Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

cancer > cell cycle 5: signalling pathways > Flashcards

cell cycle 5: signalling pathways Flashcards

1
Q

what do cells do in the absence of growth signals?

A

enter G0 phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the key components of signalling pathways?

A

kinases: regulate enzyme activity via protein phosphorylation
phosphatases: remove phosphates
adapter proteins: bring interactive partners together
GTP-binding proteins: regulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what do signalling cascades allow?

A
  • response to extracellular factors
  • signal amplification
  • signal integration
  • modulation by other pathways
  • regulation of divergent responses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is c-Myc?

A

transcription factor that stimulates cell cycle gene expression to cause entry to cell cycle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is the signalling pathway for mitogenic growth factor?

A

binds to receptor -> activates receptor protein tyrosine kinase -> small Gprotein (Ras) -> kinase cascade -> immediate early genes stimulate expresion of other genes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is the signalling pathway for peptide growth factor?

A

growth factors occur as dimers -> bring the 2 receptors close to each toher -> multiple tyrosine phosphorylations occur -> activated tyrosines act as docking points for adapter molecules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what do adaptor proteins do?

A

tyrosine phosphorylation provides docking sites for adaptor proteins -> allows protein-protein interactions to bring together proteins

eg Grb2 protein with SH3-SH2-SH3 domains (SH3 binds to proline richareas, SH2 binds to phosphorylated tyrosines)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what do GTP-binding proteins do?

A

act as molecular switches

- when signal arrives, GDP is released and GTP binds to activate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is the ERK cascade?

A

chain of proteins in the cell that communicate a signal from a surface receptor to DNA in nucleus Raf -> MEK -> ERK -> protein activation and upregulation of regulatory proteins eg c-Myc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are cyclins?

A

proteins transiently expressed at specific points in cycle to activate kinases

  • M-cyclins produce M-phase promoting factor -> trigger mitosis
  • S-cyclins produce start kinases to trigger DNA replication machinery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what do cyclin-dependent kinases do?

A
  • control cell cycle
  • present in proliferating cells throughout cell cycle
  • activity regulated by interaction with cyclins & phosphorylation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what do activated CDKs do?

A

phosphorylate proteins to drive cell cycle progression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

how is CDK activated?

A
  1. CDK and cyclin bind to form inactive cyclin
  2. CDK-activating kinase and inhibitory kinase both phosphorylate CDK (donating inhibitory & activating phosphate group)
  3. phosphatase activates CDK by removing inhibitory phosphate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what cyclins and CDKs are required from G0-G1?

A

c-Myc stimulates transcription of other genes eg cyclin D -> activates CDK4/6 to stimulate cyclin E synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what cyclins and CDKs are required at the metaphase-anaphase checkpoint?

A

CDK1/cycB pauses mitosis -> kinetchores fully attach -> cyclin B degraded -> CDK1 inactivated -> mitosis continues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is MPF?

A

mitosis promoting factor

- complex of CDK1 & cyclin B

17
Q

how is MPF activated?

A

(CDK phosphorylated twice ->) phosphatase Cdc25 removes inhibitory phosphate -> MPF phosphorylates Cdc25 -> Cdc25 activated -> positive feedback loop

18
Q

what is the retinoblastoma gene?

A

tumour suppressor gene

19
Q

what happens during retinoblastoma protein regulation?

A

when CDKs phosphorylate Rb proteins they become inactivated -> this allows transcription factors to bind and upregulate genes such as cyclin E

20
Q

what is E2F?

A

transcription factor that upregulates:

  • proto-oncogenes (eg c-Myc)
  • cell cycle genes (eg CDK2/4, cyclin A/E)
  • DNA synthesis genes (eg DNA polymerase, thymidine kinase, thymidine synthetase)
21
Q

what are the types of CDK inhibitors?

A

INK4 family: G1 phase CKIs that inhibit CDK4/6 by displacing cyclin D

CIP/KIP family: inhibit all CDKs by binding to CDK/cyclin complex -> regulate S phase CDKs

22
Q

what is herceptin?

A

antibody against HER-2 (human epidermal growth factor) receptor - binds to extracellular domain of gf

23
Q

what is Grb2?

A

adapter protein that is always found bound to Sos

24
Q

what is sos?

A

set of genes that encode guanine nucleotide exchange factors
- Ras-activating protein

25
Q

what is Ras?

A

an oncogene

26
Q

what does sos do?

A

act on Ras subfamily of small GTPases
- brought up to membrane -> binds to Ras -> forces it to release GDP -> Ras released from sos -> Ras quickly binds another guanine nucleotide -> since GTP is much more abundant than GDP Ras is usually activated

27
Q

how can Ras be oncologically activated?

A

by mutations that increase the amount of active GTP-loaded Ras

cancer (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions