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Mechanisms of Gene Regulation > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

Define/describe proto-oncogene

A

Normal gene, frequently linked to the regulation of cell proliferation; can be converted into an oncogene by overexpression or mutation

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2
Q

Define/describe oncogene

A

A gene whose protein product can make cells cancerous when it is overexpressed or mutated

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3
Q

Define/describe oncoprotein

A

Proteins encoded by oncogenes (dysregulated or activated genes) and have a potential to cause cancer

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4
Q

Define/describe retroviruses

A

A retrovirus has an RNA genome; replicates by making an RNA-DNA hybrid and then double-stranded DNA which gets integrated into host chromosomes

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5
Q

Define/describe transformation

A

The incorporation/transfer of viral/foreign DNA into host genome

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6
Q

Define/describe double minute chromosomes

A

Typically seen in tumors/for specific oncogenes, regions of DNA amplification that result in overexpression

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7
Q

Define/describe ErbA

A
  • Nuclear receptor family of TFs (hormone-dependent transcription)
  • Contains a region that can bind the thyroid hormone. After binding, the hormone-receptor complex induces transcription of thyroid hormone-responsive genes
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8
Q

Define/describe trans-splicing

A

Splicing reaction between two RNA molecules encoded by different genes, can produce chimeric RNA encoding a fusion protein

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9
Q

Define/describe tumor suppressor genes

A
  • Genes that encode proteins involved in the inhibition of cell growth/division
  • Also called anti-oncogenes or cancer preventers
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10
Q

Define/describe retinoblastoma protein

A
  • Rb-1
  • First identified tumor suppressor
  • Inhibits activation by TF E2F
  • Recruits HDACs and histone methylases
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11
Q

Define/describe wild-type

A

The “normal” allele or typical phenotype

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12
Q

Define/describe quenching

A
  • The blocking of activity
  • Ex: Rb “quenches” E2F’s activity, keeping chromatin closed and resulting in no transcription
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13
Q

Define/describe DNA tumor viruses

A

Viruses that encode proteins with oncogenic potential, disrupting normal cellular pathways

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14
Q

Define/describe haploid insufficiency

A

A disease in which one copy of a gene is mutated and the remaining wild-type copy cannot produce sufficient functional protein to prevent disease

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15
Q

Define/describe triplet repeat diseases

A

Diseases involving the abnormal amplification of a three base pair sequence

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16
Q

Define/describe RAN translation

A
  • Repeated associated non-AUG
  • Repeats hinder initiation at AUG
  • Abnormal proteins are produced
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17
Q

Define/describe interferon

A
  • A class of cytokines secreted by virus-infected cells and certain T cells
  • Induce antiviral responses by activating JAK/STAT pathway to turn on antiviral genes (proteins and miRNAs)
  • STAT heterodimer forms complex with IRF9 TF to run on target antiviral genes
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18
Q

Define/describe BRD4

A
  • Bromodomain protein
  • BRD4-NUT oncogenic fusion protein produces abnormally enhanced histone acetylation and opening in the chromatin of genes associated with growth stimulation
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19
Q

Define/describe designer zinc finger

A
  • Can be used as a drug therapy to alter gene transcription
  • Alpha helical region contacts DNA, allowing specific region of genome to be altered
  • Designer zinc fingers can be used to switch expression ON or OFF
20
Q

Define/describe RNA interference (RNAi)

A
  • Short RNA molecules which are complementary to a target mRNA can be produced and used to inhibit it post-transcriptionally
  • Therapeutic procedures involving artificial inhibitory RNAs can involve small RNAs complementary to the target mRNA which bind to it and induce its degradation or block its translation. Alternatively it can involve longer RNAs which are complementary to it and will therefore bind to it producing a double-stranded RNA molecule. This molecule will be cleaved to produce siRNAs which can bind to further copies of the target mRNA and induce its degradation
21
Q

What mechanisms do the following oncoproteins use to regulate gene expression?
a. V-ErbA
b. Myc
c. MDM2, MDM4

A

A. v-ErbA: Dominant repressor, competes for binding with promoter. Blocks hormone dependent gene expression

B. Myc: Can stimulate gene expression in 3 ways: 1. heterodimerization with Max 2. heterodimerization with PTEF-b and 3. heterodimerization with TFIIH

C. MDM2: altering TF activity by promoting/inhibiting protein : protein interactions. Promotes p53 ubiquitination, but small molecule nutlin blocks p53 interaction, allowing p53 to still inhibit tumor growth.

22
Q

How would you cure a transcriptional disease?

