ライフサイエンスコーパス: mispair

1 nsertion/deletion mispairs and not on the CC mispair.

2 mmetry between the base angles of the formed mispair.

3 t extend well past an N (7)-CH(3) 2'-F dG:dT mispair.

4 ble geometry at neutral pH, similar to a T-G mispair.

5 next correct nucleotide in the presence of a mispair.

6 to the mispair, allowing Exo1 to excise the mispair.

7 cted MMR of a substrate containing a +1 (+T) mispair.

8 strand break 5' to the mispair, excising the mispair.

9 ed to contain a G/U or 8-oxoG ( degrees G)/C mispair.

10 omains yields a functional TCR that does not mispair.

11 e it discriminates against U-oxoG and G-oxoG mispairs.

12 lity at 5' mispairs is similar to that at 3' mispairs.

13 d by replication-induced (S)G:T and S(6)mG:T mispairs.

14 -G, but they preferentially extend A:8-oxo-G mispairs.

15 ot stimulate hpol eta-catalyzed formation of mispairs.

16 in A.T pairs and in polymerase-generated G.T mispairs.

17 from 1 to 14 nucleotides and some base-base mispairs.

18 . AP) sites, and somewhat less tightly G . T mispairs.

19 ine effect was most evident for G-containing mispairs.

20 dNTP substrates for 9 of the 12 natural base mispairs.

21 icity of the reconstituted system for looped mispairs.

22 ith the formation of 8-oxodG:C and 8-oxodG:A mispairs.

23 dro-8-oxoguanine (8-oxodG) and extended both mispairs.

24 demonstrated to form product aggregates, if mispaired.

25 Fc eliminates the possibility of light chain mispairing.

26 uman airways was regulated by slipped-strand mispairing.

27 reduced recombination-induced sgRNA-barcode mispairing.

28 bs without heavy/heavy and light/heavy chain mispairing.

29 paired activity possibly caused by disulfide mispairing.

30 ecognizes A:8-oxo-G mispairs and removes the mispaired A giving way to the canonical base excision re

31 hen the substrate contained a nick 3' to the mispair, a mixture of Msh2-Msh6 (or Msh2-Msh3), Exo1, RP

32 If not repaired in time, DNA polymerases can mispair Ade with 8-oxoG in the template.

33 ches through metalloinsertion, ejecting both mispaired adenosines.

34 E. coli AlaRS has an intrinsic capacity for mispairing alanine onto nonalanyl-tRNAs including tRNA(C

35 k 3' to the mispair, to make nicks 5' to the mispair, allowing Exo1 to excise the mispair.

36 an asymmetric mutator phenotype for certain mispairs, allowing an unambiguous strand assignment for

37 repair requires MutY recognition of the OG:A mispair amidst highly abundant and structurally similar

38 tion step as well as catalytic hydrolysis of mispaired aminoacyl-tRNA(Phe) species.

39 n 1 (Pms1) endonuclease in the presence of a mispair and a nick 3' to the mispair, to make nicks 5' t

40 e oligomer results in strand cleavage at the mispair and at TT steps preceding it with little reactio

41 espectively, and support a mechanism whereby mispair and ATP binding induces a conformational change

42 of the L561A variant forming an 8-oxoG.dATP mispair and show that the propensity for forming this mi

43 ng cellular NHEJ of ends with systematically mispaired and damaged termini.

44 The results of undetectable mispairing and high biological activity have indicated t

45 t protein mass spectrometry for profiling of mispairing and other product-related impurities, includi

46 tify nucleoside analogs that mimic this base-mispairing and preferentially inhibit apicoplast DNA rep

47 TRBC), were deleted in T cells to reduce TCR mispairing and to enhance the expression of a synthetic,

48 LigA was exquisitely sensitive to 3'-OH base mispairs and 3' N:abasic lesions, which elicited 1000- t

49 was relatively tolerant of 5'-phosphate base mispairs and 5' N:abasic lesions.

50 ngle TDG subunit binds very tightly to G . U mispairs and abasic (G . AP) sites, and somewhat less ti

51 e gauge the effects of 3'-OH and 5'-PO4 base mispairs and damaged base lesions on the rate of nick se

52 ng TG, CC, +1 (+T), +2 (+GC), and +4 (+ACGA) mispairs and either a 5' or 3' strand interruption with

53 lex, respectively, which recognize base-base mispairs and insertions/deletions and initiate the repai

54 ine DNA glycosylase (TDG) excises T from G.T mispairs and is thought to initiate base excision repair

55 e +2 but not the +3 or +4 insertion/deletion mispairs and not on the CC mispair.

56 mal A.T pairs, and is most effective for G.T mispairs and other damage located in a CpG context.

57 uely proficient at bypassing subtle terminal mispairs and radiomimetic damage by direct ligation.

58 glycosylase (TDG), which removes T from G.T mispairs and recognizes other lesions, with specificity

59 A glycosylase (TDG) excises thymine from G.T mispairs and removes a variety of damaged bases (X) with

60 ylase homologue (MutYH) recognizes A:8-oxo-G mispairs and removes the mispaired A giving way to the c

61 In initial steps in MMR, Msh2-Msh6 binds mispairs and small insertion/deletion loops, and Msh2-Ms

62 heterodimer in the recognition of base-base mispairs and the suppression of homology-mediated duplic

63 ytosine producing the TpG alteration and T:G mispair, and this step is followed by thymine DNA glycos

64 ase:base mispairs, the +1 insertion/deletion mispair, and to a low level on the +2 but not the +3 or

65 arkable affinity, modestly weaker than G . T mispairs, and exhibits substantial affinity for nonspeci

66 emoves fC, with higher activity than for G.T mispairs, and has substantial caC excision activity, yet

67 ligonucleotide duplexes containing the ClU-G mispair are substantially less stable than those contain

68 Thymine-thymine mispairs are barriers to long-distance radical cation mi

69 Small looped mispairs are corrected by DNA mismatch repair.

70 The mechanism by which purine-purine mispairs are formed and extended was examined with Solfo

71 t hMutSalpha is enriched on chromatin before mispairs are introduced during DNA replication.

72 In Saccharomyces cerevisiae, mispairs are primarily detected by the Msh2-Msh6 complex

73 omic integrity, post-replicative 8-oxo-dG:dA mispairs are removed through DNA polymerase lambda (Pol

74 TDG removes thymine from mutagenic G.T mispairs arising from deamination of 5-methylcytosine (m

75 With 5'-PO4 mispairs, DraRnl seals a 5' T-G mispair as well as it does a 5' C-G pair; in most other

76 get recognition, as evidenced by lack of TCR mispairing, as well as preserved specificity.

77 ee of four possible near-cognate tRNAs could mispair at position 1 or 3 of nonsense codons and that,

78 45-mer double-stranded substrate with a U/G mispair at position 21, we showed that extracts from all

79 ertion biases arise primarily from mRNA:tRNA mispairing at codon positions 1 and 3 and reflect, in pa

80 Introduction of mispairs at the base pairs flanking 5 or substitution of

81 DNA mismatch repair corrects mispaired bases and small insertions/deletions in DNA.

82 resulted in an Msh2-Msh6 complex that bound mispaired bases but could not form sliding clamps or bin

83 MutS protein recognizes mispaired bases in DNA and targets them for mismatch rep

84 icted to cause a defect in the correction of mispaired bases inserted during DNA replication.

85 ncreases replication fidelity by eliminating mispaired bases resulting from replication errors.

86 Mlh1-Pms1 foci increased when the number of mispaired bases was increased; in contrast, Msh2-Msh6 fo

87 ponent of replication centers independent of mispaired bases; this localized pool accounted for 10%-1

88 t the mechanism by which Msh6 interacts with mispairs because key mispair-contacting residues are con

89 sealing rate varies widely, with G-T and A-C mispairs being the best substrates and G-G, G-A, and A-A

90 ng the best substrates and G-G, G-A, and A-A mispairs being the worst.

