Cell cycle Flashcards

1
Q

a) In the cell cycle, what occurs after completion of mitosis
b) What loss of function mutational event would contribute most strongly to genetic instability and the development of cancer
c) How does angiogenesis contribute to cancer development
d) How do chemical carcinogens lead to cancer
e) How does cyclin B control a CDK

A

a) Phosphorylation of the retinoblastoma protein
b) Loss of function of the retinoblastoma protein
c) It facilitates the supply of nutrients and oxygen to tumours and their metastases
d) They form covalent adducts with histone H3 thus exposing genes to excessive transcription
e) Cyclin B in complex with CDK1 is essential for CDK1 kinase activity

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2
Q

a) How is β-catenin targeted for destruction via the proteasome
b) What inhibits the phosphatase CDC25, and where in the cell cycle does this happen
c) What inhibits CDK4/6 and arrests cells, and where in the cell cycle does this happen
d) What initiates apoptosis in response to DNA damage by ionising radiation
e) What activation occurs in S-phase of the cell cycle

A

a) Adenomatous Polyposis Coli (APC) together with other proteins
b) CHK1/2 inhibit CDC25 at the G2/M checkpoint
c) INK4 proteins inhibit CDK4/6 and arrest cells in G1
d) p53
e) CDK2/cyclin A complex activation

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3
Q

a) Following DNA damage, what does activation of ATM lead to
b) What is the normal order of chromosomal events in meiosis
c) What is involved in entry to S phase of the normal cell cycle
d) What do meiotic crossovers occur between
e) Does the frequency of crossovers differ between different chromosome pairs

A

a) Leads to phosphorylation of p53
b) Replication of chromosomes in the diploid nucleus. Alignment of homologous pairs of chromosomes on the metaphase plate. Pairing and synapsis of homologous chromosomes. Segregation of sister chromatids to opposite poles. Segregation of homologous chromosomes to opposite poles
c) Separation of previously-paired chromatids
d) Occur between chromatids on homologous chromosomes, but not between sister chromatids
e) Yes

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4
Q

a) Does the frequency of crossovers differ between male and female humans
b) Is the recombination frequency between markers at opposite ends of the chromosome is 100%
c) Can there be more than one crossover between each pair of homologous chromosomes in each meiosis
d) What does SOS cause
e) What mutations can confer susceptibility to cancer

A

a) Yes
b) No
c) Yes
d) SOS causes RAS to exchange bound GDP for GTP
e) Inherited single allele mutations in tumour suppressor genes

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5
Q

a) What are CHK1/2 and their functions
b) What can DNA damage lead to
c) What targets p53 for degradation
d) What does p53 phosphorylation lead to increased levels in
e) What happens to retinoblastoma protein (RB1) during progression into G1-phase

A

a) They’re kinases that inhibit CDC25 and prevent progress through the G2/M checkpoint
b) Leads to an increase in ATM kinase activity
c) MDM2
d) Leads to increased levels of p21WAF1
e) Undergoes phosphorylation

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6
Q

a) What does AKT phosphorylate
b) In the WNT signalling pathway, where does E. β-catenin translocate to
c) What protein is most closely associated with oncogenic mutation
d) What protein is most closely associated with loss of normal function leading to an increased risk of chromosome non-disjunction
e) What protein is most closely associated with an inherited predisposition to cancers arising from a mutation that causes loss of a G1-S phase checkpoint

A

a) The mammalian target of rapamycin (mTOR) protein
b) Translocates to the nucleus from a location close to the plasma membrane
c) RAS
d) Adenomatous polyposis coli gene product (APC)
e) p53

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7
Q

a) What activates apoptosis by counteracting the phosphorylation of phosphatidylinositols by PI3K
b) What is phosphorylated by CDK1 during chromatin condensation
c) What regulates exit from mitosis through its ubiquitin ligase activity

A

a) PTEN
b) Histone H1
c) Anaphase promoting complex (APC/C)

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8
Q
A
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