Brainscape's Knowledge GenomeTM

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


See full index

Foundations Week 7 > Cell Cycle 2 > Flashcards

Cell Cycle 2 Flashcards

1
Q

High levels of cyclin correspond to what?

A

high activity of cyclin, Cdk

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

What are the three Cdks we need to know? What are they involved in?

A
  • Cdk1 (M, but also S for Cdk1/2-cycA)
  • Cdk2 (G1/S transition, S, possibly M)
  • Cdk4 (G1)
  • involved in cell cycle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

The active site of Cdks is blocked in the absence of what?

A

cyclin

*note, cyclin can also interact directly with Cdk substrates

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

Cyclins are classified into four different groups based on what?

A

when they function in the cell cycle and the timing of their expression

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

What are each of the cyclins corresponding to each phase and what Cdks do they bind to?

A

G1: cycD, binds to Cdk4
G1/S: cycE, binds Cdk2
S: cycA, binds Cdk2
M: cycB, binds Cdk1

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

cycB corresponds to what phase, binds what Cdk?

A

M phase, binds Cdk1

Cdk1-cycB

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

cycA corresponds to what phase, binds what Cdk?

A

S phase, binds Cdk2
Cdk2-cycA
Cdk1/2-cycA

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

cycE corresponds to what phase, binds what Cdk?

A

G1/S checkpoint, binds Cdk2

Cdk2-cycE

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

cycD corresponds to what phase, binds what Cdk?

A

G1 phase, binds Cdk4

Cdk4-cycD

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

Cyclins can interact directly with Cdk ______.

A

substrates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is required for full Cdk activity?

A

phosphorylation by the Cdk-activating kinases (CAKs)

Cdk7, forms trimer with cyclin H and Mat1

**

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Cdk binds cyclin, not going to get you full activity. What is needed for full activity?

A

phosphorylation by CAK

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Cdk inhibitors (CKIs) help suppress Cdk activity. In what phase are these important for?

A

G1 phase

*know p27 (inhibits G1/S and S-Cdks, activates cyclin D-Cdk4)

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

What is the E2F network?

A
  • they have DNA binding domains and drive expression of E2F network; and dimerization

**

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the job of the retinoblastoma protein?

A

to regulate E2F

fix

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

What happens if pRB does not act?

A
  • no control of E2F-dependent gene expression

* pRB keeps E2F form binding *** and DNA

16
Q

Mitogen

A

growth factor

17
Q

When cyc-Cdk acted on by mitogens, what happens?

A

fill in

18
Q

as soon as pRB is phosphorylated

A

E2F is made

fill

19
Q

What two responses occur secondary to double-strand break?

A

huge signal transduction

  • rapid response
  • delayed response
20
Q

ATM (kinase), phosphorylates another kinase (Chk2) which phosphorylates Cdc25A, causing something to be broken down
Cdk2-cyclin is kept inactive (no start)

A

fix/fill

diagram

22
Q

Immediate cell cycle arrest is caused by which response to a double-strand break?

A

rapid response

23
Q

ATM has two roles, what are they?

A
  • phosphorylate Chk2

- phosphorylate p53, making it stable and active

24
Q

If DNA cannot be repaired, what does p53 do?

A

illicits programmed cell death

25
Q

What is one of the most highly mutated?? thing in cancer?

A

p53

26
Q

What is the evolution of a tumor?

A
  • begins with mutations that provide a cell with competitive growth advantage
  • over many years, descendants of that mutant cells acquire additional mutations to overcome a variety of regulatory barriers that block cell proliferation
  • additional mutations promote genomic instability to enhance the rate of mutation
27
Q

What is the advantage of tumor cells?

A
  • no longer responds to growth factors, unregulated, can grow as much as it wants; gives it advantage over regular cells
  • can’t undergo programmed cell death
  • multiple mutations occur causing above changes and more

fill in
eventually, cell becomes malignant and invades other areas?

28
Q

What are oncogenes?

A
  • hyperactive cancer-promoting mutant gene
  • tend to be genetically dominant
  • normal gene version is called a proto-oncogene
29
Q

90% of all human cancers are carcinomas - what is this?

A

a malignant tumor of epithelia

probably because epithelial tissues proliferate throughout life

30
Q

know p16 NK4a?

A

old, aging cells express this
puts break on cell division
binds Cdk4 and inactivates that complex
it is a tumor suppressor gene

fix

30
Q

Many human cancers are associated with mutations in one component of what?

A

the pRB module

**
only one mutation in pRB module is necessary to drive cell cycle entry

Foundations Week 7 (10 decks)

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