91 e N-terminal and linker domains, which, when mispaired between yeast and human enzymes, induces cell

92 cture of the receptor and to competition and mispairing between endogenous and transgenic receptors.

93 Mixed dimers, formed by mispairing between the endogenous and transgenic TCRs, m

94 e difference in incorporation efficiency for mispairs between the mutants and the wild-type RB69 pol

95 formation and Mlh1-Pms1 recruitment but not mispair binding alone correlated best with genetic data

96 ctive responses to nucleotide binding and/or mispair binding and used them to study the conformationa

97 In one, mispair binding by either the MutS homolog 2 (Msh2)-MutS

98 domain and communicating regions but not the mispair binding domain of Msh2-Msh3 are responsible for

99 otein family dimers around the DNA; however, mispair binding protects additional regions from deuteri

100 arative study of Msh2-Msh3 and Msh2-Msh6 for mispair binding, sliding clamp formation, and Mlh1-Pms1

101 r a 5' or 3' strand interruption occurred by mispair binding-dependent 5' excision and subsequent res

102 ct evidence has suggested that the Msh2-Msh6 mispair-binding complex undergoes conformational changes

103 Remarkably, the Msh3-specific mispair-binding domain (MBD) licences a chimeric Msh2-Ms

104 Homology modeling of the mispair-binding domain (MBD) of Msh3 using the related M

105 This chimera possessed the mispair-binding specificity of Msh3 and revealed that co

106 stand the contribution of doubly light chain mispaired bispecific IgG was demonstrated.

107 ATP binding causes the mispair-bound Msh2-Msh6 mismatch recognition complex to

108 The exchangeable protons of the ClU-G mispair broaden rapidly with an increase in temperature,

109 uggest that pol X accommodates the oxoGsyn:A mispair by sampling closed active conformations that mir

110 n the subsequent excision processing of 6-TG mispairs by MMR.

111 hus, recognition of small insertion/deletion mispairs by Msh3 appears to require a greater degree of

112 crimination via "negative selection" against mispairs by using residues in the NBP, particularly the

113 res processing of uracil lesions (likely U/G mispairs) by MSH2 and MLH1 (likely noncanonical MMR).

114 These mispairs can evade Watson-Crick fidelity checkpoints and

115 However, in all mispairing cases, phosphodiester bond formation was inef

116 ation is important because the resulting G.T mispairs cause C -> T transition mutations, and mC is ab

117 r, TDG removes thymine from mutagenic G .: T mispairs caused by 5-methylcytosine (mC) deamination and

118 This mispairing causes alterations in gene expression, and ce

119 e reduced stability of a duplex containing a mispair, consistent with previous reports with Escherich

120 ich Msh6 interacts with mispairs because key mispair-contacting residues are conserved in these two p

121 role in controlling the extension of various mispairs containing O(6)-MeG.

122 pport the view that high affinity binding to mispair-containing DNA and low affinity binding to fully

123 sh3 interactions with bent, strand-separated mispair-containing DNA are more critical for the recogni

124 ew that degradation of irreparable O(6)-mG-T mispair-containing DNA by the MMR system and CAF-1-depen

125 dependent packaging of irreparable O(6)-mG-T mispair-containing DNA into nucleosomes suppresses its d

126 ndent incorporation of irreparable O(6)-mG-T mispair-containing DNA into nucleosomes suppresses its d

127 ns using purified S. cerevisiae proteins and mispair-containing DNA substrates.

128 causes degradation of irreparable O(6)-mG-T mispair-containing DNA, triggering cell death; this proc

129 We determined that mispair-containing DNAs were bent more by MutS than comp

130 lcytosine to thymine creates mutagenic G . T mispairs, contributing to cancer and genetic disease.

