ライフサイエンスコーパス: dG

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

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

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

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

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

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

7 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-

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

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

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

11 ced intercalated 10R-(+)-cis-anti-B[a]P-N(2)-dG (G*), manifests large differences in nucleotide excis

12 ically identical benzo[a]pyrene-derived N(2)-dG adduct (B[a]P-dG) in which the B[a]P rings reside in

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

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

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

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

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

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

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

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

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

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

23 rolytic reactivity at neutral pH for bulky 8-dG adducts is N-linked > C-linked > O-linked, which corr

24 for the hydrolytic reactivity of O-linked 8-dG adducts in the gas-phase, as determined using electro

25 rotonation for highly chlorinated O-linked 8-dG adducts in water.

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

27 ,2-GG) or an acetylaminofluorene adduct (AAF-dG).

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

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

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

31 '-deoxyguanosin-8-yl)-2-acetylaminofluorene (dG-C8-AAF) adducts that differ by a single acetyl group.

32 pano-2'-deoxyguanosine adducts (alpha-OH-Acr-dG and gamma-OH-Acr-dG).

33 ne adducts (alpha-OH-Acr-dG and gamma-OH-Acr-dG).

34 We demonstrate here that Acr-dG adducts can be efficiently repaired by the nucleotide

35 nic fluoroaminofluorene-deoxyguanine adduct (dG-FAF, N-(2'-deoxyguanosin-8-yl)-7-fluoro-2-aminofluore

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

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

38 contact with C8 (2.94 A) of the 3'-adjacent dG nucleotide that may represent a pseudo hydrogen bond.

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

40 Interestingly, although AL-dG adducts progressively disappear from the DNA of labor

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

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

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

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

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

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

47 f N-(2'-deoxyguanosin-8-yl)-2-aminofluorene (dG-C8-AF) and N-(2'-deoxyguanosin-8-yl)-2-acetylaminoflu

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

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

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

51 -7-deazapurine nucleosides related to dA and dG bearing 7-octadiynyl or 7-tripropargylamine side chai

52 metabolic activation, AA reacts with dA and dG residues in DNA to form aristolactam (AL)-DNA adducts

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

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

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

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

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

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

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

60 ow dPer distinguishes between O(6)-Bn-dG and dG in DNA.

61 comprised of just two base pairs (dA-dT and dG-dC), is conserved throughout all life, and its expans

62 base pair, and when combined with dA-dT and dG-dC, it provides a fully functional six-letter genetic

63 ydrogen bond for a halogen bond in dA:dT and dG:dC base pairs, which allows 1 or 2 hydrogen bonds, re

64 cleotides (dA(BA)MP, dA(BA)TP, dG(BA)MP, and dG(BA)TP) were prepared by the direct Heck coupling of n

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

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

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

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

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

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

71 al activity (mutagenicity) of C(8)-arylamine-dG adducts with adduct conformation (anti vs syn) playin

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

73 Pyr)dG), thienyl ((Th)dG), benzofuryl ((Bfur)dG), indolyl ((Ind)dG), and benzothienyl ((Bth)dG) are d

74 The (Fur)dG, (Bfur)dG, (Ind)dG, and (Bth)dG derivatives were incorporated i

75 t position G(4) has been replaced by O(6)-Bn-dG and cytosine C(9) has been replaced with dPer to form

76 show how dPer distinguishes between O(6)-Bn-dG and dG in DNA.

77 cket that allows the benzyl group of O(6)-Bn-dG to intercalate between Per and thymine of the 3'-neig

78 ver, in solution, the benzyl ring of O(6)-Bn-dG undergoes rotation on the nuclear magnetic resonance

79 benzyl-2'-deoxyguanosine nucleoside (O(6)-Bn-dG), formed by exposure to N-benzylmethylnitrosamine.

80 7)T(8)Y(9)G(10)C(11)G(12))-3']2 (X = O(6)-Bn-dG, Y = dPer) reveals that dPer intercalates into the du

81 laced with dPer to form the modified O(6)-Bn-dG:dPer (DDD-XY) duplex [5'-d(C(1)G(2)C(3)X(4)A(5)A(6)T(

82 Finally, although mutagenic TLS across BPDE-dG largely depends on RAD18, experiments using Polk(-/-)

83 mutagenic, but not accurate, TLS across BPDE-dG.

84 dihydrodiol epoxide-derived dG adduct (BPDE-dG) using a plasmid bearing a single BPDE-dG and genetic

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

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

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

88 e(s) could insert a nucleotide opposite BPDE-dG.

89 DE-dG) using a plasmid bearing a single BPDE-dG and genetically engineered mouse embryonic fibroblast

90 The (Fur)dG, (Bfur)dG, (Ind)dG, and (Bth)dG derivatives were incorporated into the G(3) position

91 ), indolyl ((Ind)dG), and benzothienyl ((Bth)dG) are described.

