ライフサイエンスコーパス: dG

1 dG is formed quantitatively in the presence of excess be

2 dG(N(1)-H)(*) is produced by the formal dehydration of a

3 dG(N(1)-H)(*) was generated photochemically (lambda(max)

4 dG(N(1)-H)(*) were formed as a result of the indirect an

5 dG(N2-H)(.) is directly observed upon nanosecond laser f

6 At 138 dG, isolated hearts were studied using a Langendorff pre

7 n (105-138 days of gestation (dG); term ~145 dG) in isobaric chambers.

8 (86 to 95 days of gestation [dG]; term, 183 dG) on day 0 (all dams) and then at 7-day intervals thro

9 gle-nucleotide resolution for the I-A type 2'dG-sensing riboswitch from Mesoplasma florum by NMR spec

10 we have solved the crystal structure of a 2'-dG-II aptamer domain bound to 2'-deoxyguanosine.

11 s of 2'-deoxyguanosine riboswitch (called 2'-dG-II).

12 To understand how 2'-dG-II riboswitches recognize their cognate ligand and ho

13 iboguanosine, suggesting that a subset of 2'-dG-II riboswitches may bind either molecule to regulate

14 Unlike 2'-dG-I riboswitches, the 2'-dG-II class only requires local changes to the ligand bi

15 Notably, members of the 2'-dG-II family have variable ability to discriminate betwe

16 Defining the 2'-dG-II riboswitches is a two-nucleotide insertion in the

17 Unlike 2'-dG-I riboswitches, the 2'-dG-II class only requires loca

18 f the four possible stereoisomeric BP-N (2) -dG adducts, which gives insights how Rev1 achieves error

19 merase, Dpo4, bypasses a (+)-cis-B[a]P-N (2)-dG adduct in DNA.

20 ur structures provide a view of cis-BP-N (2)-dG adducts in a DNA polymerase active site, and offer a

21 structures of yeast Rev1 with three BP-N (2)-dG adducts, namely the 10S (+)-trans-BP-N (2)-dG, 10R (+

22 ine to generate four stereoisomeric BP-N (2)-dG adducts.

23 Our data show that when (+)-cis-B[a]P-N (2)-dG is the templating base, the B[a]P moiety is in a non-

24 G adducts, namely the 10S (+)-trans-BP-N (2)-dG, 10R (+)-cis-BP-N (2)-dG, and 10S ( - )-cis-BP-N (2)-

25 (+)-trans-BP-N (2)-dG, 10R (+)-cis-BP-N (2)-dG, and 10S ( - )-cis-BP-N (2)-dG.

26 -cis-BP-N (2)-dG, and 10S ( - )-cis-BP-N (2)-dG.

27 )-dG on-column, corresponding to 1 BPDE-N(2)-dG adduct per 10(11) nucleotides (1 adduct per 10 human

28 al and functional studies of this model N(2)-dG adduct, reliable and rapid access to fdG-modified DNA

29 nds of spontaneous DNA damage including N(2)-dG adducts and alkylated bases.

30 om human DNA upon acid hydrolysis, BPDE-N(2)-dG adducts have rarely if ever been observed directly in

31 ranslesion synthesis (TLS) across these N(2)-dG adducts is error free.

32 nsmoker DNA containing 3.1 and 1.3 BPDE-N(2)-dG adducts per 10(11) nucleotides, respectively.

33 rometry (LC-MS)-based detection of BPDE-N(2)-dG in BaP-treated rodents, and indirectly through high-p

34 talled at (-)-trans-anti-benzo[a]pyrene-N(2)-dG lesion on the leading strand was efficiently and quic

35 it of detection (LOD) of 1 amol of BPDE-N(2)-dG on-column, corresponding to 1 BPDE-N(2)-dG adduct per

36 DNA, resulting in the formation of BPDE-N(2)-dG, an adduct formed between deoxyguanosine and a diol e

37 CH(3) 2'-F dG and, by inference, N (7)-CH(3) dG have miscoding and mutagenic potential.

38 Because N(7) -CH(3) dG is unstable, leading to deglycosylation and ring-open

39 uct N (7)-methyl deoxyguanosine (N(7) -CH(3) dG) is one of the most abundant lesions in mammalian DNA

40 er terminating in a dC residue opposite a 5' dG provides the greatest degree of fluorophore quenching

41 a triplex composed of two bm-Calpha-PNA-C(5):dG(5) duplexes built on a core (bm-Calpha-PNA-T(7))(2):d

42 is produced only in individuals who carry a dG allele of a genetic variant rs368234815-dG/TT.