131 liding clamps formed by binding both ATP and mispairs could result from the simultaneous action of tw

132 art through their strong selectivity against mispaired deoxyribonucleotides.

133 om the mismatch, and ATP is required for the mispair-dependent interaction between Msh2-Msh6 and Mlh1

134 Here we describe the reconstitution of a mispair-dependent Mlh1-Pms1 endonuclease activation reac

135 tic homolog, was required for formation of a mispair-dependent Msh2-Msh6-Mlh1-Pms1 ternary complex.

136 ssibly GG mispairs, whereas Msh2-Msh6 formed mispair-dependent sliding clamps and recruited Mlh1-Pms1

137 of MutS that binds MutL and is required for mispair-dependent ternary complex formation and MMR.

138 Escherichia coli MutS forms a mispair-dependent ternary complex with MutL that is esse

139 nd show that the propensity for forming this mispair depends on an enlarged polymerase active site.

140 population of WC-like guanine-thymine (G-T) mispairs depends on the environment, such as the local n

141 otide residue, and primer extension beyond a mispair differed not only between these two mutants but

142 ation is especially noteworthy due to strong mispair discrimination.

143 During base excision repair of this mispair, DNA polymerase (pol) beta is confronted with ga

144 5G/Y567A) that enabled us to capture nascent mispaired dNTPs.

145 The presence of a mispair does not induce the polymerase to adopt a low ca

146 With 5'-PO4 mispairs, DraRnl seals a 5' T-G mispair as well as it do

147 Slipped-strand mispairing during replication is likely to have generate

148 Bulged and mispaired eG contexts, which can form during DNA replica

149 es at a high frequency due to slipped-strand mispairing events that occur during DNA replication.

150 ck base pair with template dG and not during mispairing events.

151 hrough does not promote novel or alternative mispairing events; rather, readthrough effectors cause q

152 (Exo1) from a single-strand break 5' to the mispair, excising the mispair.

153 synthesis to fill in the gaps resulting from mispair excision.

154 s the single-base deletion frequency and the mispair extension efficiency of these polymerases.

155 This mispair extension property of H285D is attributed to a g

156 trical size and shape on polymerase-mediated mispair extension.

157 mC deamination by a deaminase, giving a G.T mispair followed by TDG-initiated BER.

158 ation of ClU in a DNA template could promote mispair formation and mutation, in accord with previous

159 exonuclease activity of WRN prevents stable mispair formation by hpol eta.

160 These results suggest that during mispair formation the newly forming base pair is in a Ho

161 s were examined by comparing the kinetics of mispair formation with adenine versus 1-deaza- and 7-dea

162 pol nu catalyzes both correct and mispair formation with high catalytic efficiency.

163 s ionization of the ClU N3 proton, promoting mispair formation, but it also renders the glycosidic bo

164 Thus complex mispairs formed by an oxidized base and a ribonucleotide

165 nd, the structure of N7mdG:dT shows that the mispair forms three hydrogen bonds and adopts a Watson-C

166 on by initiating base excision repair of G.T mispairs generated by a deaminase enzyme.

167 omain IV) excises thymine from mutagenic G.T mispairs generated by deamination of 5-methylcytosine (m

168 However, this workflow may produce unwanted mispaired IgG species in addition to the desired bispeci

169 thods to identify and quantify low levels of mispaired IgG.

170 e past, the methoxy groups do not facilitate mispairing, implying that they are not recognized by any

171 However, only the G/U mispair in native CRE resulted in substantial developmen

172 56dupA and c.676dupC) in FERMT1, and slipped mispairing in direct nucleotide repeats was identified a

173 ow that chain termination is caused by tG:dG mispairing in the enzyme active site.

174 inding domain, which binds preferably to G.T mispairs in a methylated CpG site.

175 on, we show here that wobble dG*dT and rG*rU mispairs in DNA and RNA duplexes exist in dynamic equili

176 s BER of mutagenic and cytotoxic G:T and G:U mispairs in DNA.

