Brainscape's Knowledge GenomeTM

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


See full index

POM UNC > Cell Cycle > Flashcards

Cell Cycle Flashcards

1
Q

What are the phases of the cell cycle?

A

G0 (quiescent phase, active but no growth) G1 (growth, proteins being made) S (DNA synthesis) G2 (more growth) M (mitosis)

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

What is quiescence?

A

The state most living cells reside in. Active, operating, but not growing or proliferating.

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

What is senescence?

A

When telomeres run out a cell stops replicating and eventually is degraded.

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

Where do the major checkpoints for cell proliferation occur? Why at these locations?

A

Between G1-S, and between G2-M
DNA replication is irreversible, so a cell needs to be sure it wants and is ready to replicate DNA. Same with cell division.

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

What cyclins and CDKs are present at the transition from G1-S phase?

A

Cyclin D CDK4 work together to activate EF2 and transcribe a lot of RNA that’s used in Synthesis of new DNA

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

What cyclins and CDKs are present at the transition from G2-M phase?

A

Clycin B CDK 1

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

What cyclins and CDKs are present at the transition from S-G2 phase?

A

CDK 2 Cyclin E

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

What protein acts on DNA to encourage S phase?

A

EF2

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

What protein acts on DNA to encrouage G1 phase?

A

c-myc

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

What happens to initiate G1 phase?

A

extracellular cues will activate a GPCR or RTK or a cytokine receptor. These receptors induce a signaling cascade that ultimately phosphorylates c-myc. C-myc induces transcription of various proteins that encourage the cell to grow, or are part of a cell’s growth. C-myc binds to the E promoter box on DNA.

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

What happens to initiate S phase?

A

Cyclin D and CDK 4 bind. CDK4 is naturally available in the cell but can’t be active without Cyclin D. CDK4-cyclin D complex phosphorylates Rb, which unbinds from EF2. EF2 is able to induce transcription of key proteins for S phase initiation. Cyclin D-CDK4 are active throughout G1

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

What happens to complete S phase?

A

DNA polymerase copies new strands of DNA. It needs DNA helicase to open up double-stranded DNA. Cyclin E & CDK 2 & Cyclin A bind and work to guarantee that helicase does not bind to any single stranded DNA that’s already been replicated. Cyclin A & CDK 2 & Cyclin E work together to activate helicase. Single Stranded DNA Binding Proteins are what indicate to the cell that DNA replication is still incomplete.

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

What is Rb?

A

Rb was discovered in riboblastoma. It’s a tumor suppressor protein that keeps EF2 from actively transcribing cells. When Rb is phosphorylated (by CDK4 Cyclin D) it disengages from EF2 and EF2 is able to act as a positive transcription factor.

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

What is c-myc?

A

C-myc is a transcription factor, often used as the effector molecule at the end of signaling cascades, particularly for cascades that are trying to induce G1 phase cell grown.

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

What is a tumor suppressor gene?

A

A defensive gene. Tumor suppressor genes keep cellular processes in check. They might regulate growth, proliferation, cell-to-cell interactions, angiogenesis. A mutation in a single tumor suppressor gene is often not enough to cause a change in cellular behavior, because they’re present on both chromsomes. Enough mutant tumor suppressor genes leads to cancerous cells. Mutations in Rb (always phosphorylated, or maybe deleted). If you delete one Rb gene you still have another.

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

What is an oncogene?

A

Oncogenes are offensive cancerous genes. They actively increase the likelihood of a cell becoming cancerous. A single oncogene is enough to induce a change, because it’s an active change, not an absence. If you delete one gene (maybe a tumor suppressor gene) the other gene could still function. But if you add an oncogene there’s immediate change in cellular behavior. (cylcin D overexpression, ras not needing to bind to RTK)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are some CDK inhibitors? Which CDKs do they act on?

A

P(protein) 16 (size in kDaltons)
P16, P21, P53
P16 competitively binds with CDK4, against cyclin D. So P16 stops/limits entry into S phase.
P21 blocks CDK1 (M phase) CDK2 (S, G2 phase), by binding to the CDK-cyclin dimer and blocking the catalytic cleft.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is Rb’s relationship with E2F?

A

Rb is naturally bound to E2F and inhibits E2F from acting on DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How are cyclin concentrations managed over the course of the cell cycle?

A

Cyclins are managed by ubiquitination. Cyclins are naturally not phosphorylated, but once they begin activity in the cell they’ll have phosphates bound. Ubiquitin protein identifies these active cyclins and marks them for degradation by proteasomes. So as a cyclin becomes more and more active it increases the rate of decay.

20
Q

When does DNA helicase bind to DNA? Why can it not bind in other phases of the cell cycle?

A

DNA helicase actually binds to DNA during G1 phase, even though replication doesn’t start until S phase. This is because we only want each strand of DNA to be copied once. If you go willy-nilly you’ll end up with overexpression of certain genes, underexpression of others. No good. DNA helicase’s activity is managed by CDK2, Cyclin E, and Cyclin A

21
Q

What pair of proteins ensure DNA helicase avoids binding to previously bound strands of DNA?

A

CDK2, Cyclin A & Cyclin E

22
Q

What pair of proteins activate DNA helicase?