43 ,2-GG) or an acetylaminofluorene adduct (AAF-dG).

44 nked dG bases at a 90 degrees angle, the AAF-dG fully intercalates into the duplex to stabilize the k

45 gh levels of N-(deoxyguanosin-8-yl)-AalphaC (dG-C8-AalphaC) DNA adducts were formed in hepatocytes.

46 cimen, whereas N-(deoxyguanosin-8-yl)-4-ABP (dG-C8-4-ABP) was identified in one subject (30 adducts p

47 n bypassing the C8-2'-deoxyguanosine adduct (dG-C8-IQ) formed by 2-amino-3-methylimidazo[4,5-f]quinol

48 The adducted dG maintains the anti-conformation about the glycosyl bo

49 via covalent modification of the 5'-adjacent dG, but there is no evidence for electron transfer by th

50 In the absence of a reducing agent, dG(N(1)-H)(*) oxidizes 3, decreasing the dG yield to ~50

51 O (6)-alkyl-dG) and minor-groove N (2)-alkyl-dG lesions in human cells, where the alkyl groups are et

52 Replication across the two N (2)-alkyl-dG lesions was error-free, and Pol nu and Pol theta were

53 air and translesion synthesis of O (6)-alkyl-dG lesions and provide a better understanding of the rol

54 O (6)-alkyl-dG lesions mainly induced G->A mutations that were modul

55 eplicative bypass of a series of O (6)-alkyl-dG lesions, with the alkyl group being a Me, Et, nPr, iP

56 promote TLS across major-groove O (6)-alkyl-dG lesions.

57 tation frequencies for all three O (6)-alkyl-dG lesions.

58 the straight- and branched-chain O (6)-alkyl-dG lesions.

59 e O (6)-alkyl-2'-deoxyguanosine (O (6)-alkyl-dG) and minor-groove N (2)-alkyl-dG lesions in human cel

60 O (6)-alkyl-2'-deoxyguanosine (O (6)-alkyl-dG) lesions are among the most mutagenic and prevalent a

61 e ethyl, n-butyl (nBu), and, for O (6)-alkyl-dG, pyridyloxobutyl.

62 the photogenerated benzyl cations alkylated dG, dC, and dA, ICL assay with variation of DNA sequence

63 ee, replicative bypass of alpha-dC and alpha-dG yielded mainly C-->A and G-->A mutations.

64 ed a major role in bypassing alpha-dC, alpha-dG and alpha-dT in vivo.

65 tial levels of the alpha-anomer of dG (alpha-dG) in calf thymus DNA and in DNA isolated from mouse pa

66 ions, abolished the G-->A mutation for alpha-dG, pronouncedly reduced the C-->A mutation for alpha-dC

67 The abundance of alpha-dG in mammalian tissue and the impact of the alpha-dNs o

68 BP), N-(deoxyguanosin-8-yl)-4-aminobiphenyl (dG-C8-4-ABP); the HAA 2-amino-1-methyl-6-phenylimidazo[4

69 ced 8-(deoxyguanosin-N(2)-yl)-1-aminopyrene (dG(1,8)), one of the DNA adducts derived from 1-NP, can

70 the presence of complementary DNAs dA(8) and dG(6) at neutral pH, bm-Calpha-PNA 1 forms a higher orde

71 H115A mutation disrupted MgdGTP binding and dG:dGTP ternary complex formation but not dG:dCTP ternar

72 duced electron transfer between coumarin and dG slows down ICL formation.