177 thus confirming the danger of unrepaired G/U mispairs in promoters.

178 We show that mispairs in yeast that escape MMR during replication can

179 Msh2-Msh3 heterodimer recognizes various DNA mispairs, including loops of DNA ranging from 1 to 14 nu

180 of glycosylases that excise thymine from G.T mispairs, including thymine DNA glycosylase (TDG).

181 mutants to investigate the requirements for mispair interaction by Msh3.

182 The base pairing in the G*G mispair is achieved via Hoogsteen hydrogen bonding with

183 mispair is replaced by uracil show that the mispair is both a highly reactive site and a barrier to

184 prisingly, pol X's insertion rate of the G*G mispair is comparable to that of the four Watson-Crick b

185 se in temperature, indicating that the ClU-G mispair is less stable and opens more easily than the su

186 The melting temperature of the ClU-G mispair is not experimentally distinguishable from that

187 Experiments in which a thymine in the mispair is replaced by uracil show that the mispair is b

188 The kinetic basis for extension of mispairs is defective discrimination by I260Q at the lev

189 In particular, MUTYH activity on 8-oxodG:rA mispairs is fully inhibited, although its binding capaci

190 other respects, the ligation fidelity at 5' mispairs is similar to that at 3' mispairs.

191 odimers, half molecules, and antibodies with mispaired light and heavy chains.

192 ed active-site specificity toward the G-dTTP mispair may be associated with its cellular function(s).

193 These effects of the thymine-thymine mispairs may be associated with its wobble base pair str

194 ethylG by human pol iota, in contrast to the mispairing modes observed previously for O(6)-methylG in

195 ly in the repair of small insertion/deletion mispairs; mutations of the first class also caused defec

196 replicating reporter plasmids that contain a mispaired N(4)C-ethyl-N(4)C (C-C), N3T-ethyl-N3T (T-T),

197 polymerases, the recognition and removal of mispaired nucleotides (proofreading) by the exonuclease

198 by nuclease, guide RNA and the positions of mispaired nucleotides.

199 This may reflect mispairing of adenine with 8-oxoguanine in DNA attacked

200 Errors in protein synthesis due to mispairing of amino acids with tRNAs jeopardize cell via

201 Mispairing of polymeric guanine (polyG) tracts within ea

202 , a major limitation to this approach is the mispairing of the introduced chains with the endogenous

203 However, mispairing of the therapeutic alphabeta chains with endo

204 The resulting potentially mutagenic mispairs of uracil (U), thymine (T) or 5-hydroxymethylur

205 r, when a TT step contains a thymine-thymine mispair, one electron oxidation of the oligomer results

206 rmini, either by extending directly from the mispair or by primer-template misalignment.

207 ene family appears to reflect slipped-strand mispairing or domain duplication, allowing for redundanc

208 likely tautomeric forms." Indeed, among many mispairing possibilities, either tautomerization or ioni

209 sAb) constructs revealed that although chain mispairing primarily depends on the antibody sequence an

210 ent with the observed reduction in k(pol) in mispaired primer extension being due to the position of

211 ays an unusual efficiency for to extend from mispaired primer termini, either by extending directly f

212 y described here, we show that I260Q extends mispaired primer termini.

213 ficient than wild-type pol beta at extending mispaired primer termini.

214 Unexpectedly, a mispaired primer terminus accesses the exo site more fre

215 consistent with the interpretation that the mispaired primer terminus affects the geometry of the dN

216 ne DNA glycosylase (hTDG) removes T from G.T mispairs, producing an abasic (or AP) site, and follow-o

217 AG and AT promoters relative to AA or singly mispaired promoters.

218 h1-Pms1 endonuclease active site, as well as mispair recognition and Mlh1-Pms1 recruitment by Msh2-Ms

219 otic DNA mismatch repair (MMR) downstream of mispair recognition and Mlh1-Pms1 recruitment, including

220 hinery-coupled and -independent pathways for mispair recognition by Msh2-Msh6, which direct formation

221 that act as if they inactivate the Msh2-Msh3 mispair recognition complex thus causing weak MMR defect

222 aromyces cerevisiae msh3 designed to disrupt mispair recognition fell into two classes.