A

CDK2, Cyclin A & Cyclin E

23
Q

What role does ubiquitination play in the regular cell cycle?

A

It’s used in two key areas: the management of cyclins (binds to and ultimately degrades all cyclins with phosphate groups) and in the regulation of p53. Mdm2 is normally bound to p53 and attracts ubiquitin. p53 is ultimately decayed from this. BUT! in situations of DNA damage or incomplete replication p53 is phosphorylated and kicks off Mdm2

24
Q

What are some common ways that the function of EF2 is mutated in cancer?

A

If you delete Rb, or mutate Rb to seem phosphorylated, or increase presence of Cyclin D, CDK4 or convince CDK4 it doesn’t need Cyclin D

25
Q

What are some common ways the function of p53 is altered in cancers?

A

If you delete Mdm2, or mutate p53 so it thinks it’s phosphorylated

26
Q

How does the cell respond to DNA damage?

A

The cell will send signals that ultimately phosphorylate p53. P53 will kick off mdm2 and activate p21. p21 will inhibit cyclin/CDK from activating transcription of proteins. This keeps cell from replicating.

27
Q

What is mdm2?

A

A factor that binds to and marks p53 for degradation

28
Q

What is p53 used for?

A

p53 is used to regulate cells with incomplete DNA replication or DNA damage.

29
Q

What is p16 used for?

A

P16 is used to block CDK4 from binding Cyclin D, stopping the transition into the S phase

30
Q

What is p21 used for?

A

Used to stop CDK1 and CDK2 protein complexes from activating transcription by binding and sterically hindering any other molecules from binding the CDK/cyclin complex. CDK1 is M phase transition, CDK2 is S phase.

31
Q

What are DNA tumor viruses?

A

A virus that carries oncogenes. The virus carries oncogenes so it can stimulate the cell’s production of necessary cellular building blocks. The virus doesn’t have any native cellular mechanisms so it has to steal from the host cell. To do this is easiest when the host cell is trying to proliferate (more materials available)

32
Q

How does HPV lead to cervical cancer?

A

HPV leads to two key mutations. E7 is a protein (transcribed from viral DNA) that convinces Rb to leave EF2, allowing EF2 to transcribe DNA unchecked. HPV also transcribes for E6, a protein that binds to p53. It and marks p53 for death. This means p53 can’t stop DNA damage from proliferating. These alone are not enough to cause cancer (that’s why it doesn’t start right when people start having sex) but it is enough to start cells down the path towards cancer.

33
Q

What is the difference between an immortal and cancerous cell?

A

Immortal cells have an error in telomerase, and maybe a couple other errors, but they still require external influences to proliferate. They don’t pile up on each other, but are limited by spatial requirements. They have a slightly unstable genome (telomerase and other things could be mutated) but it hasn’t gone crazy like in cancer.

34
Q

Why do targeted cancer drugs often lead to recurrence?

A

If you identify the most prevalent type of cancer cell and target its characteristics, you can crush that cancer. But there are other types of cancer hiding around the body (either earlier or later mutations) and these will then begin to proliferate.

35
Q

What are hallmarks of cancerous cells?

A

Angiogenesis, immortal telomerase, metastasis stabilized, mutant regulatory proteins in cell cycle, avoiding immune destruction, tumor promoting inflammation, resisting cell death, deregulating cellular energetics (mitochondria just book it)

36
Q

What is cdc25?

A

cdc25 is a phosphatase that activates CDK1 Cyclin B, the cyclin/cdk complex active for M phase to occur. cdc25 is inhibited by a signal cascade initiated by SSBP, telling the cell that there is still unreplicated DNA. SSBP interacts with detector, which interacts with 2 kinases, which inhibit cdc25.

37
Q

How is incomplete replication regulated by the cell?

A

SSBP are recognized by detector proteins. A signaling cascade results in inhibition of cdc25, which is a phosphatase key in activating Cyclin B CDK1 (M phase)

38
Q

What is an unstable genome?

A

point mutations, insertions, deletions, failed chromosome separation, etc.

39
Q

What signaling cascades often activate c-myc?

A

Ras, RTK, Cytokine Receptors

40
Q

CDKs are always present in the cell. Why are they not active?

A

They need to bind to Cyclins before they can phosphorylate their end targets

41
Q

What kind of environments can pull a cell out of quiescence?

A

Tissue damage, empty space around the cell, hormone signals from other cells.

42
Q

What is retinoblastoma? How is it inherited?

A

cancer in the retina. It’s inherited by having one mutant chromosome passed to the child, and a second chromosome accidentally mutate to have no rb. Without rb cancer grows rapidly.

43
Q

What are some different ways to induce production of S phase-necessary proteins?

A

Delete Rb. Delete P16. Trick cdk4 to acting without cyclin

44
Q

What are ways that phosphate groups can activate or inhibit the cyclin-cdk complex?

A

Phosphate on cyclin can inhibit, phosphate on CDK activator loop can activate

45
Q

What’s the difference between cell growth and cell proliferation?

A

Cell growth means getting bigger. Cell proliferation means splitting

POM UNC (21 decks)

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