73 ation of dC, with misincorporation of dA and dG in 5-10% of products.

74 inked by glyoxal are dG-gx-dC, dG-gx-dA, and dG-gx-dG.

75 Furthermore, the levels of dG-gx-dC and dG-gx-dA correlated with HbA1c with statistical signific

76 ction and quantification of the dG-gx-dC and dG-gx-dA cross-links based on stable isotope dilution (S

77 atients (n = 38), the levels of dG-gx-dC and dG-gx-dA in leukocyte DNA were 1.94 +/- 1.20 and 2.10 +/

78 fication was 94 and 90 amol for dG-gx-dC and dG-gx-dA, respectively, which is equivalent to 0.056 and

79 rm of N7mdG in the base pairings with dC and dG.

80 dG:dG are very similar to those of dG:dC and dG:dG, respectively, indicating the involvement of the k

81 the 3' penultimate position opposite another dG increased the quenching further.

82 a Hoogsteen base pair with the template anti-dG.

83 cleoside adducts cross-linked by glyoxal are dG-gx-dC, dG-gx-dA, and dG-gx-dG.

84 ovide insights into the TLS across N(2)-aryl-dG damaged DNAs by Pol IV.

85 MT protection can be limiting because 8-aryl-dG adducts suffer from greater rates of acid-catalyzed d

86 Our studies focus on 8-aryl-dG adducts with 8-substituents consisting of furyl ((Fur

87 iciency for DNA substrates containing 8-aryl-dG adducts.

88 ncoming rNTP to pair with the template base (dG) or 7,8-dihydro-8-oxo-2'-deoxyguanosine with a signif

89 t the excision repair maps for CPDs and BPDE-dG adducts generated by tXR-Seq for the human genome.

90 s) and BaP diol epoxide-deoxyguanosine (BPDE-dG), which are removed from the genome by nucleotide exc

91 , we report the sequence specificity of BPDE-dG excision repair using tXR-seq.

92 ion, which alkylates guanines at both the C8-dG and N2-dG positions.

93 s conformation is compared to that of the C8-dG-IQ adduct in the same sequence, which also formed a '

94 In addition, the C8-dG-IQ adduct was oriented with the IQ CH3 group and H4a

95 However, the C8-dG-IQ adopted the syn conformation placing the Watson-Cr

96 r)dG), phenyl ((Ph)dG), 4-cyanophenyl ((CNPh)dG), and quinolyl ((Q)dG).

97 le Pol X prebinds MgdCTP weakly, the correct dG:dCTP ternary complex is readily formed in the presenc

98 to the covalent fixation of the crosslinked dG bases at a 90 degrees angle, the AAF-dG fully interca

99 (d2Ih), 5',8-cyclo-2'-deoxyguanosine (cyclo-dG), and the free base guanine (Gua).

100 dducts cross-linked by glyoxal are dG-gx-dC, dG-gx-dA, and dG-gx-dG.

101 contains the modified base deoxyarchaeosine (dG(+)) in its genome.

102 Deoxyguanosine (dG) adducts of the PAH benzo[a]pyrene (B[a]P), 10-(deoxy

103 three epimeric lesions of 2'-deoxyguanosine (dG) and liquid chromatography-tandem mass spectrometry a

104 en believed to react with 2'-deoxyguanosine (dG) generating 2'-deoxyguanosin-N1-yl radical (dG(N1-H)(

105 onfirmed that 100% of the 2'-deoxyguanosine (dG) residues are replaced by modified bases.

106 reference for reaction at 2'-deoxyguanosine (dG) sites.

107 our-electron oxidation of 2'-deoxyguanosine (dG) yields 5-guanidinohydantoin (dGh) as a product.

108 the heterocyclic ring in 2'-deoxyguanosine (dG), the initial electrophilic intermediate displays a w

109 tron oxidation product of 2'-deoxyguanosine (dG), the most readily oxidized native nucleoside.