223 ted by either the Msh2-Msh6 or the Msh2-Msh3 mispair recognition heterodimer.

224 n protein could substitute for the Msh2-Msh6 mispair recognition protein and showed a different speci

225 The Msh2-MutS homolog 3 mispair recognition protein could substitute for the Msh

226 However, colocalization of the S. cerevisiae mispair recognition proteins with the replicative DNA po

227 to the Msh3 MBD model appears to distinguish mispair recognition regions from DNA stabilization regio

228 distortion is only involved at the earliest mispair recognition steps of MMR: MutL does not trap ben

229 h2-Msh6 localizes PCNA to repair sites after mispair recognition to activate the Mlh1-Pms1 endonuclea

230 h3 and Msh2-Msh6 are two partially redundant mispair-recognition complexes that initiate mismatch rep

231 ombined with the poor extension of the dA.rA mispair reduce transcriptional mutagenesis.

232 base-base and small insertion/deletion (ID) mispairs, respectively, despite the fact that cells cont

233 ofuran (i.e. T:G, A:G, and tetrahydrofuran:G mispairs) resulted in a 10-, 13-, and 4-fold decrease in

234 ot scrambled CRE or scrambled CRE with a G/U mispair, resulted in increased embryo death.

235 nformational changes upon binding of ATP and mispairs, resulting in the formation of Msh2-Msh6 slidin

236 ass ability varies widely, with increases in mispair severity gradually reducing bypass products from

237 ncluding bispecific antibodies and potential mispaired side products, in cell culture media, or other

238 of a single receptor chain results in chain mispairing, simultaneous editing of alpha- and beta-chai

239 These include slipped strand mispairing, site-specific recombination and epigenetic r

240 type and distribution of half antibodies and mispaired species impurities but not the quality ranking

241 one correlated best with genetic data on the mispair specificity of Msh2-Msh3- and Msh2-Msh6-dependen

242 The mispair specificity of sliding clamp formation and Mlh1-

243 ations through the process of slipped strand mispairing (SSM) by DNA polymerase during replication.

244 We report a general strategy to prevent TCR mispairing: swapping constant domains between the alpha

245 utcomes requires systematic profiling across mispaired target DNAs.

246 c misincorporation model suggesting that G-T mispair tautomerization occurs in the ajar polymerase co

247 gate these environmental effects, herein G-T mispair tautomerization processes are studied computatio

248 kinetics, and fundamental mechanisms of G-T mispair tautomerization, which plays a role in a wide ra

249 us TCR chains, resulting in the formation of mispaired TCR dimers and decreased or unspecific reactiv

250 isinsertions and that, in shark B cells, the mispairs tend to be extended rather than proofread.

251 ds to be accompanied by the extension of the mispaired terminus thus formed.

252 is more tolerant of 5' T-oxoG and 5' G-oxoG mispairs than the equivalent configurations on the 3' si

253 rmations induced by small insertion/deletion mispairs than with those induced by large insertion/dele

254 short-lived, low-populated Watson-Crick-like mispairs that are stabilized by rare enolic or anionic b

255 G), which excises thymine from mutagenic G.T mispairs that arise by deamination of 5-methylcytosine (

256 G mispairs that lead to mutations, the role played by tran

257 d Mlh1-Pms1 on 7 of the 8 possible base:base mispairs, the +1 insertion/deletion mispair, and to a lo

258 With 3'-OH mispairs, the DraRnl sealing rate varies widely, with G-

259 During formation of purine-purine mispairs, the k pol/ K d (dNTP) values for the insertion

260 s dependent on error-prone processing of G.U mispairs, these cell free assays provide a practical met

261 athway is blocked due to the 5'-flanking T:G mispair; this reduces OGG1, AP endonuclease 1, and DNA p

262 sponsible for the ability of H285D to extend mispairs through disruption of contacts near the C-termi

263 be guided by information on potential chain mispairing to enable timely decision making and risk mit

264 ploit the reduced thermodynamic stability of mispairs to distinguish U:A from U:G pairs.

