Brainscape's Knowledge GenomeTM

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


See full index

MAMS BCH > Quiz 4 > Flashcards

Quiz 4 Flashcards

1
Q

Purines

A

Adenine
Guanosine
Xanthine
Hypoxanthine

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

Pyrimidines

A

Cytosine
Uracil
Thymine

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

Uracil nucleoside and nucleotide

A

Uracil - Uridine - Uridylate

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

Cytosine nucleoside and nucleotide

A

Cytosine - Cytidine - Cytidylate

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

Hypoxanthine nucleoside and nucleotide

A

Hypoxanthine - Inosine - Inosinate

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

Xanthine nucleoside and nucleotide

A

Xanthine - Xanthosine - Xanthylate

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

PRPP Synthetase inhibitors

A

IMP, AMP, GMP, ADP,GDP

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

PRPP Aminotransferase inhibitors

A

IMP, AMP, GMP, ADP, GDP, ATP, GTP

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

Adenylosuccinate synthetase inhibitor

A

AMP

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

IMP Dehydrogenase inhibitor

A

GMP

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

Purine salvage pathways

A

Hypoxanthine/Guanine to IMP,GMP
Adenine to AMP

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

Carbamoyl-P Synthetase II Inhibitor

A

UMP, UDP, UTP, CTP

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

Carbamoyl-P Synthetase II Activator

A

ATP

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

Aspartate Transcarbamoylase Inhibitor

A

CTP

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

Aspartate Transcarbamoylase Activator

A

ATP

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

Difference between CPS1 and CPS2

A

1 is in the mitochondria and for the urea cycle, 2 is in the cytosol

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

Nucleoside Diphosphate Kinase specificity

A

Can be used for any of the diphosphate to produce CTP

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

2 sites of ribonucleotide reductase regulation

A

Site 1: dATP binding inhibits enzyme
Site 2: binding of triphosphate triggers reduction to diphosphates

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

dATP or ATP binding to site 2 is reduced to

A

UDP, GDP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

dTTP binding to site 2 is reduced to

A

GDP
reduction of UDP, CDP is inhibited

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

dGTP

A

ADP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Thymidylate synthase inhibitor

A

F-dUMP
- made from fluoruracil, fluorodeoxyuridine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Dihydrofolate reductase inhibitor

A

Aminopterin
Amethopterin (methotrexate)
- these are folate analogs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Why is dTMP a good target for chemo

A

It is only used for DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Allopurinol

A

Inhibits Xanthine Oxidase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What causes gout

A

Too much purine synthesis leading to accumulation of uric acid
- deposits in joints/kidney
- caused by foods high in nucleic acids, proteins, alcohol, diuretics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Lesch-Nyhan syndrome

A

Absence of HGPRT
- symptoms: gout, self-mutilation, intellectual disability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

3 ways chemotherapy works on cancer

A

1) blocks nucleotide biosynthesis
2) kills proliferating cells
3) blocks DNA replication (nucleotide analogues)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Fluorouracil, Fluorodeoxyuridine

A

Creates F-dUMP which works as a nucleotide biosynthesis inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Methotrexate

A

Folate antagonist, kills proliferating cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

AraC

A

Arabinose analog of deoxycytosine
- blocks DNA replication with nucleotide analogues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Acyclovir, Gancylovir, AZT

A

Chain terminators
- acyclovir, gancyclovir for Herpes
- AZT for AIDS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

5-iododeoxyuridine, araA, araC

A

Chain elongation inhibitors
- 5-iodo for Herpes
- araA for viral encephalitis
- araA is a more potent inhibitor of viral polymerase vs host polymerase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

B form vs A form hydration

A

B from is hydrated, while A form is present in low humidity
- changes the shape of the helix

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Z form DNA significance

A

GCGCGCGCGC
- spreads out genes being actively transcribed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Secondary DNA stabilizing factors

A

H bonds, vDw, ions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Secondary DNA destabilizing factors

A

electrostatic repulsion, phosphate at pH 7 (negatively charged)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Why does ssDNA absorb more light

A

Absorbs more light (260 nm) bc the bases are exposed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Tm

A

50% of DNA denatured

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

5 types of drugs included in HAART

A

1) Nucleoside reverse transcriptase inhibitors
2) Non-nucleoside RTI (NRTIs)
3) Protease Inhibitors
4) Entry Inhibitors
5) HIV Integrase Inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Non-nucleoside reverse transcriptase inhibitors (NRTIs)

A

Inhibit addition of nucleotides to chains using a nucleoside analog
- acyclovir, AZT

42
Q

Negative supercoil

A

Underwound

43
Q

Positive supercoil

A

Overwound

44
Q

Is natural DNA negative or positive

A

Negatively supercoiled

45
Q

Topoisomerase 1

A

break one strand, change by +1 or -1 supercoils
- requires DNA to be strained + or -
- does not affect unstrained DNA

46
Q

Topoisomerase 2

A

cuts 2 strands, changes number of supercoils by 2
- can add supercoils to new DNA in prokaryotes only

47
Q

How do topoisomerase inhibitors work

A

Inhibit re-ligation function by the enzyme

48
Q

Topoisomerases 1/2 in prokaryotes and eukaryotes

A

Different version in each

49
Q

Histones

A

small, positive proteins

50
Q

H1 function

A

Linker DNA, higher-order structures

51
Q

H2A, H2B, H3, H4 function

A

Nucleosome core
- DNA wrapped around is same length as Okazaki

52
Q

Solenoid

A

35-40x shortening of DNA
- 6 nucleosomes per turn

53
Q

Highly repetitive sequences

A
  • short, tandem, AT-rich
  • 10% of genome
  • telomeres
  • greater than 300,000 copies per genome
54
Q