110 ification (LOQ) of the major deoxyguanosine (dG) adducts of these carcinogens ranged between 1.3 and

111 l, anthracenyl, and pyrenyl)-deoxyguanosine (dG) modified phosphoramidite building blocks and the cor

112 Distal dG's are also oxidatively damaged by the peroxyl radical

113 The Dpo4.DNA-dG(1,8) binary structure shows that the aminopyrene moie

114 In the Dpo4.DNA-dG(1,8).dCTP ternary structure, the aminopyrene moiety o

115 tructures of N7mdG or dG paired with dC, dT, dG, and dA.

116 d repair polymerase that catalyzes efficient dG:dGTP incorporation in addition to correct repair.

117 re able to incorporate N(2) -4-ethynylbenzyl-dG into the nucleus.

118 through incubation of N(2) -4-ethynylbenzyl-dG with wild-type and pol kappa deficient mouse embryoni

119 have evolved distinct mechanisms to express dG-free DNA.IMPORTANCE Bacteriophages are in a constant

120 eta and Dpo4 can bypass the N(7) -CH(3) 2'-F dG adduct, albeit with some stalling, but hpol kappa is

121 We conclude that N (7)-CH(3) 2'-F dG and, by inference, N (7)-CH(3) dG have miscoding and

122 g an analog of this lesion (N(7) -CH(3) 2'-F dG) and examined its miscoding potential with four Y-fam

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

124 and increases the efficiency of beta-C-Fapy*dG insertion opposite dC.

125 4,6-Diamino-5-formamidopyrimidine (Fapy*dG) is an abundant form of oxidative DNA damage that is

126 When Fapy*dG is in its nucleotide triphosphate form, Fapy*dGTP, it

127 zeta) to incorporate an A opposite AFB1-Fapy-dG and extend from this mismatch, biological evidence su

128 ificant increases in the levels of AFB1-Fapy-dG in Neil1(-/-) vs. wild-type liver DNA.

129 opened AFB1-deoxyguanosine adduct (AFB1-Fapy-dG).

130 yielding formamidopyrimidine AFB1 (AFB1-Fapy-dG).

131 In COS7 cells, NM-Fapy-dG caused targeted mutations, predominantly G --> T tran

132 Although formation of NM-Fapy-dG in cellular DNA has been demonstrated, its potential

133 -NM-substituted formamidopyrimidine (NM-Fapy-dG).

134 atalyze high-fidelity synthesis past NM-Fapy-dG, but only on a template subpopulation, presumably con

135 lucidate the mechanisms of bypass of NM-Fapy-dG, we performed replication assays in vitro with a high

136 pha-anomer as a major contributor to NM-Fapy-dG-induced mutagenesis in primate cells.

137 is 0.19 amol for dG-gx-dC and 0.89 amol for dG-gx-dA, which is 400 and 80 times more sensitive, resp

138 The detection limit is 0.19 amol for dG-gx-dC and 0.89 amol for dG-gx-dA, which is 400 and 80

139 mit of quantification was 94 and 90 amol for dG-gx-dC and dG-gx-dA, respectively, which is equivalent

140 -adjacent nucleobases, with a preference for dG.

141 ural substrate binding and the most frequent dG:dGTP misincorporation of AsfvPolX remain poorly under

142 (.) following hydrogen atom abstraction from dG is unlikely to be a major pathway when HO(.) reacts w

143 using structuring parameters calculated from dG'/dt, for the characterisation of the pectin sugar aci

144 ith 8-substituents consisting of furyl ((Fur)dG), phenyl ((Ph)dG), 4-cyanophenyl ((CNPh)dG), and quin

145 mpared to 5'-O-DMT for incorporation of (Fur)dG into DNA substrates critical for determining adduct i

146 The most acid-sensitive (Fur)dG was chosen for optimization of solid-phase DNA synthe

147 is in 0.1 M aqueous HCl determined that (Fur)dG was the most acid-sensitive (55.2-fold > dG), while (

148 ird of gestation (105-138 days of gestation (dG); term ~145 dG) in isobaric chambers.

149 at midgestation (86 to 95 days of gestation [dG]; term, 183 dG) on day 0 (all dams) and then at 7-day

150 )dG was the most acid-sensitive (55.2-fold > dG), while (Q)dG was the most resistant (5.6-fold > dG).

151 ile (Q)dG was the most resistant (5.6-fold > dG).

152 ent targeting the amino nitrogen of guanine (dG-N2) provides direct evidence for Watson-Crick (G)N2H2

153 by glyoxal are dG-gx-dC, dG-gx-dA, and dG-gx-dG.

154 These results identify dG oxidation to d2Ih to occur in high yields leading to

155 he hydrophobic residues Val120 and Leu123 in dG:dGTP misincorporation and can provide information for

156 ymes necessary to synthesize and incorporate dG(+).

157 the primer/template junction pair, while its dG moiety projected into the cleft between the Finger an

158 mational change to adopt a Watson-Crick-like dG*dTTP base pair and a closed protein conformation.

159 e, whereas replication past the cross-linked dG component occurred at a mutation frequency of approxi

160 l)-1-butanone (NNK), O(6)-methyl-dG (O(6)-Me-dG) and O(6)-pyridyloxobutyl-dG (O(6)-POB-dG), formed in

161 ernary Pol.DNA.dNTP complexes between MeFapy-dG-adducted DNA template:primer duplexes and the Y-famil

162 4-oxo-5-N-methylf ormamidopyrimidine (MeFapy-dG) arises from N7-methylation of deoxyguanosine followe

163 lication bypass investigations of the MeFapy-dG adduct revealed predominant insertion of C opposite t

164 ative of error-free replication, with MeFapy-dG in the anti conformation and forming Watson-Crick pai

165 -1-(3-pyridyl)-1-butanone (NNK), O(6)-methyl-dG (O(6)-Me-dG) and O(6)-pyridyloxobutyl-dG (O(6)-POB-dG

166 lacing the Watson-Crick edge of the modified dG into the major groove.

167 cedented strategies to achieve the mutagenic dG:dGTP incorporation.

168 alkylates guanines at both the C8-dG and N2-dG positions.

169 The conformation of a site-specific N2-dG-IQ adduct in an oligodeoxynucleotide duplex containin

170 otope standards [(15)N5]dG-gx-dC and [(15)N5]dG-gx-dA as internal standards, enzyme hydrolysis to rel

171 tion of the stable isotope standards [(15)N5]dG-gx-dC and [(15)N5]dG-gx-dA as internal standards, enz

172 The resulting AFB1-N7-dG adduct undergoes either spontaneous depurination or i

173 of DNA alkylation by NMs is a cationic NM-N7-dG adduct that can yield the imidazole ring-fragmented l

174 The structures of N7mdG:dC and N7mdG:dG are very similar to those of dG:dC and dG:dG, respect

175 mplates that contain 7dG in place of natural dG residues replicate with high efficiency and >99% over

176 attenuated the mutation rates for O (6)-nBu-dG and O (6)-pyridyloxobutyl-dG.

177 u alone reduced mutations only for O (6)-nBu-dG, and sole loss of Pol theta attenuated the mutation r

178 nd dG:dGTP ternary complex formation but not dG:dCTP ternary complex formation.

179 ydrogen bonds with the templating nucleotide dG and adopts a chair-like triphosphate conformation.

180 dehydration of a hydroxyl radical adduct of dG as well as by deprotonation of the corresponding radi

181 of substantial levels of the alpha-anomer of dG (alpha-dG) in calf thymus DNA and in DNA isolated fro

182 observation suggests that the generation of dG(N1-H)(.) via dG(N2-H)(.) following hydrogen atom abst

183 e report the first independent generation of dG(N2-H)(.) in high yield via photolysis of 1.

184 cesses are initiated after the generation of dG:dU mismatches by activation-induced cytidine deaminas

185 ttached to the exocyclic N(2)-amino group of dG.

186 Furthermore, the levels of dG-gx-dC and dG-gx-dA correlated with HbA1c with statist

187 itus (T2DM) patients (n = 38), the levels of dG-gx-dC and dG-gx-dA in leukocyte DNA were 1.94 +/- 1.2

188 so observed, giving characteristic masses of dG + 31.

