PCB4234 Exam 2

What is the initial event in intracellular signaling?

a) Protein-protein interaction

b) Post-translational modification

c) Ligand binding to a cell surface receptor

d) Gene expression

C

Which of the following is NOT a –crine mechanism of intercellular signaling?

a) Autocrine

b) Paracrine

c) Endocrine

d) RPTK

D

What is crucial for relaying signals within a cell?

a) Protein-protein interactions (PPI)

b) Gene expression

c) DNA replication

d) Glycosylation

A

What is key to pleiotropic signal transduction?

a) Protein-protein interactions

b) Post-translational modification (PTM)

c) Gene silencing

d) mRNA splicing

B

What can be the 'ultimate molecular destiny' of signal transduction?

a) Protein phosphorylation

b) Receptor binding

c) Gene expression

d) mRNA translation

C

Which of the following is an example of an extracellular stimulus?

a) Protein kinase

b) GTPase

c) Growth factor

d) Adaptor protein

C

What is the result of extracellular stimuli interacting with their receptors?

a) Changes in DNA sequence

b) Modifications of intracellular proteins

c) Direct alteration of cellular function

d) Immediate cell death

B

What is an example of intracellular signaling?

a) ErbB signaling

b) Autocrine signaling

c) Paracrine signaling

d) Endocrine signaling

A

What type of receptor is RPTK?

a) Receptor protein tyrosine kinase

b) G-protein coupled receptor

c) Ligand-gated channel

d) Interferon receptor

A

What is the function of PTKs in integrin signalling?

a) To bind ligands

b) To transduce signals

c) To modify DNA

d) To activate GTPases

B

What is the role of the Gly12 residue in Ras protein?

a) Activating GTPase activity

b) Keeping GTPase dormant

c) Binding to EGFR

d) Phosphorylating PI3K

B

What does PI3K phosphorylate to form PIP3?

a) Akt

b) PIP2

c) PTEN

d) Ras

B

What is the function of PTEN?

a) To activate Akt

b) To counter-regulate Akt activity

c) To phosphorylate PIP2

d) To bind to Ras

B

What is the GEF activity associated with in GPCR pathways?

a) Effectors

b) Transmembrane and cytoplasmic domain of the receptor

c) GAPs

d) RGSs

B

What is the GAP activity associated with in GPCR pathways?

a) The receptor

b) G-GTP

c) Effectors (RGSs)

d) Transmembrane domain

C

What is a characteristic of 'dual address' signaling proteins?

a) They only function in the cytoplasm

b) They travel between subcellular locations to transduce signals

c) They are only involved in gene expression

d) They modify DNA directly

B

What is the role of adaptor proteins in signaling pathways?

a) To serve as interacting bridges

b) To directly modify downstream proteins

c) To initiate gene expression

d) To degrade signaling molecules

A

What is the ultimate outcome of the EGFR-mediated signaling pathway?

a) Protein degradation

b) Lipid modification

c) Gene expression

d) Receptor internalization

C

What characterizes oncogenic signaling in terms of cellular life and death?

a) Decreased life and increased death

b) Increased life and decreased death

c) Balanced life and death

d) No change in life or death

B

What is the primary function of tumor suppressor genes (TSGs)?

a) To promote cell proliferation

b) To activate oncogenes

c) To restrain cell proliferation

d) To induce angiogenesis

C

What is required for the phenotypes of some tumors, according to the source?

a) Activation of multiple proto-oncogenes

b) Loss of tumor-suppressing gene function

c) Increased DNA transfer efficiency

d) Hyperactivation of a single proto-oncogene

B

How can the loss of a TSG's function from a cancer cell be rescued?

a) By introducing an oncogene

b) By fusing the cancer cell with a normal cell

c) By increasing DNA methylation

d) By inhibiting protein translation

B

According to the 'two-hit hypothesis', what must occur in familial retinoblastoma for a tumor to form?

a) Two random mutations in the RB allele before conception

b) One inherited mutated RB allele and one random mutation after conception

c) Two random mutations in the RB allele after conception

d) No mutations are required; it is purely hereditary

B

According to the 'two-hit hypothesis', what must occur in sporadic retinoblastoma for a tumor to form?

a) One inherited mutated RB allele and one random mutation after conception

b) One random mutation in the RB allele before conception

c) Two independent somatic mutations after conception

d) No mutations are required; it arises spontaneously

C

What is LOH an abbreviation of?

a) Loss of Homology

b) Locus of Heterogeneity

c) Loss of Heterozygosity

d) Level of Homogeneity

C

What is mitotic recombination?

a) Homologous recombination between two chromatids

b) Non-homologous end joining

c) DNA replication without cell division

d) Transcription of mRNA

A

What is gene conversion?

