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Cancer Biology > Chapter Five > Flashcards

Chapter Five Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

What is a good definition for the cell cycle?

A

The stages that a cell goes through between divisions.

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2
Q

What is a mitogen?

A

Something that induces cell division.

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3
Q

What are the three stages of the cell cycle?

A

Interphase
Mitosis
Cytokinesis

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4
Q

What is mitosis?

A

The segregation or division of nucleus

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5
Q

Cyclins are expressed _________.

A

Cyclically.

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6
Q

When are cdks present?

A

They are always present, but rely on cyclins.

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7
Q

When G0 is referred to as the quiescent phase, what does this mean?

A

It means that cells are doing normal functions.

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8
Q

Before the G1 restriction point, mutagens are required for progression into cell division.

What are such examples of mitogens?

A

PDGF
EGF

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9
Q

How does EGF result in progression into the cell cycle?

A

MAPK will phosphorylate transcription factors like AP-1 stuff and Myc that will promote expression of genes needed for cell cycle progression.

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10
Q

What are genes that are transcribed in G1?

A
  1. Cyclins
  2. Checkpoint proteins
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11
Q

Cell cycle progression is ___________, ___________, and _____________.

A
  1. Unidirectional
  2. Bistable (on or off)
  3. Regulated by checkpoints.
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12
Q

What are cyclins?

What do they do to CDK’s?

How does their concentration change during the cell cycle?

A

They are regulatory subunits (coassign with other proteins) of cyclin-dependent kinases.

They induce a conformational change in the catalytic subunit of the CDK, exposing the active site (kinase domain)

Their concentration changes during the cell cycle.

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13
Q

What are CDK’s?

How does their concentration change during the course of the cell cycle?

A

They are ser thr kinases that regulate the cell cycle progression, and are activated by cyclins.

They stay the same.

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14
Q

What is the first cyclin to be expressed?

Who expresses it?

A

Cyclin D

AP-1

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15
Q

What activates the expression of Cyclin E?

A

Cyclin D

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16
Q

What is the G1 checkpoint?

A

It occurs before the cell goes into the S phase.

It arrests the cell cycle in response to DNA damage.

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17
Q

What is the G2 checkpoint?

A

It occurs before the cell goes into mitosis at the end of G2

It arrests the cell cycle in response to damaged or unreplicated DNA

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18
Q

What is the M-phase checkpoint?

A

it occurs during metaphase of mitosis

it arrests the cell cycle in response to misalignment on the mitotic spindle.

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19
Q

If checkpoints are working correctly, what are the consequences?

A

There will be genomic and chromosomal instability.

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20
Q

What are some things that cdks are responsible for phosphorylating?

A

Transcriptional regulators
Cytoskeleton proteins
Nuclear pore proteins
Histones

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21
Q

What is the result of cdks on each of these?

A. Transcriptional regulators
B. Cytoskeleton proteins
C. Nuclear pore proteins

A

A. Changes in gene expression

B. Chromosomal condensation

C. Nuclear breakdown

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22
Q

What is the cell cycle progression controlled by?

A
  1. Protein phosphorylation by kinases
  2. Protein dephosphorylation by phosphatases
  3. Ubiquitination - tagging stuff that marks it to be degraded
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23
Q

How can cdk activity be regulated?

A
  1. Associate with cyclins - it will work
  2. Association with cdk inhibitors - it won’t work
  3. Addition of an inhibitory kinase
  • likely by wee kinase
  1. Addition of an activating phosphate
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24
Q

What about the conformation of the inactive cdk prevents it from working?

A
  1. Blocks substrate binding
  2. Blocks the correct alignment of ATP
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25
Q

What does cyclin binding do to cdk?

A

it causes a conformational change.

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26
Q

What are the two families of inhibitors of CDKs?

A

p16 (INK) family - bind cdk 4 and 6 inhibiting the binding of cdks to cyclin D

p21 (Cip/Kip) family - block the ATP binding site of cdk2
cdk still binds to cyclin

27
Q

What can cyclin dependent kinases do that keeps the cell cycle going?

A

They prevent p21 family activity, so cdk2 is able to be activated by cyclin E

28
Q

What about inhibitors are important for progression of the cell cycle?

A

Inhibitors being inactivated are important for progression.

29
Q

How does Wee1 kinase inhibit cdks?

A

It phosphorylates 2 sites on the amino terminal end of the cdk, which interferes with ATP binding.

30
Q

What are the two steps to activate cdks that have been inhibited via phosphorylation?

A
  1. cdc25 phosphatase must take these phosphates off
  2. Central threonine must be phosphorylated by CAK (CDK activating kinase)
31
Q

What is the RB protein?

A

A nuclear, tumor suppressor that regulates E2F activity

It is also a key substrate of cyclin-D to cdk 4/6 complex.

