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BMS I > DNA Replair > Flashcards

DNA Replair Flashcards

1
Q

Replication Error

A

MMR

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2
Q

Single base dmg

A

BER

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3
Q

Bulky DNA adduct during trx

A

trx coupled NER repair

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4
Q

Bulky DNA adduct not during trx

A

GGNER

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5
Q

SSB

A

SSB repair

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6
Q

DSB

A

nonhomo end joining

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7
Q

DSB

A

homo recomb

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8
Q

MMR Proteins

A

endo/exonuc, helicase, polymerase, ligase

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9
Q

BER Proteins

A

glycosylase, endonuc, deoxyribse P lyase, polymerase, ligase

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10
Q

NER Proteins

A

Helicase, excinuclease, polymerase, ligase

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11
Q

SSB Proteins

A

Hydro/transferase, polymrase, ligase

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12
Q

NHEJ Proteins

A

broken DNA sensor nucelases, polyermase, ligase

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13
Q

Hom Recomb protiens

A

recombinases and endonuceleases

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14
Q

Proteins that recognize mismatch

A

MutS/L (proks), MSH2/6 (mismatch), MSH2/3 (small insertions/deletions)

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15
Q

Strand specificity

A

Proks-DNA methylation

Euks-nicks between Okazaki Frags

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16
Q

MMR steps

A

Strand recognition, endonuc cleaves on sides of mismatch, helicase/exonuclease remove new DNA, DNA pol III fills+ligase

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17
Q

HNPCC

A

Lynch syndrome, defects in MSH2 or MLH1 (can’t recognize mismatch)

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18
Q

BER pathway

A

glycosylase cleaves glycosidic bond between sugar and phosphate, AP endonuc cleaves backbone, lyase removes backbone, DNA Pol I beta fills gap+ligase

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19
Q

AP endonuclease

A

BER-cleaves sugar backbone

20
Q

Lyase

A

BER-removes backbone

21
Q

WRN helicase

A

involved in base excision repair, defects cause werners syndrome

22
Q

werners syndrome

A

deffect in wrn helicase, premature aging and disposition for cancer

23
Q

TT dimers cause…

A

significant DNA distortion=use NER

24
Q

causes to use repair

A 
MMR-mistake
BR-spontaous de-amination among others
NER-carcinogens/sunlight
SS breaks-oxidative damage
DSB-ionizing radiotion, oxidizing agents, mechanical stress, toposimoerase inhibs
25
Q

Glycosylase

A

recognize damaged bases in BR pathway

26
Q

GGner proteins

A

xpe, xpc, common pathway, UvrA in proks

27
Q

TCner proteins

A

c/a and csb and rna pol III and common pathway

28
Q

common pathway proteins

A

xpa-rpa, TFIID (XPB/XPD helicases), XPG 3’ nuclease, PCNA-pol delta, XPF 5’ nuclesase

29
Q

GGner pathway

A

Recognize distortion by xpe, xlc, uvra
Protein assembly of repair complex XPA
Excinuclease activity at 3’ and 5’ (XPF/XPG-UvrC in proks)
Helciase unwinds (XPB/XPD domains of TFIID binding complex)-UvrB in proks
DNA pol I fills gap
DNA ligase seals DNA

30
Q

XP disease

A

Mutations in XPC, XPE, XPD, XPA-cancer and extremely sensitive skin-sometimes neuronal degeneration

31
Q

TC ner pathway

A

Distortion blocks RNA pol II progression, csA or csB ubi the polymerase, RNA pol displacement, Recruitment of common pathway proteins, helices unwind replication fork more, excinuclease makes 5’ and 3’ incisions, damaged oligonuc out, DNA pol I fills gap, ligase

32
Q

PCNA

A

processivty protein-ONLY IN PROKS

33
Q

CS

A

mutation in CSA or B, mental retardation, sun sensitive, no risk for cancer b/c cell will apoptose vs accumulate problems like in XP

34
Q

SSB repair pathway

A

assocoiated with loss of 1 nucleotide
Parp 1-recognizes SSB
XRCC recruited-scaffold for other proteins
APTX (and other proteins) processes 3’ and 5’ ends
Restoration of proper 3’ and 5’ ends
DNA pol beta adds nun
ligation

35
Q

Parp1

A

recognies SSB

36
Q

XRCC/APTX

A

Scaffold

3’ and 5’ processivity

37
Q

AOA1

A

Ataxia Oculmotor Apraxia
Defect in APTX
limited eye movement, cognitive impairment, involuntary movements, NO NON NEUROLOGICAL FEATURES

38
Q

Apraxia

A

limited movement by command

39
Q

NHEJ pathway

A

no homology requirement/any stage of cell cycle
mutagenic (very mutagenic over time)

Ku70/80 detects dna broken and binds
DNA PKcs-artemis facilites aligment
WRN helicase opens
FEN1/Artemis removes overhangs if needed
Polymerase by pol mu and lambda
ligase
40
Q

Ku proteins/DNA PKcs-artemis

A

Detects dsb

faciliates alignment and removes overhangs if needed

41
Q

When can do homo recomb

A

S and G2 and must be extremely homoloogous, also not mutagenic

42
Q

homo recomb process

A

RAD52 binds to ends to help align, Rad51 looks for homologoies, Human BRCA1/2 regulate Rad51, nuclease and helicase makes nick, RAD51 promotes ATP dependent strand invasion, undamaged chromosome is template

43
Q

FEN1

A

removes nucleotides (nuclease)

44
Q

RAD51/52

A

Align Homo recomb/looks for homologous and promotes ATP dependent strand invasion

45
Q

BRCA1/2

A

regulate Rad51 (looking for homologies/ATP dependent strand invasion)

46
Q

AT

A

Ataxia Telangiasticia

ATM protein doesn’t work
Cell won’t slow down cell cycle to do homo recomb and signals homo recommit proteins to go there
lymphoid cancer and skin sensitivity

47
Q

ATM protein

A

slows cell down so can do homo recomb+signals homo recomb proteins to go there

BMS I (30 decks)

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