265 e presence of a mispair and a nick 3' to the mispair, to make nicks 5' to the mispair, allowing Exo1

266 lU-A base pair studied previously, the ClU-G mispair undergoes a pH-dependent structural change, assu

267 and purine analogs for the Escherichia coli mispaired uracil glycosylase (MUG).

268 a target for removal by the Escherichia coli mispaired uracil glycosylase, which senses damage-relate

269 s indicate that the preference of hSMUG1 for mispaired uracil over uracil paired with adenine is best

270 with previous reports with Escherichia coli mispaired uracil-DNA glycosylase.

271 corporation of correctly base paired (R) and mispaired (W) analogues demonstrated a strong linear fre

272 increase in deoxythymidine 5'-triphosphate-G mispairs was confirmed by performing steady state single

273 se-mediated extension past lesion-containing mispairs was examined.

274 The structures of the purine-purine mispairs were examined by comparing the kinetics of misp

275 erent specificity of repair of the different mispairs whereas addition of MutL homolog 1-postmeiotic

276 ertion/deletions and CC, AA, and possibly GG mispairs, whereas Msh2-Msh6 formed mispair-dependent sli

277 r of both small and large insertion/deletion mispairs, whereas the second class caused defects only i

278 ever, m(5)C deamination yields mutagenic G.T mispairs, which are implicated in genetic disease, cance

279 the formation of Watson-Crick-like (WC-like) mispairs, which have been proposed to give rise to spont

280 tly increased the rate of all three 'X-dCTP' mispairs, which Polzeta4 alone made extremely inefficien

281 s and a potent pre-mutagenic lesion prone to mispair with 2'-deoxyadenosine (dA).

282 oG) is a dangerous DNA lesion because it can mispair with adenine (A) during replication resulting in

283 Because 8-oxoG can mispair with adenine during DNA synthesis, it is of inte

284 s high mutagenic potential as it is prone to mispair with deoxyadenine (dA).

285 closed state is achieved for the A*G and G*G mispair with the incoming dGTP in anti conformation, whi

286 guingly, the simulations reveal that the G*G mispair with the incoming nucleotide in the syn configur

287 One of these enzymes, MutY, excises an A mispaired with 8-oxoG as part of the process to restore

288 MutY homolog-dependent excision of adenines mispaired with 8-oxoguanine (G(O)) also act as MMR initi

289 easurements of the quantum yield of 8-DEA-tC mispaired with adenosine and, separately, opposite an ab

290 ity of PolB1 was the highest when 8-oxoG was mispaired with an incorrect nucleotide and could therefo

291 ycol (Tg), 5,6-dihydroxy-5,6-dihydrothymine, mispaired with deoxyguanosine.

292 By contrast, dsTCR chains mispaired with endogenous chains cannot properly assembl

293 nd and when correctly paired with adenine or mispaired with guanine.

294 emains closed in single-stranded DNA or when mispaired with T.

295 t unrepaired O(6)-methyldeoxyguanine lesions mispaired with thymine during the first replication cycl

296 e damage is 8-oxo-2'-deoxyguanosine (8-oxoG) mispairing with adenine (Ade), which can occur in two wa

297 DNA polymerases, is highly mutagenic due to mispairing with adenine.

298 mplating base, thereby competing against the mispairing with the templating base.

299 e mismatch repair complex MSH2-MSH6 binds to mispairs with only slightly higher affinity than to full

300 e-specific differences were observed for one mispair, with WT RT preferentially resolving dC-rC pairs