a) DNA polymerase using homologous chromosomal DNA as a template during replication

b) RNA polymerase switching to DNA synthesis

c) Conversion of a proto-oncogene to an oncogene

d) Direct conversion of one gene into another

A

What is hemizygosity?

a) Duplication of a chromosome

b) Chromosomal deletion leading to loss of one allele

c) Mutation in both alleles of a gene

d) Inversion of a chromosomal segment

B

What is the result of epigenetic hypermethylation of a TSG promoter?

a) Increased gene expression

b) DNA amplification

c) Functional LOH

d) Increased protein translation

C

What is RFLP analysis used for?

a) Sequencing entire genomes

b) Tracking the inheritance of DNA sequences and identifying LOHs

c) Measuring protein phosphorylation

d) Analyzing RNA splicing patterns

B

What does SNP analysis help to do?

a) Measure telomere length

b) Identify protein-protein interactions

c) Rapidly map TSGs with LOHs

d) Quantify mRNA levels

C

What is a common epigenetic mechanism for inactivating TSGs in cancer cells?

a) Histone acetylation

b) Promoter methylation

c) DNA replication

d) Increased protein translation

B

What does the APC TSG normally do?

a) Promotes angiogenesis

b) Serves as a brake on -catenin signaling

c) Activates Ras

d) Inhibits apoptosis

B

What is the consequence of loss of Apc gene function?

a) Decreased cell proliferation

b) Constitutive activation of -catenin signalin

c) Increased DNA repair

d) Decreased angiogenesis

B

What is the role of pVHL in the presence of oxygen?

a) Mediates ubiquitylation and degradation of HIF1α

b) Stabilizes HIF1α

c) Activates VEGF

d) Inhibits angiogenesis

A

What happens to HIF1α in the absence of pVHL, even with oxygen?

a) It is degraded

b) It is accumulated

c) It is ubiquitylated

d) Its expression is decreased

B

What is the function of the cell cycle clock?

a) To replicate DNA

b) To govern cell growth, division, proliferation, differentiation and senescence

c) To repair damaged DNA

d) To initiate apoptosis

B

What are cell cycle checkpoints?

a) Monitoring mechanisms ensuring proper completion of each phase

b) Points where cells undergo apoptosis

c) Locations of DNA replication

d) Sites of protein synthesis

A

What is the restriction point (R-point) in the cell cycle?

a) A decision point for the cell to continue, remain in G1, or enter G0

b) The point where DNA replication begins

c) The point where cells commit to apoptosis

d) The start of mitosis

A

What is the function of cyclins in the cell cycle?

a) To phosphorylate DNA

b) To inhibit CDK activity

c) To direct CDKs to the right substrates

d) To degrade proteins

C

What do CDK inhibitors (CDKIs) do?

a) Inhibit the activities of cyclin-CDK complexes

b) Activate DNA replication

c) Promote cell growth

d) Initiate apoptosis

A

What is the function of pRb in relation to the R-point?

a) To activate the cell cycle

b) To serve as a guardian of the R-point gate

c) To inhibit DNA replication

d) To initiate apoptosis

B

What happens when pRb is hyperphosphorylated?

a) E2F transcription factors are released

b) The cell cycle is inhibited

c) DNA replication stops

d) Apoptosis is initiated

A

What is the role of E2F transcription factors?

a) Driving force of R-point transition

b) Inhibiting cell growth

c) Promoting DNA repair

d) Activating apoptosis

A

What is the effect of Myc overexpression on the R-point transition?

a) It inhibits R-point transition

b) It can bypass the need for mitogens to impose R-point transition

c) It promotes DNA repair

d) It initiates apoptosis

B

What is the role of Id proteins in cell differentiation?

a) To promote differentiation

b) To inhibit differentiation

c) To activate apoptosis

d) To repair damaged DNA

B

What does Skp2 do?

a) Activates p27

b) Mediates p27 degradation

c) Inhibits cyclin D1

d) Promotes DNA repair

B

What is a potential consequence of too many activators or too few inhibitors of the R-point regulating machinery?

a) DNA repair

b) Apoptosis

c) Human cancer

d) Cellular senescence

C

What is the role of p53 in response to metabolic disorders or genetic damages?

a) To promote cell proliferation

b) To act as a police officer, correction officer, and death executioner

c) To initiate DNA replication

d) To inhibit cell growth

B

What was p53 initially thought to be?

a) A protooncogene

b) A tumor suppressor gene

c) A DNA repair enzyme

d) An apoptotic factor

A

What is a key characteristic of mutant p53 proteins?

a) They activate DNA repair

b) They act as dominant-negative mutants

c) They promote cell differentiation

d) They inhibit apoptosis

B

What does MDM2 do to p53?

