphate group. Still inactive

41
Q

What is the third (final) step of Cyclin-CDK complex formation?

A

Inactive complex is ridden of inhibitory phosphate via activating protein phosphatase to result in an active complex.

42
Q

How does positive feedback increase the level of active Cyclin-CDK complex?

A

Active CDK complex acts as a kinase to phosphorylate the inactive phosphatase cdc25. This leads to an increase in active cdc25 which in turn phosphorylates inactive complex to form active complex.

43
Q

How are cyclin-CDK complexes turned off?

A

Ubiquitination: leads to cyclin destruction and thus complex deactivation

44
Q

How do cyclins give directions and timing to the cell cycle?

A

c-Myc gives rise to cyclin D/CDK 4/6

This in turn stimulates expression of cyclin E, then A and b respectively.

45
Q

Why do we have cyclical activation?

A

As cyclins can be degraded

46
Q

What is the Rb gene?

A

Tumour suppressor gene that acts as a molecular brake

47
Q

What happens when Rb is missing or inactive?

A

We develop cell cycle progression problems and thus a retinoblastoma (eye tumour)

48
Q

How does Rb stop cell proliferation?

A

Active Rb sequesters/holds transcription factor E2F in an inactive state which normally increases expression of cell cycle proteins e.g. thymidine kinase and DNA polymerase.

49
Q

How does Rb allow cell proliferation?

A

When a growth factor binds to a mitogen receptor, intracellular signalling leads to G1/S-CDK complex which phosphorylates active Rb to inactive Rb, releasing E2F and allowing cell cycle progression.

50
Q

What is p53?

A

Tumour suppressing gene that arrests cell with damaged DNA in G1.

51
Q

What does p53 do?

A

When there is DNA damage, p53 will activate protein kinases to arrest the cell

52
Q

What happens with p53 in the absence of DNA damage?

A

p53 is degraded in proteosomes

53
Q

What is the advantage of initially making p53 regardless of DNA damage?

A

p53 can be rapidly activated to arrest the cell before further cell cycle progression if there’s DNA damage

54
Q

What happens with p53 when there’s DNA damage?

A

Protein kinases are activated and activate/stabilise p53 with phosphorylation (addition of phosphate). p53 then binds to regulating region of the p21 gene to express p21.

55
Q

What is the p21 translation product?

A

CDK inhibitor protein

56
Q

What does the CDK inhibitor protein from p21 do?

A

It deactivates the active G1/S-CDK complex to stop cell cycle progression, stopping the cell cycle of a cell with damaged DNA.

57
Q

What are 5 example oncogenes?

A

EGFR/HER2
Ras
Cyclin D1
c-Myc

58
Q

What are EGFR/HER2?

A

Oncongenes that are mutationally activated/overexpressed in breast cancer. E.Herceptin antibody is used in treatment of HER2+ metastatic breast cancer.

59
Q

What is Ras?

A

Oncogene that is mutationally activated in many cancers.

60
Q

What is cyclin d1?

A

Cyclin that is overexpressed in 50% of breast cancers

61
Q

What is c-myc (oncogene)?

A

Oncogene that is overexpressed in many tumours.

PoM (27 decks)

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