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POM (Principles of Medicine) > Cell replication > Flashcards

Cell replication Flashcards

1
Q

What is the cell cycle?

A
  1. cell growth and chromosome replication
  2. chromosome segregation
  3. cell division
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2
Q

What is the orderly sequence of events in which a cells duplicates?

A
  • duplication
  • division
  • coordination
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3
Q

Different cells divide at different rates

A

fastest: embryonic and yeast cells

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4
Q

What does the rate of division depend on?

A
  • the type of cell
  • complexity of system
  • necessity for renewal
  • state of differentiation (some cells never divide)
  • tumour cells
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5
Q

What are the phases of the cell cycle?

A

G1 phase
S phase
G2 phase
M phase (mitosis)

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6
Q

What does G phase stand for?

A

gap

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7
Q

What is the interphase?

A

G1 + S + G2

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8
Q

What is G0?

A

quiescent phase

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9
Q

What happens in the absence of stimulus to cells?

A

they go into G0

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10
Q

Which cells arent dormant, but are non-dividing?

A

neurons
skeletal muscle
hepatocytes

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11
Q

How does the cell decide if it can enter the cycle?

A

Monitoring external environment: - nutriets

- growth factors

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12
Q

When does a cell pause?

A

DNA repair

undergo apoptosis

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13
Q

Why do cells ever leave G0?

A

signalling cascades

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14
Q

What are the signalling cascades?

A
  • response to extracellular factors (growth factors stimulate entry from G0 into the G1 phase)
  • signal amplification
  • signal integration/ modulation by other pathways
  • Ras/ Raf /MEK/ ERK (kinases- enzymes)
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15
Q

What do the kinase enzymes do in the cell cycle?

A
  • protein synthesis increased
  • protein degradation decreased
  • -> overall net growth of the cell
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16
Q

What is c-Myc ?

A

transcription factor

drives the production of specific cell cycle genes

induced the expression of Cyclin D which drives entry into S phase

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17
Q

What do growth factor signalling pathways induce?

A

the expression of c-Myc

  • c-Myc promotes G0 to G1 transition
  • c-Myc is an oncogene - overexpressed in many tumours
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18
Q

What is the key role of Cyclic dependant kinases (Cdks)?

A

phosphorylation + dephosphorylation

  • key signaling events
  • serine/ threonine/ tyrosine
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19
Q

What else do Cdks allow?

A

exquisite control of events:

  • cdks present in proliferating cells
  • BUT only active when a cyclin is bound
20
Q

Why are they called cyclins?

A

bc their concs within the cell fluctuate

21
Q

What cyclin is active during mitosis?

A

Cdk complex

22
Q

What is the pathway of cell cycle entry?

A

growth factor –>
C-Myc –>
Cyclin D –>
cyclin D/ Cdk 4/ 6 complex

23
Q

What are the checkpoints that can arrest the cell cycle?

A

G1: - damaged DNA
- unfavourable extracellular environment
S: damaged or incompletely replicated DNA
G2: damaged or incompletely replicated DNA
M: chromosome improperly attached to mitotic spindle

24
Q

What are protein kinase cascades?

A

Kinases activate a molecule by phosphorylation

phosphorylation of one kinase then allows it to phosphorylate another kinase and a third kinase and so on

25
Q

What do protein kinase cascades lead to?

A
  • signal amplification
  • diversification
  • opportunity for regulation
26
Q

What are phosphatases?

A

they reverse phosphorylation

27
Q

Where are cyclin-dependent kinases present?

Cdk1, Cdk2, Cdk4, Cdk6

A

in proliferating cells throughout the cell cycle

28
Q

How is the activity of Cdk’s regulated?

A
  • interaction with cyclins

- phosphorylation

29
Q

Cyclins?

CyclinA, CyclinB, CyclinD, CyclinE

A

transiently expressed at specific points in the cell cycle

  • regulated at level of expression
  • synthesised, then degraded
30
Q

What drives the cell cycle forwards?

A

Positive feedback

31
Q

What drives the entry to the S phase?

A

active S-Cdk

32
Q

What drives the entry to the M phase?

A

active M-Cdk

33
Q

What are the 3 steps required to activate the cdk?

A
  1. phosphorylation
  2. dephosphorylation
  3. binding of the cyclin (s or M)
34
Q

How are cyclins turned off?

A 
by ubiqutination (post-it notes- destroy me)
and then destruction
35
Q

When cyclins become sequentially active what do they stimulate?

A

synthesis of genes requires for the next phase

36
Q

What is a retinoblastoma?

A
  • a molecular “brake”
  • if its missing or inactive –> issues of cell cycle progression
  • a tumour suppressor
    abundant in all nucleated cells
37
Q

What does a growth factor do?

A

drives cell proliferation

38
Q

What does a retinoblastoma (Rb) act as?

A

a brake on cell proliferation

39
Q

What happens when TFs are bound to the retinoblastoma?

A

Tfs cannot turn of genes needed for cell cycle progresion:
eg DNA polymerase
thymidine kinase

40
Q

What does the prolyphertion of Rb release?

A

the brake in a prolypherating cell

  • Activation of intracellular signaling leads to production of G1-Cdk and G1/S–Cdk complexes
  • can phosphorylate Rb inducing the inactivation of Rb and release of the TF.
  • Target genes such as DNA polymerase and thymidine kinase can now activated.
41
Q

What do E2F family members regulate?

A

the expression of several genes need for cell cycle progression

42
Q

What does p53 do?

A

arrests cells with damaged DNA in G1

43
Q

What happens in absence of DNA damage?

A

p53 is degraded in proteasomes

p53 also induces the production of the Cdk inhibitor p21

44
Q

What happens if there is DNA damage?

A
  • stable, activated p53
  • active p53 binds to regulatory region of p21 Gene
  • transcription –> p21 mRNA
45
Q

What are p21 family members?

A

inhibitors of cyclin: Cdk complexes

46
Q

What are the oncogenes?

A
  • EGFR/HER2 mutationally activated of over expressed in breast cancers
    Herceptin antibody for the treatment of HER2+ metastatic breast cancer
  • Ras mutationally activated in many cancers
  • Cyclin D1 overexpressed in 50% of breast cancers
  • C-Myc
    overexpressed in many tumours
47
Q

What are tumour suppressors?

A
  • Rb
    loss of function mutations in 80% of small cell lung cancers
  • p53
    loss of function mutations inover 50% of all human cancers

POM (Principles of Medicine) (17 decks)

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