A
  • Could target chromatin modifying proteins
  • Could target epigenetic modifications by targeting modification directly (azacytidine), inhibiting enzymes that produce modification (histone acetylases), inhibiting enzymes that remove modification (histone deacetylases), inhibit interactions of the modification with other factors (bromodomain : acetyl groups)
  • Nucleic acid therapies
  • Design zinc fingers to switch expression OFF or ON
23
Q

What type of factors that regulate gene expression can be mutated in human diseases?

A
  • TFs
  • BTC components
  • CMCs
  • Co-activators
  • RNA processing
24
Q

Describe RAN translation details

A

The ribosome does not initiate translation at the normal AUG translation initiation codon. Rather it initiates translation within the CGG repeat sequence to produce polyglycine or polyalanine depending on whether translation takes place in the GGC or GCG reading frame

25
Q

Describe molecular details for all p53-linked functions

A
  • p53 can interact with GIGs (genes whose proteins inhibit growth), inducing growth arrest
  • p53 can also interact with GSGs (genes whose proteins stimulate growth) through direct mechanisms and indirect mechanisms
26
Q

What general and/or specific genes are regulated by p53? What are p53’s tumor suppressor functions?

A
  • p53 is a tumor suppressor that is involved in the activation of expression of genes that inhibit growth (can induce growth arrest)
  • Is considered a sensor of DNA damage
  • It is induced by DNA damage
  • Mutated in many cancers
27
Q

How do viruses manipulate gene expression?

A
  • Degrade cellular RNAs
  • Decapping enzymes block cap-dependent translation
  • Have IRESs in viral mRNAs
  • Viral “cap” proteins to allow host cell ribosomes to translate uncapped viral transcripts
28
Q

How do retroviruses become tumorigenic?

A

The virus integrates next to proto-oncogene, followed by incorrect incision, resulting in cancer-causing virus carrying oncogene

29
Q

How can chromosome translocation result in a change in gene expression?

A
  • It can put regulatory elements on chromosomes, resulting in higher levels of expression
  • It can result in the orientation of transcription being changed (head-to-head orientation // divergently transcribed), resulting in an increase in oncogene expression
30
Q

What are the 4 consequences of Jun binding to ccl2 gene?

A
  • Histone phosphorylation
  • Histone acetylation
  • Recruitment of NFkB
  • Recruitment of RNAP II

All result in increased transcription of ccl2 gene

31
Q

Leucine zippers promote…

A

Jun/Fos heterodimers

32
Q

Jun and Fos normally promote…

A

cellular growth via transcription of various genes

33
Q

Phosphorylation of Jun disrupts…

A

NuRD interactions

34
Q

Can v-ErbA bind thyroid hormone or activate transcription? How is v-ErbA oncogenic?

A
  • Cannot bind TH or activate transcription
  • It is oncogenic because it is a dominant repressor and it blocks hormone-dependent gene expression
35
Q

Describe the v-ErbA inhibitory domain

A
  • v-ErbA contains an inhibitory domain that recruits a co-repressor
  • The inhibitory domain is essential for transformation
36
Q

v-ErbA must do what to transform?

A

Repress transcription

37
Q

c-erbA is involved with the development of

A

RBCs

38
Q

What does v-erbA do?

A

Inhibits c-erbA, letting the blood cells to continue replicating

39
Q

What does v-ErbA encode that allows cells to grow without growth factor stimulation?

A

A truncated EGF receptor

40
Q

What are the three ways that Myc can stimulate gene expression?

A
  • Myc can heterodimerize with Max, resulting in enhanced transcriptional initiation
  • Myc can heterodimerize with PTEF-b, resulting in enhanced transcriptional elongation
  • Myc can heterodimerize with TFIIH, stimulating the activity of GMT, resulting in enhanced translation
41
Q

What are the consequences of genome translocations?

A
  • Gene overexpression
  • Oncogenic fusion proteins
42
Q

Describe the direct mechanisms by which p53 represses GSGs

A
  • Compete for activator binding sites
  • Close chromatin
  • Bind up activators
43
Q

Describe the indirect mechanisms by which p53 represses GSGs

A
  • p21 (inhibits cyclin-dependent kinases needed for growth; p21 is a growth arrest gene)
  • Turn on miRNAs
  • Turn on lncRNAs
44
Q

How is p53 regulated or thwarted?

A
  • Deletion of the gene
  • Mutation
  • MDM2 overexpression
45
Q

Mutant p53 can bind…

A
  • Alternative sequences in promoters that wt p53 won’t
  • Other TFs
46
Q

What is MDM2?

A

An oncogenic protein that misdirects or inactivates p53 activity

47
Q

How can p53 evade MDM2?

A

Via acetylation, which inhibits MDM2 interaction and recruits TAF1 (TFIID component)

Mechanisms of Gene Regulation (4 decks)

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