32
Q

What is E2F?

What is included on the functional heterodimer?

A

It is a family of transcription factors that regulate expression of cell cycle genes (things like cyclin E, cyclin A, and cdk 2)

It has an EF2 subunit with a DP subunit.

33
Q

Describe the structure of the whole RB protein.

A

It is a pocket protein with a A domain and a B domain joined by a linker region.

HDAC and E2F bind to the pocket region

34
Q

What does RB do for the cell cycle?

A

It blocks TF’s (E2F)

It holds onto HDACs that take acetyl groups off the DNA making it more condensed

35
Q

What happens to the RB complex when cyclin D phosphorylates

A

The first phosphorylation kicks the HDAC it is holding onto on the B domain off, allowing the cyclin E gene to be transcripted.

36
Q

What happens when RB becomes hyperphosphorylated by cyclin D and E?

A

RB becomes inactive allowing the cell cycle to move into S phase.

37
Q

RB being inactivated is what checkpoint?

A

G1 checkpoint.

38
Q

What does the G2 checkpoint do?

A

It blocks the entry into M phase if the DNA is damaged or not replicated properly.

39
Q

When DNA damage is noticed, what happens?

A

ATR or ATM kinases are activated.

40
Q

What do ATR/ATM kinases do?

A

They will phosphorylate Chk1 (ATR) or Chk2 (ATM)

41
Q

What do Chk1 and Chk2 do?

A

They inactivate cdc 25 phosphatase

When this is inactive, CDKs cannot be activated.

42
Q

What is decatenation?

What happens and what enzymes are involved?

A

It is part of the G2 checkpoint and aims to detangle the intertwined sister chromatids

Topoisomerase II creates DNA ds breaks that are then fixed by repair.

43
Q

What does the mitotic checkpoint entail?

A

It involves checking the spindle assembly - ensuring the correct chromosomal segregation and production of two genetically identical nuclei.

44
Q

What normally happens in metaphase?

A

The spindle microtubules attach to the centromere of chromosomes.

45
Q

If normal activity doesn’t happen correctly, what occurs?

A

The unattached chromatid pairs will recruit checkpoint proteins that inhibit the APC.

46
Q

What is APC?

A

It is Anaphase Promoting Complex.

47
Q

If correct attachment occurs, what happens?

A

The APC inhibition is relieved and cohesin is removed.

48
Q

In simple terms what controls APC?

A

It is controlled by M phase cyclin-cdk.

49
Q

What does APC do?

A

It activates separase, which hydrolyzes cohesin.

50
Q

What do the Aurora Kinases do?

A

The regulate chromosome segregation and spindle checkpoint.

51
Q

What does Aurora A do?

A

It localizes to the centromeres during interphase and is important for the assembly of the spindle apparatus.

52
Q

What does Aurora B do?

A

It is important for bipolar spindle attachment, the spindle checkpoint, and monitoring chromosomal segregation.

53
Q

What does Aurora C do?

A

It localizes to the spindle poles late in mitosis.

54
Q

Growth signal autonomy is one of the hallmarks of cancer. What is this chapter did you learn that causes this?

A
  1. There are mutations within the GF signalling pathway
  2. There are mutations in the genes that code for cell cycle proteins
55
Q

There is a mutation within cdk 4 that blocks binding to INK 4 inhibitors in some melanomas.

What will this result in?

A

CDK will never be able to be inactivated.

56
Q

There is a chromosomal translocation that involves the overexpression of cdk6 seen in some leukemias.

What would be the result?

A

CDK6 would be more easily activated.

57
Q

There is overexpression via gene amplification in breast cancer and squamous cell carcinomas.

What is the result?

A

The cell cycle moves forward much easier.

58
Q

There is a deletion of the p16 gene is mesothelioma and pancreatic carcinoma.

What is the result?

A

There is no way to turn off CDKs that are inhibited by the p16 (INK) inhibitors.

59
Q

What is the most common characteristic of human solid tumors?

A

Aneuploidy.

60
Q

What can aneuploidy be caused by?

A
  1. Defective centromeres
  2. Improper cytokinesis
  3. Changes in the mitotic checkpoint
  • weakened if there are individual components are missing
61
Q

What is mosaic variegated aneuploidy?

What is it caused by?

A

It is when some cells have the normal amount of chromosomes, but others display varied aneuploidy

It is caused by mutations in genes that code for checkpoint proteins.

62
Q

CDKs are overexpressed in many cancers.

What is Flavopiridol?

What does it do?

How is Flavopiridol given?

A

It is the first cdk inhibitor.

It is a competitive inhibitor of cdk activity that targets the ATP binding site.

It will induce cell cycle arrest at G1/S and G2/M

Given via IV

63
Q

What would chk1 and chk 2 inhibitors do?

A

They would prevent cell cycle arrest, because normally=

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