Cell Replication Flashcards

1
Q

What are the phases of the cell cycle?

A

G0
G1
S
G2
M

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2
Q

Which phases take place during interphase state?

A

G1+S+G2

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3
Q

In which phase does DNA replication occur?

A

S Phase (interphase)

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4
Q

In which phase does mitosis occur?

A

M Phase

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5
Q

What is G0 Phase?

A

Gap, no cell division

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6
Q

What happens at G1 checkpoint?

A

Checked if environment favours cell replication

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7
Q

What happens at G2 checkpoint?

A

Checked if all DNA is replicated and no DNA damage is present

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8
Q

What happens at M checkpoint?

A

Checked if all chromosomes are properly attached to the spindle and ready for cell cleavage

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9
Q

What happens if G2 checkpoint is not passed?

A

DNA repair or Apoptosis

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10
Q

What stimulates the cells in G0 phase to enter G1 phase?

A

Growth factors

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11
Q

What is c-Myc?

A

a transcription factor that stimulates the expression of cell cycle genes (also proto-oncogene)

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12
Q

What is the likely outcome of overexperssion of c-Myc?

A

Tumour growth

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13
Q

What is Cdk and which cells would have it?

A

Cyclin dependent kinase found in. proliferating cells

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14
Q

When is Cdk active, what does it do?

A

Active when cyclin is present, carries out phosphorylation of proteins

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15
Q

Which amino acids are substrates for Cdk and why?

A

Serine, tyrosine and threonine as they all have hydroxyl groups

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16
Q

Why are cyclins boh produced and degraded at the same time?

A

Different cyclins with different concentrations at different times to control the cell cycle

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17
Q

Put the molecules in order to make cascade: Cdk 4/6:cyclin D complex, cyclin D, growth factors, c-Myc

A
18
Q

What do the checkpoints check for in the cell (generalised)?

A
19
Q

What are the advantages of kinase-kinase regulations?

A

Signal amplification
Diversification
Opportunity for regulation
(reversal by phosphatases)

20
Q

What are the names of Cdk molecules present in proliferating cells?

A

Cdk 1, 2, 4, 6

21
Q

What are the names of cyclins transiently expressed at specific points in the cell cycle?

A

Cyclin A, B, D, E

22
Q

How is Cdk activity regulated?

A

Interaction with cyclins
Phosphorylation

23
Q

How is a Cdk:cyclin complex activated?

A

Through phosphorylation and removal of inhibitory phosphate

24
Q

What kind of feedback does the active Cdk provide?

A

Positive feedback for activation or inhibiton of kinases

25
Q

What are the 2 types of cyclins?

A

S cyclin (for Interphase)
M cyclin (for Mitosis)

26
Q

What is the degradation mechanism of cyclins?

A

Ubiquitination/ubiquitylation tags cyclins for degradation in proteasome

27
Q

What is the order of Cdk:cyclin complexes activated sequntially starting from stimulation by c-Myc?

A

4/6:D
2:E
2:A
1:B

28
Q

What is the role of Retinoblastoma (Rb) protein?

A

Tumour supression - inactivating transcription factors

29
Q

How is Rb protein inactivated?

A

Through phosphorylation

30
Q

What is E2F and how does it contribute to the cell cycle?

A

E2F is a transcription factor and regulates the expression of several genes need for cell cycle progression - can be inactivated by Rb

31
Q

What causes DNA damage?

A

X-rays

32
Q

What is Rb protein named after?

A

Eye tumour in children caused by inactive or missing Rb

33
Q

Which protein is activated in case of DNA damage and how?

A

p53 is activated through phosphorylation by protein kinase

34
Q

How does p53 interfere with the cell cycle?

A

Upregulates production of p21 which inhibits cdk:cyclin complexes

35
Q

What happens to active p53 in absence of DNA damage?

A

Degraded in proteasome

36
Q

Which oncogenes are overly expressed in breast cancer?

A

EGFR/HER2 and/or Cyclin D1

37
Q

What does the overexpression of EGFR/HER2 result in?

A

Breast cancer

38
Q

What is the treatment for HER2+ metastatic breast cancer?

A

Herceptin antibodies

39
Q

What is Ras?

A

An oncogene - mutationally activated in many cancers (e.g. pancreatic, lung, colorectal, thyroid)

40
Q

What does the overexpression of Cyclin D1 result in?

A

Breast cancer

41
Q

What is the cause of 80% of small cell lung cancers?

A

loss of function in mutated Rb protein

42
Q

What is the cause of 50% of all human cancers?

A

loss of function in mutated p53