189 ormations, indicating that N7-methylation of dG does not promote a promutagenic replication.

190 Mutation frequency (MF) of dG-C8-IQ was reduced by 38-67% upon siRNA knockdown of p

191 and H2O adducts resulting from oxidation of dG in the nucleoside, single-stranded, and duplex oligod

192 and high-yielding photochemical precursor of dG(N(1)-H)(*) that will facilitate mechanistic studies o

193 ize the chemical structure and properties of dG-AP cross-links generated in duplex DNA.

194 ofiles were mapped when aqueous solutions of dG were allowed to react with NH4Cl in the presence of t

195 The absorption spectrum of dG(N2-H)(.) is corroborated by DFT studies, and anti- an

196 ts showed no evidence for tautomerization of dG(N2-H)(.) to dG(N1-H)(.) within hundreds of microsecon

197 dC and N7mdG:dG are very similar to those of dG:dC and dG:dG, respectively, indicating the involvemen

198 y out the majority of the error-prone TLS of dG-C8-IQ, whereas pol eta is involved primarily in its e

199 reductant results in a quantitative yield of dG and two-electron oxidation products of 8-oxodGuo.

200 that the ICL reaction occurred with opposing dG/dC but not with staggered dA/dA.

201 ctural basis for dCTP incorporation opposite dG(1,8), we solved the crystal structures of the complex

202 ficient at nucleotide incorporation opposite dG-C8-IQ.

203 an dCTP incorporation opposite either 7dG or dG.

204 or substrates with a 5'-phosphorylated dC or dG residue on the 3' side of the ligation junction.

205 ermined eight crystal structures of N7mdG or dG paired with dC, dT, dG, and dA.

206 icularly susceptible to oxidation, and 8-oxo-dG (OG), when produced in situ or incorporated by DNA po

207 ely 2-fold higher than that induced by 8-oxo-dG adduct.

208 igating the pathophysiological role of 8-oxo-dG and 8-oxo-dA in AMD and other oxidative damage-relate

209 ry method for simultaneous analysis of 8-oxo-dG and 8-oxo-dA in human retinal DNA.

210 ge-as indicated by the accumulation of 8-oxo-dG and gammaH2AX-which was suppressed by the NADPH oxida

211 cumulation of reactive oxygen mediated 8-Oxo-dG and spontaneous pyroptotic signaling.

212 appa-catalyzed dCMP insertion opposite 8-oxo-dG approximately 10-fold and extension from dC:8-oxo-dG

213 e lesion, as well as extension from dC:8-oxo-dG base pairs.

214 ximately 10-fold and extension from dC:8-oxo-dG by 2.4-fold.

215 , WRN limits the error-prone bypass of 8-oxo-dG by hpol kappa, which could influence the sensitivity

216 Here we show that WRN stimulates the 8-oxo-dG bypass activity of hpol kappa in vitro by enhancing t

217 d kinetic data that fully characterize 8-oxo-dG bypass by Pol lambda.

218 In nuclear DNA, the levels of 8-oxo-dG in controls and AMD donors averaged 0.54 and 0.96, an

219 In mtDNA, the levels of 8-oxo-dG in controls and AMD donors averaged 170 and 188, and

220 flexible active site that can tolerate 8-oxo-dG in either the anti- or syn-conformation.

221 is behaviour for the GO system (BER of 8-oxo-dG lesions).

222 also shows a high C-->A error rate on 8-oxo-dG templates ( approximately 10(-4)).

223 sions such as 8-oxo-2'-deoxyguanosine (8-oxo-dG) and 8-oxo-2'-deoxyadenosine (8-oxo-dA) in diseased R

224 e 7,8-dihydro-8-oxo-2'-deoxyguanosine (8-oxo-dG) during translesion DNA synthesis.

225 8-oxo-7,8-dihydroxy-2'-deoxyguanosine (8-oxo-dG) has high mutagenic potential as it is prone to mispa

226 helicase known to influence repair of 8-oxo-dG.

