module 5 Flashcards

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1
Q

parent strand/ template

A

Provide a platform for complementary base pairing to form a new duplex

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2
Q

daughter strand

A

newly synthesized strand of DNA 5>3; made by the addition of a nucleotide that is complementary to the parent strand of DNA

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3
Q

DNA polymerase I

A

Prokaryotic removed and replaced the primer

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4
Q

DNA polymerase III

A

Prokaryotic major replication polymerase

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5
Q

DNA polymerase alpha

A

Initiates replication by synthesizing primer

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6
Q

DNA polymerase beta

A

Replaces nucleotide in DNA repair

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7
Q

DNA polymerase epsilon

A

Major replication polymerase leading strand

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8
Q

DNA polymerase delta

A

Major replication polymerase lagging strand

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9
Q

primer

A

Short sequence of RNA that stabilizes the initial nascent daughter strand to parent strand

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10
Q

helicase

A

Separated duplex

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11
Q

RPA

A

Replication protein A
Single strand binding protein
Protect ssDNA
Prevent complementary base pairing

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12
Q

ssDNA BP

A

Used in bacteria
Protect ssDNA
prevent complementary base pairing

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13
Q

RFC

A

Replication factor c
Loads PCNA clamp
Used in eukaryotes

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14
Q

PCNA

A

Proliferating cell nuclear antigen
DNA clamp loading structure
Works with RFC in eukaryotes

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15
Q

primase

A

Used in bacteria
Add __NTP primer

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16
Q

topoisomerase

A

Enzyme that breaks binds of double stranded DNA to unwind and release supercoiling and synthesize starts

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17
Q

flap endonuclease/ FEn

A

In eukaryotes
Works with RNAse to remove primers

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18
Q

lagging strand

A

synthetic direction away from the growing fork

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19
Q

leading strand

A

can be replicated continuously and polymerization of the new strand moves with the fork

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20
Q

okazaki fragment

A

Lagging strand synthesized in short units (prokaryotic)

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21
Q

beta clamp

A

Used in bacteria
Clamp loaders

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22
Q

telomerase

A

Enzyme that elongates telomeres at lagging strand to provide a template
Has TERT, TERC
Adds repeating sequence
After extension, recruits DNA pol alpha

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23
Q

reverse transcriptase

A

extends the telomere lagging strand; enzyme used to generate complementary DNA from an RNA template

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24
Q

methyguanine methyltransferase

A

MGMT
Corrects alkylated guanine
Uses cystine residue to catalyze the reaction to methylate guanine

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25
Q

thymine dimer

A

Covalent bonding of adjacent thymines in DNA
caused by UV radiation

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26
Q

XPC

A

Functions to build scaffold that would have helicase and endonuclease activity

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27
Q

CSB

A

Works with XPC to recognize and repair DNA
Recognition protein

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28
Q

nucleotide excision repair

A

Fixes Large modifications covalently bonded to base intra cross link/ diners

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29
Q

base excision repair

A

Corrects small changes to DNA base
-Glycosylase recognize mismatch and flip it out, APE nicks one side of sugar and recruits phosphodiesterase to remove DNA sugar
-DNA pol beta adds new nucleotide
-last phosphodiester bond made by ligase

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30
Q

deamination

A

Loss of amine group
Replaced by oxygen to create free radical which is highly reactive

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31
Q

thymine glycol

A

when thymine is oxygenated twice and releases free radical oxygen which can impact the genome

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32
Q

thymine glycosylase

A

enzyme that targets and removes only thymine from sugar

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33
Q

uracil glycosylase

A

Flips incorrect uracil out to be cleaved

34
Q

a-basic

A

When removal of base sugar creates apyrimidic or apurinic site

35
Q

a-puranic

A

When purine is missing during BET process
(G and a)

36
Q

a-pyrimidimic

A

When pyrimidine is missing during BET process (T and C)

37
Q

endonuclease

A

enzymes that cleave the phosphodiester bond within a polynucleotide chain; create nicks

38
Q

exonuclease

A

enzymes that work by cleaving nucleotides one at a time from the end of a chain

39
Q

ligase

A

Completes last phosphodiester bond

40
Q

MMR

A

mismatch repair
-done for mispairs and loops from insertion/ deletion events
repair system to correct mispaired bases in double stranded DNA from replication