Moderately repetitive sequences

A
  • code for highly-used genes
  • SINES/LINES space out actively transcribed genes
55
Q

Unique or single-copy sequences

A
  • only 1% made (housekeeping genes)
  • grouped in families
  • pseudogenes: non-functional unique sequences
56
Q

Myotonic Dystrophy Type 1

A
  • more CTG repeats increases severity (onset age decrease)
  • due to polymerase slipping on repeats
57
Q

What is anticipation

A

increase in severity of a disease with each successive generation

58
Q

Origin of replication

A

P - OriC
E - ARS

59
Q

Protein that binds origin

A

P - dnaA complex
E - ORC

60
Q

Helicase protein

A

P - dnaB/dnaC complex
E - MCM

61
Q

Protein that stabilizes ssDNA

A

P - SSB
E - RPA

62
Q

Protein that increases processivity

A

P - ß-subunit polymerase 3
E - PCNA

63
Q

Clamp loader

A

P - gamma complex
E - RFC (replication factor C)

64
Q

Protein that makes RNA primer

A

P - dnaG (part of primosome)
E - DNA pol ⍺

65
Q

Protein that removes RNA primers

A

P - DNA Pol 1
E - RNAse H and Fen1

66
Q

How do dnaA and ORC function?

A

Bind DNA binding domain and using positive histone-like proteins, causing DNA to split apart at nearby 3 AT-rich regions

67
Q

How does priming work in prokaryotic replication

A

Provides an uncreated 3’ OH, allowing DNA polymerase to bind
- RNA primer is 5-10 nts

68
Q

DNA Pol I

A

Primer excision and DNA repair
- 3’ exonuclease: proofreading, removes wrong brase
- 5’ exonuclease: removes primers (nick translation)

69
Q

Nick translation

A

5’ exonuclease removes one base at a time until it gets to DNA
- DNA ligase then seals the open gap

70
Q

DNA Pol III

A

bulk of replication, high processivity and rate

71
Q

Core enzyme of DNA Pol III

A

Dimer of ⍺, ε, θ

72
Q

ß-sliding clamp

A

Improves processivity, contains negative amino acids on interior to help DNA slide through

73
Q

Function of χ subunit on 𝛾 complex

A

Helps transition DNA Pol III from RNA primer to making DNA

74
Q

Replisome

A

Creation of a loop at at replication fork so DNA Pol III goes in the same direction on the lagging and leading strand

75
Q

Proofreading in prokaryotes

A

epsilon subunit removes mismatched base with 3’ to 5’ exonuclease

76
Q

Termination in prokaryotes

A
  • ter sites: x6, 3 each side apposed 180º from OriC
  • TUS protein: binds ter sites in opposite direction
  • Type II topoisomerase: separates new interlinking strands, then religates
77
Q

Protein that synthesizes DNA

A

P - DNA Pol III
E - DNA Pol ε, ẟ, 𝛾

78
Q

DNA Pol 𝛾

A

Only in mitochondria

79
Q

DNA Pol ε

A

Leading strand replication

80
Q

DNA Pol ẟ

A

Lagging strand replication
- High processivity with PCNA, low without

81
Q

DNA Pol ε

A

Leading strand replication
- High processivity regardless of PCNA

82
Q

Licensing

A

Assembly of pre-replication complex on ARS in eukaryotes
- ORC, inactive MCM, Cdc6, Cdt1

83
Q

Firing

A

Helicase activation, which activates complex to begin replication

84
Q

hTERT

A

Protein component of Telomerase
- reverse transcriptase

85
Q

hTR

A

Template for hTERT (RNA component)

86
Q

t-loop

A

Leftover overhang that comes in and displaces ds-DNA to make D-loop-t-loop

87
Q

Dyskeratosis Congenita

A

Mutations in hTERT/hTR cause premature mortality

88
Q

Normal methylation in prokaryotes

A

Adenine and Cytosine

89
Q

Normal methylation in eukaryotes

A

Only Cystosine

90
Q

Methylation Heritability

A

1) Sites chosen during gametogenesis and embyrogenesis
2) not all C’s methylated
3) maintenance methylase after replication

91
Q

How does methylation control gene expression

A

Un-methylated promoter: expressed
Methylated promoter: not expressed

92
Q

5-azacytidine

A

N instead of CH3 prevents methylation
- allows gene expression

93
Q

Transition mutation

A

Purine-Pyrimidine to Purine-Pyrimidine
- GC -> AT

94
Q

Transversion mutation

A

Purine-Pyrimidine to Pyrimidine-Purine
- AT -> TA
- can’t be fixed

95
Q

Photodimerization

A

Dimerization of adjacent intra-strand pyrimidines by UV
- creates Thymine dimers

96
Q

8-oxoguanine mispaired with Adenine

A

Caused by ROS

97
Q

Types of single-strand repair

A

1) direct base repair
2) excision repair
3) mismatch repair

98
Q

Mechanism of direct repair of base in single-stranded repair

A

MGMT transfers methyl group onto itself from O6-alkylguanine
- alkylates itself and restores Guanine

99
Q

Mechanism of NER in prokaryotes

A

1) UvrAB recognizes damage and bends DNA
2) UvrA leaves, UvrC joins
3) 3’ cut, 5’ cut, helices removes damaged piece
4) DNA Pol I replaces excised DNA, ligase seals nick

100
Q

Mechanism of base excision repair in prokaryotes

A

1) Uracil-DNA n-glycosylase recognizes and removes damaged base from backbone
2) Endonuclease creates 5’ nick
3) Backbone removed and replaced with new base by DNA Pol I 5’ endonuclease

101
Q
A

MAMS BCH (20 decks)

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