a) Activates p53

b) Ubiquitylates p53, leading to degradation

c) Phosphorylates p53

d) Inhibits p53 transcription

B

What is the effect of DNA damage on p53 protein levels?

a) Decreased p53 levels

b) Increased p53 levels

c) No change in p53 levels

d) Increased p53 degradation

B

What can increased p53 levels lead to?

a) DNA replication

b) Cell growth

c) Cytostatic state, senescence, or apoptosis

d) Angiogenesis

C

What is the role of p14ARF?

a) To activate MDM2

b) To inhibit MDM2, stabilizing p53

c) To promote cell proliferation

d) To initiate DNA replication

B

What is autophagy?

a) Programmed cell death

b) Cellular self-eating

c) DNA repair mechanism

d) Promotion of cell growth

B

What is the role of Bcl-2 family proteins?

a) To balance pro-apoptotic and anti-apoptotic signals

b) To promote cell proliferation

c) To activate DNA replication

d) To inhibit cell growth

A

What happens during apoptosis?

a) Cytochrome c is released from mitochondria

b) DNA replication is activated

c) Cells undergo necrosis

d) Cells increase in size

A

What is the apoptosome?

a) A complex that activates initiator caspases

b) A mitochondrial channel

c) A DNA repair complex

d) A protein degradation machine

A

What is the function of caspases in apoptosis?

a) To inhibit apoptosis

b) To cleave death substrates and execute apoptosis

c) To promote cell proliferation

d) To repair damaged DNA

B

Which of the following represents intercellular signaling via physical contact?

a) Autocrine

b) Paracrine

c) Endocrine

d) Juxtacrine

D

What is the ultimate outcome of intercellular signaling?

a) Protein phosphorylation

b) Activation of cell surface receptors

c) Gene expression

d) Modification of signaling proteins

C

Which of the following is NOT a component of a signal transduction pathway?

a) Extracellular stimuli

b) Cell surface receptors

c) Intracellular protein modifications

d) Ribosome assembly

D

What type of receptor is EGFR?

a) Receptor tyrosine kinase

b) G-protein coupled receptor

c) Ligand-gated ion channel

d) Nuclear receptor

A

What can result from constitutive activation of EGFR?

a) Cell cycle arrest

b) Apoptosis

c) Oncogenic signaling

d) DNA repair

C

Which of the following is NOT a common characteristic of cancer cells' signaling abnormalities?

a) Constitutive activation

b) Altered interactions

c) Pleiotropic effects

d) Decreased protein synthesis

D

Which protein is activated downstream of EGFR?

a) Akt

b) Ras

c) PTEN

d) MDM2

B

What type of protein regulates the Ras cycle?

a) Kinases and phosphatases

b) GEFs and GAPs

c) Adaptor proteins

d) Death receptors

B

What is the usual function of TSGs?

a) To promote cell proliferation

b) To restrain cell proliferation

c) To induce angiogenesis

d) To promote metastasis

B

What type of action do TSGs generally have?

a) Dominant

b) Recessive

c) Co-dominant

d) Epistatic

B

What does the 'two-hit hypothesis' explain?

a) The activation of oncogenes

b) How TSG inactivation contributes to tumors

c) The process of metastasis

d) The mechanism of DNA repair

B

What is the result of DNA polymerase using a homologous chromosome carrying a mutation as a template?

a) DNA amplification

b) Gene conversion

c) Chromosomal translocation

d) Increased transcription

B

Which process can cause LOH through chromosomal deletion?

a) Hemizygosity

b) Mitotic recombination

c) Gene conversion

d) DNA methylation

A

Which of the following is NOT an example of a TSG?

a) Rb

b) P53

c) APC

d) Ras

D

What does the APC TSG regulate?

a) Ras activity

b) β-catenin signaling

c) HIF1α activity

d) Cell cycle progression

B

What is a major function of the cell cycle clock?

a) To replicate DNA

b) To govern cell growth, division, and differentiation

c) To repair damaged DNA

d) To initiate apoptosis

B

What is a cell cycle checkpoint's primary role?

a) To initiate DNA replication

b) To ensure proper completion of each phase

c) To activate apoptosis

d) To promote cell growth

B

Which point determines whether cells continue through the cycle, remain in G1, or enter G0?

a) S phase

b) M phase

c) Restriction point (R-point)

d) G2 phase

C

What is the role of CDKs in the cell cycle?

a) They are the catalytic units that drive progression

b) They inhibit cyclin activity

c) They degrade proteins

d) They repair damaged DNA

A

Which cyclin-CDK complex is inhibited by the INK4 family of CDKIs?

a) E-CDK2

b) A-CDK2

c) D-CDK4/6

d) B-CDC2

C

What does pRb regulate in the cell cycle?