41
Q

MutS

A

Complex that checks for base stacking
-won’t stack if bases mismatched

42
Q

MutL

A

Coordinate between mutS and mutH to put Nick where mismatch occurred

43
Q

MutH

A

Recognize heavy methylated site for bacteria

44
Q

MSH2

A

in eukaryotes
do recognition in MMR (G) for small loops and mistmatches
recognize on large loops

45
Q

MSH3

A

recognize on large loops

46
Q

MSH6

A

in eukaryotes
do recognition in MMR for mismatched pairs

47
Q

MLH1

A

forms dimer during MMR

48
Q

PMS2

A

forms dimer during MMR
endonuclease activity
Nicks the strand where the mis match occurred

49
Q

IDL

A

insertion daughter strand
candidates for what causes DNA mismatches that need repaired

50
Q

Ku 70/80

A

Proteins that interact w DNA protein kinase C
Used in NHEJ

51
Q

MRE11-NBS1-Rad50 (trimer)

A

coordinates with pyH2AX
interacts with phosphorylated yH2X

52
Q

NHEJ repair

A

always will result in deletion mutation
rare in bacteria, yeast, and Drosophilia
NonHomologous end joining repair
Used when double strand break occurs

53
Q

holliday junction

A

occurs after DNA synthesis
homologous or nonhomologous repairs of a strand
Formed after rad 51 causes strand invasion

54
Q

strand invasion

A

done by RAD51
one strand goes in and uses other strand as a template
forms loop in uncut duplex

55
Q

TERT

A

Telomerase Reverse Transcriptase
protein enzyme that can extend the telomeres

56
Q

TERC

A

Telomerase RNA
recruits DNA Pol alpha. DNA Pol alpha has a platform to
create the last Okazaki fragment

57
Q

Rad51

A

Used in homologous recombination
Coordinates strand invasion process

58
Q

Aneuploidy

A

Aberrant chromosome complements

59
Q

benign tumor

A

Confined to local site or origin

60
Q

malignant tumor

A

Faster rate of growth, rate may be same and apoptosis decreased so appears to grow faster
-poorly demarcated borders, invasive growth

61
Q

5-fluro uracil

A

topical drug that halts DNA synthesis and that can be used to treat basal cell carcinoma

62
Q

temozolamide

A

adds methyl groups to guanine during MGMT

63
Q

iomeguatrib

A

cancer therapeutic; drug that targets MGMT so DNA repair is inhibited killing the cells much the same way as temozolamide

64
Q

PAHs

A

Polycyclic Aromatic Hydrocarbons
DNA damaging agent

65
Q

loss of heterozygosity

A

Happens in mitosis from chromosome non disjunction
Extra copies of chromosomes, degrades good chromosome
Homozygous mutant results

66
Q

heterogenetic

A

produced by infection outside the body

67
Q

hyperchromatic

A

malignant cells become this
nucleus that looks darker than normal when examined under the microscope

68
Q

protooncogene

A

Cyclin
Growth factor
Receptor
Produce proteins which function to enhance cell growth/division

69
Q

tumor suppressor gene

A

Regulate cell growth
Make sure stop correctly
P21 inhibits cell cycle
2 hits required

70
Q

metastasis

A

Spread of cancer behind the primary tumor
-invasion into the extra cellular matrix
-vascular dissemination

71
Q

anaplasia

A

lack of differentiation or poorly differentiated

72
Q

differentation

A

extent to which parenchymal cells resemble normal cells
Benign- well differentiated
Malignant- less differentiated/ undifferentiated

73
Q

contact inhibition

A

arresting cell growth when cells come in contact with each other

74
Q

epigenetic mechanisms

A

Promotion of cancer by gene expression or misregulation rather than mutations

75
Q

initiation

A

Works with promotor to induce tumor, will not cause by itself

76
Q

promotion

A

Have to have enough promoter to induce tumor with initation
If enough spacing between promoters, won’t cause tumor
-chemical irritant, dietary fat etc

77
Q

mutator phenotype

A

characteristic behavior of a cell that has lost DNA repair ability

78
Q

non-disjunction

A

describes incorrect chromosome separation during M phase

79
Q

angiogenesis

A

Formation of new blood vessels into the tumor
-supplies nutrients and oxygen and route for metastasis

80
Q

hypo methylation

A

Loss inhibition
Genes that should be silenced are expressed

81
Q

hyper methylation

A

Silence gene activity

82
Q

ROSs

A

oxidative chemicals that can be initiators of cancer; can damage cellular proteins, lipids and DNA