227 in genomic integrity, post-replicative 8-oxo-dG:dA mispairs are removed through DNA polymerase lambda

228 kinetic preference for synthesis of an A:oxo-dG Hoogsteen pair.

229 nesium, DinB2 is adept at synthesizing A:oxo-dG or C:oxo-dG pairs.

230 2 is adept at synthesizing A:oxo-dG or C:oxo-dG pairs.

231 an incorporate any dNMP or rNMP opposite oxo-dG in the template strand with manganese as cofactor, wi

232 s consisting of furyl ((Fur)dG), phenyl ((Ph)dG), 4-cyanophenyl ((CNPh)dG), and quinolyl ((Q)dG).

233 adduct of PhIP, N-(deoxyguanosin-8-yl)-PhIP (dG-C8-PhIP) was identified in 11 out of 35 patients, at

234 yridine (PhIP), N-(deoxyguanosin-8-yl)-PhIP (dG-C8-PhIP); and the dG adducts of the NOC 4-(methylnitr

235 st, we demonstrate that PhIP induced C8-PhIP-dG adducts and DNA strand breaks.

236 Although C8-PhIP-dG adducts are mutagenic, their interference with the DN

237 kinetics of AGT-dependent repair of O(6)-POB-dG in duplex DNA.

238 Me-dG) and O(6)-pyridyloxobutyl-dG (O(6)-POB-dG), formed in liver, lung, bladder, pancreas, or colon

239 rihydroxy-7,8,9,10-tetrahydrobenzo[a]pyrene (dG-N (2) -B[a]PDE) were not detected in any specimen, wh

240 rihydroxy-7,8,9,10-tetrahydrobenzo[a]pyrene (dG-N(2)-B[a]PDE); the aromatic amine 4-aminobiphenyl (4-

241 hyl-dG (O(6)-Me-dG) and O(6)-pyridyloxobutyl-dG (O(6)-POB-dG), formed in liver, lung, bladder, pancre

242 s for O (6)-nBu-dG and O (6)-pyridyloxobutyl-dG.

243 , 4-cyanophenyl ((CNPh)dG), and quinolyl ((Q)dG).

244 st acid-sensitive (55.2-fold > dG), while (Q)dG was the most resistant (5.6-fold > dG).

245 2'-Deoxyguanosin-N1-yl radical (dG(N(1)-H)(*)) is the thermodynamically favored one-elec

246 ) generating 2'-deoxyguanosin-N1-yl radical (dG(N1-H)(.) ) via addition to the nucleobase pai-system

247 The 2'-deoxyguanosin-N2-yl radical (dG(N2-H)(.) ) formed was proposed to rapidly tautomerize

248 efficiency and fidelity with which a reduced dG-AP cross-link-containing plasmid was replicated in cu

249 f duplexes containing the native and reduced dG-AP cross-link, respectively.

250 inosine, while the firehammerviruses replace dG with 2'-deoxy-7-amido-7-deazaguanosine (dADG), noncan

251 Fletcherviruses replace dG with 2'-deoxyinosine, while the firehammerviruses rep

252 a dG allele of a genetic variant rs368234815-dG/TT.

253 rroborated by DFT studies, and anti- and syn-dG(N2-H)(.) are resolved for the first time.

254 exes of Dpo4 and DNA containing a templating dG(1,8) lesion in the absence or presence of dCTP.

255 r two hydrogen bonds, whereas the templating dG is anchored by a hydrogen bond with the side chain of

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

257 by inhibiting the formation of Hoogsteen tG:dG base pairs.

258 rporation is 5-fold higher opposite 7dG than dG and only slightly lower than dCTP incorporation oppos

259 er rates of acid-catalyzed depurination than dG and are sensitive to the acidic deblock conditions re

260 phage and bacterial genomes, suggesting that dG(+) is not a rare modification.