a) DNA replication

b) Apoptosis

c) E2F transcription factors

d) Protein synthesis

C

What is the effect of mitogen stimulation on pRb?

a) It activates pRb

b) It leads to hypophosphorylation of pRb

c) It degrades pRb

d) It inhibits pRb

B

What is a major function of p53?

a) To promote cell proliferation

b) To activate oncogenes

c) To act as a genome guardian and induce apoptosis

d) To promote angiogenesis

C

How are p53 levels usually controlled in normal cells?

a) By increased transcription

b) By ubiquitylation and degradation

c) By phosphorylation

d) By activating DNA repair

B

What is the role of apoptosis in the context of oncogene activation?

a) To promote cell proliferation

b) To activate DNA repair

c) To act as a check on uncontrolled proliferation

d) To promote angiogenesis

C

What is the function of the INK4 family of CDK inhibitors?

a) To inhibit D-CDK4/6 complexes at G1

b) To promote DNA replication

c) To activate apoptosis

d) To inhibit all cyclin-CDK complexes

A

What is the role of E2F transcription factors in the cell cycle?

a) To drive R-point transition

b) To inhibit cell growth

c) To promote DNA repair

d) To activate apoptosis

A

What is the role of MDM2 in regulating p53?

a) To activate p53
b) To ubiquitylate p53 and promote its degradation

c) To phosphorylate p53

d) To inhibit p53 transcription

B

What is a common characteristic of cancer cells' strategies to evade apoptosis?

a) To decrease expression of anti-apoptotic proteins

b) To promote DNA repair

c) To increase expression of anti-apoptotic proteins

d) To activate cell cycle checkpoints

C

What is the significance of the R-point in the cell cycle?

a) It's where DNA replication begins

b) It's where mitosis occurs

c) It's a critical decision point for cell cycle progression

d) It's where cells undergo apoptosis

C

What is the effect of TGF-β signaling on Myc transcription?

a) It activates Myc transcription

b) It represses Myc transcription

c) It has no effect on Myc transcription

d) It degrades Myc protein

B

Which of the following accurately describes the two-hit hypothesis in the context of tumor suppressor genes?

a) Activation of two oncogenes is required for tumor formation.

b) One activating and one inactivating mutation are needed for tumor development.

c) Two inactivating mutations in a tumor suppressor gene are required for tumor formation.

d) One mutation is sufficient due to the dominant-negative effect of mutated tumor suppressor genes.

C

What is the primary mechanism by which pRb controls the cell cycle?

a) By directly phosphorylating cyclins.

b) By degrading CDK inhibitors.

c) By binding to and inhibiting E2F transcription factors.

d) By promoting DNA replication.

C

How does DNA methylation contribute to tumorigenesis?

a) By activating oncogenes through increased transcription.

b) By silencing tumor suppressor genes through epigenetic modifications.

c) By increasing genetic stability through enhanced DNA repair mechanisms.

d) By promoting chromosomal stability through enhanced telomere maintenance.

B

Which of the following best describes the role of Myc in cancer development?

a) It acts as a tumor suppressor by promoting cell cycle arrest.

b) It acts as an oncogene by promoting cell cycle progression and proliferation.

c) It plays a role in DNA repair, preventing genetic instability.

d) It promotes cell differentiation, thus preventing uncontrolled growth.

B

What is the role of post-translational modifications (PTMs) in cancer signaling?

a) To directly alter the DNA sequence for gene expression.

b) To ensure that protein-protein interactions never occur.

c) To allow for pleiotropic signal transduction.

d) To completely halt signal transduction.

C

What is the function of the anaphase promoting complex (APC)?

a) Promotes cell growth by stimulating ribosome assembly.

b) Activates receptor tyrosine kinases.

c) Regulates β-catenin signaling

d) Stimulates apoptosis in cancerous cells.

C

What is one way cancer cells counteract apoptosis to ensure their survival?

a) Enhancing the expression of pro-apoptotic proteins such as Bax and Bak.

b) Increasing the activity of caspases, leading to cell death.

c) Decreasing the expression and/or activity of pro-apoptotic proteins or increasing the expression and/or activity of anti-apoptotic proteins.

d) Promoting high levels of autophagy to recycle damaged cellular components.

C

What process does the pVHL tumor suppressor gene regulate to prevent tumor formation?

a) Stimulates β-catenin degradation.

b) Promotes cell cycle arrest by activating pRb.

c) Inhibits HIF1α activity, preventing increased angiogenesis.

d) Repairs damaged DNA by recruiting DNA repair enzymes.

C

What are the key roles of p53 in response to DNA damage?

a) DNA replication, promoting uncontrolled cell growth

b) Cell growth, promoting protein synthesis

c) Cell cycle arrest, DNA repair, and apoptosis

d) Angiogenesis, stimulating blood vessel growth

C