ライフサイエンスコーパス: mispair

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

2 mmetry between the base angles of the formed mispair.

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

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

5 next correct nucleotide in the presence of a mispair.

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

7 (removal) of IUdR-DNA, principally the G:IU mispair.

8 omains yields a functional TCR that does not mispair.

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

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

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

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

13 ot stimulate hpol eta-catalyzed formation of mispairs.

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

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

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

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

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

19 icity of the reconstituted system for looped mispairs.

20 0 side chain to serve as a sensor of nascent mispairs.

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

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

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

24 ll the bases within the crossover region are mispaired.

25 paired activity possibly caused by disulfide mispairing.

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

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

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

29 ches through metalloinsertion, ejecting both mispaired adenosines.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

46 also play a role in the repair of base-base mispairs and in the suppression of homology-mediated dup

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

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

49 phorylate Chk1 in the presence of O(6)-meG/T mispairs and MMR proteins.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

64 Small looped mispairs are corrected by DNA mismatch repair.

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

66 The mechanism by which purine-purine mispairs are formed and extended was examined with the h

67 The latter mispairs are fundamental units of RNA secondary structur

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

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

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

71 enetic and bioinformatic tools and show that mispairs are significantly more important for aminoacyla

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

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

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

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

76 45-mer double-stranded substrate with a U/G mispair at position 21, we showed that extracts from all

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

93 Mispair binding analysis with purified Msh2-Msh3 and DNA

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

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

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

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

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

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

100 mispairs that was consistent with functional mispair binding.

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

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

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

104 e found that a chimeric protein in which the mispair-binding domain (MBD) of Msh6 was replaced by the

105 The Escherichia coli mispair-binding protein MutS forms dimers and tetramers

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

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

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

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

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

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

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

113 er and the recognition of insertion/deletion mispairs by the Msh2-Msh3 heterodimer.

114 ognition of base-base and insertion/deletion mispairs by the Msh2-Msh6 heterodimer and the recognitio

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

116 These mispairs can evade Watson-Crick fidelity checkpoints and

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

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

119 This mispairing causes alterations in gene expression, and ce

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

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

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

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

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

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

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

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

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

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

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

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

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

133 Removal of mispairs created by annealing of the single-stranded oli

134 art through their strong selectivity against mispaired deoxyribonucleotides.

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

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

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

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

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

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

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

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

143 ation is especially noteworthy due to strong mispair discrimination.

144 sed affinity of Msh2 for ADP, and binding to mispaired DNA stabilized the binding of ATP to Msh6.

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

146 5G/Y567A) that enabled us to capture nascent mispaired dNTPs.

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

148 DNA glycosylase (which can excise U from U:G mispairs) does not (unlike enforced UNG or SMUG1 express

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

150 those of others, we propose a model of slip mispairing during error-prone repair synthesis to explai

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

166 s were examined by comparing the kinetics of mispair formation with adenine versus 7-deazaadenine and

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

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

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

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

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

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

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

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

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

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

177 56dupA and c.676dupC) in FERMT1, and slipped mispairing in direct nucleotide repeats was identified a

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

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

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

181 atched bases and elucidates how destabilized mispairs in DNA may be recognized.

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

183 entities and tasks of six mutant G-U and A-C mispairs in Escherichia coli tRNA(Gly) using genetic and

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

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

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

187 mechanistic differences between correct and mispaired incorporation.

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

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

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

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

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

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

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

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

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

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

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

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

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

201 s that were consistent with a slipped-strand mispairing mutation model, as well as a smaller number o

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

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

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

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

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

207 Mispairing of dGTP and dTTP was similar and occurred wit

208 Mispairing of polymeric guanine (polyG) tracts within ea

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

210 However, mispairing of the therapeutic alphabeta chains with endo

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

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

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

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

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

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

217 appa (Pol kappa) is a proficient extender of mispaired primer termini on undamaged DNAs and is implic

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

240 TDG(67-308) removes U and T from U/G and T/G mispairs, respectively, with similar rates as native hTD

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

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

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

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

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

246 , indicating that Msh3-like behaviors beyond mispair specificity are not features controlled by the M

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

248 The mispair specificity of sliding clamp formation and Mlh1-

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

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

251 Base mispairing, temperature and the presence of an interstra

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

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

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

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

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

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

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

259 hibited robust binding to specific base-base mispairs that was consistent with functional mispair bin

260 Because the mispairs the primers create are efficiently removed by t

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

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

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

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

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

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

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

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

269 xtend the different unnatural base pairs and mispairs under steady-state conditions.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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