261 of the isolated ICL products indicated that dGs were the preferred alkylation sites in DNA for the b

262 The dG-AP cross-link in duplex DNA was remarkably stable, de

263 The dG-C8 adducts of AalphaC and MeIQx, and the B[a]P adduct

264 oxyguanosin-8-yl)-PhIP (dG-C8-PhIP); and the dG adducts of the NOC 4-(methylnitrosamino)-1-(3-pyridyl

265 tic digestion of DNA duplexes containing the dG-AP cross-link.

266 Three plasmid vectors containing the dG-C8-IQ adduct at the G1-, G2- or G3-positions of the N

267 nt, dG(N(1)-H)(*) oxidizes 3, decreasing the dG yield to ~50%.

268 stablish a minimal kinetic mechanism for the dG(1,8) bypass by Dpo4.

269 cells, with the bypass efficiencies for the dG- and AP-containing strands being 40% and 20%, respect

270 ition C(9) is replaced with dPer to form the dG:dPer (DDD-GY) [5'-d(C(1)G(2)C(3)G(4)A(5)A(6)T(7)T(8)Y

271 r with dG, two nucleotides upstream from the dG(1,8) site, creating a complex for "-2" frameshift mut

272 ary structure, the aminopyrene moiety of the dG(1,8) lesion, is sandwiched between the nascent and ju

273 s establish the chemical connectivity of the dG-AP cross-link released from duplex DNA and provide a

274 The intrinsic chemical stability of the dG-AP cross-link suggests that this lesion in duplex DNA

275 ltaneous detection and quantification of the dG-gx-dC and dG-gx-dA cross-links based on stable isotop

276 insertion of dCTP was preferred opposite the dG-FAF adduct in a single nucleotide gap assay consisten

277 lar to the dA*dCTP-Mg2+ complex, whereas the dG*dTTP-Mn2+ complex undergoes a large-scale conformatio

278 intermediate' protein conformation while the dG*dTTP-Mg2+ complex adopts an open protein conformation

279 irus-infected PHHs from individuals with the dG allele, where it was poorly secreted but highly funct

280 SLC43A3 mRNA predicted sensitivity to 6-thio-dG and therefore SLC43A3 could serve as a promising biom

281 Moreover, 6-thio-dG overcomes resistance to checkpoint blockade in advanc

282 ld serve as a promising biomarker for 6-thio-dG sensitivity in patients with NSCLC.

283 6-thio-dG treatment causes telomere-associated DNA damages that

284 eting drug, 6-thio-2'-deoxyguanosine (6-thio-dG), leads to tumor regression through innate and adapti

285 ge mediator 6-thio-2'-deoxyguanosine (6-thio-dG).

286 ly four NSCLC lines were resistant to 6-thio-dG.

287 for patients that may not respond to 6-thio-dG.

288 ll lines (73 of 77) were sensitive to 6-thio-dG; only four NSCLC lines were resistant to 6-thio-dG.

289 idence for tautomerization of dG(N2-H)(.) to dG(N1-H)(.) within hundreds of microseconds.

290 ormed was proposed to rapidly tautomerize to dG(N1-H)(.) .

291 )Ph) showed a similar photoreactivity toward dGs and dAs.

292 gests that the generation of dG(N1-H)(.) via dG(N2-H)(.) following hydrogen atom abstraction from dG

293 crystal structures of polbeta complexed with dG*dTTP and dA*dCTP mismatches in the presence of Mg2+ o

294 m, in which the major reaction of HO(.) with dG was proposed to involve hydrogen atom abstraction fro

295 :MgdGTP), and ternary (Pol X:DNA:MgdGTP with dG:dGTP non-Watson-Crick pairing) forms, along with func

296 er, dCTP forms a Watson-Crick base pair with dG, two nucleotides upstream from the dG(1,8) site, crea

297 to be a major pathway when HO(.) reacts with dG.

298 axation dispersion, we show here that wobble dG*dT and rG*rU mispairs in DNA and RNA duplexes exist i

299 ation dispersion recently showed that wobble dG.dT and rG.rU mismatches in DNA and RNA duplexes trans

300 In the present work, dG was oxidized by HO(*) via the Fe(II)-Fenton reaction