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Molecular Basis Of Disease/ Microbiology And Immunology > Cell Growth And Differentiation > Flashcards

Cell Growth And Differentiation Flashcards

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Biology 101 flashcards
1
Q

What are the three main groups of disease?

A

Developmental conditions, neoplasia and others

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2
Q

What are developmental conditions?

A

Related to cell growth or differentiation

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3
Q

What are neoplasia (and metaplasia)?

A

Cancers and tumours

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4
Q

What are the two main groups of cell growth?

A

Hypertrophy and hyperplasia

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5
Q

What is hypertrophy?

A

Bigger cells (more proteins and membrane)

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6
Q

What drives hypertrophy?

A

Elevated protein synthesis

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7
Q

What is hyperplasia?

A

More cells

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8
Q

What is hyperplasia caused by?

A

Cell division or proliferation

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9
Q

What does cell differentiation begin with?

A

Exit from the cell cycle

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10
Q

What are the three broad classes of extracellular signals?

A

Paracrine, autocrine, endocrine

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11
Q

What do paracrine signals do?

A

Stimulate proliferation of a different cell type that has the appropriate cell surface receptor

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12
Q

Where are paracrine factors produced?

A

Locally

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13
Q

What are autocrine signals produced by?

A

Cell that also expresses the appropriate cell surface receptor

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14
Q

How do endocrine signals work?

A

Released systematically for distant effects

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15
Q

What are the type of proteins used in cell growth and differentiation?

A

Proteins that:
Stimulate proliferation and promote survival
induce differentiation and inhibit proliferation
Induce apoptosis

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16
Q

What do mitogens do?

A

Stimulate proliferation and promote survival

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17
Q

What are the phases of the cell cycle?

A

Mitosis, G1, S phase, G2

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18
Q

What are quiescent cells and what phase are they in?

A

Cells that have left the cell cycle- G0

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19
Q

Can quiescent cells rejoin the cell cycle?

A

Yes

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20
Q

What is FACS used to measure?

A

DNA content of every cell in a population

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21
Q

What are the controls of the cell cycle checkpoints?

A

Specific protein kinases and phosphatases

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22
Q

What do the controls of the cell cycle checkpoints ensure?

A

Strict alteration of mitosis and DNA replication

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23
Q

What are the three cell cycle checkpoints (and when do they happen)?

A 
Restriction point (end of G1)
G2/M phase checkpoint 
Mitotic checkpoint
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24
Q

What is checked at the restriction point?

A

DNA not damaged
Cell size
Metabolite/nutrient stores

25
Q

What does the G2/M checkpoint check?

A

DNA completely replicated

DNA not damaged

26
Q

What is colchicine used for?

A

Immune supression

27
Q

What is checked at the mitotic checkpoint?

A

Chromosomes aligned on the spindle

28
Q

When do extrinsic factors act on the cell cycle?

A

G1

29
Q

What does CDK stand for?

A

Cyclin dependent kinases

30
Q

What does CDK do?

A

Catalytic subunit

31
Q

What does cyclin do?

A

Regulatory subunit

32
Q

What is cyclin expression induced by?

A

Growth factors

33
Q

What does an active cyclin-CDK complex do?

A

Phosphorylates specific substrates

34
Q

What destroys the cyclin-CDK complex?

A

Proteasomes

35
Q

What does post-translational phosphorylation result in?

A

Activation, inhibition or destruction

36
Q

What is the retinoblastoma protein (RB)?

A

Key substrate of G1 and G1/S cyclin dependent kinases

37
Q

How does RB normally work?

A

Unphosphorylated RB binds E2F transcription factor preventing its stimulation of S-phase protein expression

  • > RB is phosphorylated and E2F dissociates in the presence of cyclin D-CDK4 and cyclin E-CDK2
  • > E2F stimulates expression of more cyclin E and S phase proteins
  • > DNA replication starts
38
Q

What are some cyclin E and S phase promoters?

A

DNA polymerase, thymidine kinase, PCNA

39
Q

What are some sequential activites in the cell cycle?

A

Mitogens in G1 phase signal to the nucleus

  • > drives early gene expression
  • > encode delayed genes
  • > cyclin D able to form active complexes with CDK4/6
  • > hypophosphorylates RB
  • > allows some cyclin E expression which causes hyperphorphorylation of RB
  • > activation of E2F responsive genes
  • > cyclin E and CDK 2 phosphorylates and activates cyclin A and CDK 1
  • > same happens to cyclin B and CDK1
  • > RB dephosphorylation mediated by PP1
40
Q

What does DNA damage trigger?

A

Cell cycle arrest or apoptosis

41
Q

What is stopping of the cell cycle driven by?

A

CDKI genes

42
Q

What things attempt DNA repair?

A

Nucleotide or base excision enzymes, mismatch repair etc

43
Q

What causes programmed cell death?

A

BCL2 family or caspases

44
Q

What happens if the cell senses DNA damage?

A

Cell cycle stops, DNA repair attempted, if not possible -> programmes cell death

45
Q

What happens to TP53 in the normal cell?

A

Completely and continously destroyed by a proteasome

46
Q

What happens to TP53 if there is DNA damage?

A

Kinases are activated

  • > phosphorylates TP53
  • > phosphorylated TP53 can’t be destroyed by proteasome
  • > phosphorylated TP53 then accumulates
47
Q

What are the functions of TP53?

A

Expression of CKI causing cell cycle arrest

DNA repair - if not possible it causes apoptosis

48
Q

What mutations are the most frequent in cancer?

A

TP53 loss of function

49
Q

What are the ways in which TP53 loss of function mutations cause cancer?

A

Prevent cell cycle arrest, apoptosis and DNA repair

50
Q

How does the prevention of DNA repair lead to cancer?

A

More mutations -> more heterogenity -> more adaptation -> cancer progression

51
Q

What are the types of chemo drugs?

A

S phase, M phase and colchicine

52
Q

What do S phase drugs do?

A

DNA damage

53
Q

What do M phase drugs do?

A

Mess up the mitotic spindle

54
Q

What are the types of M phase drugs?

A

Vinca alkaloids, paclitaxel

55
Q

What do vinca alkaloids do?

A

Stabalise free tubulin
Prevent microtubule polymerisation
Arrest cells in mitosis

56
Q

What does paclitaxel do?

A

Stabalise microtubules
Prevents depolymerisation
Arrest cell in mitosis

57
Q

What are the two types of S phase drugs?

A

5-fluorouracil and cisplatin

58
Q

How does 5-fluorouracil work?

A

Prevents synthesis of thymidine

59
Q

How does cisplatin work?

A

Binds to DNA causing damage and blocking repair

Molecular Basis Of Disease/ Microbiology And Immunology (57 decks)

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