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 In contrast, dG-FAF adduct at the replication fork for the Kfexo(-) c

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

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

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

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

102 y strong at repeated poly(dA:dT) and poly(dC:dG) tracts.

103 onists of TLR7, 8 and 9 containing a 7-deaza-dG or arabino-G modification in the immune-stimulatory m

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

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

106 (O)-linked biaryl ether 8-2'-deoxyguanosine (dG) adducts produced by phenolic toxins following metabo

107 erties of C(8)-heteroaryl-2'-deoxyguanosine (dG) adducts with C(8)-substituents consisting of furyl (

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

109 p) lesions resulting from 2'-deoxyguanosine (dG) or 8-oxo-7,8-dihydro-2'-deoxyguanosine (dOG) oxidati

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

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

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

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

114 a benzo[a]pyrene dihydrodiol epoxide-derived dG adduct (BPDE-dG) using a plasmid bearing a single BPD

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

132 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

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

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

135 -adjacent nucleobases, with a preference for dG.

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

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

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

139 C(8)-substituents consisting of furyl ((Fur)dG), pyrrolyl ((Pyr)dG), thienyl ((Th)dG), benzofuryl ((

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

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

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

143 The (Fur)dG, (Bfur)dG, (Ind)dG, and (Bth)dG derivatives were inco

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

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

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

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

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

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

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

151 The (Fur)dG, (Bfur)dG, (Ind)dG, and (Bth)dG derivatives were incorporated into the G

152 Th)dG), benzofuryl ((Bfur)dG), indolyl ((Ind)dG), and benzothienyl ((Bth)dG) are described.

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

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

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

156 dG was 2-7 times slower than that of O(6)-Me-dG adducts.

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

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

159 4-oxo-5-N-methylf ormamidopyrimidine (MeFapy-dG) arises from N7-methylation of deoxyguanosine followe

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

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

162 -1-(3-pyridyl)-1-butanone (NNK), O(6)-methyl-dG (O(6)-Me-dG) and O(6)-pyridyloxobutyl-dG (O(6)-POB-dG

163 Similar excesses of N(2)-(1-MIM)-dG over N(6)-(1-MIM)-dA adducts were found in all cellul

164 Arylamine-modified dG lesions were studied in two fully paired 11-mer duple

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

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

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

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

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

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

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

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

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

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

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

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

177 4-Cl-Ph-O-dG and 2,6-dichloro-Ph-O-dG (DCP-O-dG), respectively.

178 0.37 for 4-Cl-Ph-O-dG and 2,6-dichloro-Ph-O-dG (DCP-O-dG), respectively.

179 +) pKa values of 0.92 and 0.37 for 4-Cl-Ph-O-dG and 2,6-dichloro-Ph-O-dG (DCP-O-dG), respectively.

180 the unsubstituted adduct 8-phenoxy-dG (Ph-O-dG).

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

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

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

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

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

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

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

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

189 dSp products upon one-electron oxidation of dG in chiral hybrid or propeller G-quadruplexes that exp

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

191 (rigid vs flexible) and with the presence of dG nucleosides in close proximity to a JOE residue.

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

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

194 family, the greater repair susceptibility of dG-C8-AAF in all sequences stems from steric hindrance e

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

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

197 ly inhibited by the oxidized nucleoside 8-OH-dG.

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

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

200 with the corresponding nucleotides opposite dG.

201 an dCTP incorporation opposite either 7dG or dG.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

221 8-oxo-7,8-dihydroxy-2'-deoxyguanosine (8-oxo-dG) has high mutagenic potential as it is prone to mispa

222 on, 7,8-dihydro-8-oxo-2'-deoxyguanine (8-oxo-dG).

223 Changes in serum levels of 8-oxo-dG-modified DNA and total protein carbonylation correspo

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

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

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

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

228 2 is adept at synthesizing A:oxo-dG or C:oxo-dG pairs.

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

230 t to the minor groove alignment of the B[a]P-dG adduct, and the implications of the DB[a,l]P-dG confo

231 benzo[a]pyrene-derived N(2)-dG adduct (B[a]P-dG) in which the B[a]P rings reside in the B-DNA minor g

232 adduct, and the implications of the DB[a,l]P-dG conformational motif for the recognition of such DNA

233 he intercalated conformation of the DB[a,l]P-dG lesion in contrast to the minor groove alignment of t

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

235 ddition of CTP opposite the phenanthriplatin-dG adduct in an error-free manner, with specificity for

236 , error-prone bypass of the phenanthriplatin-dG lesion, which resembles DNA polymerases that similarl

237 f 1.1 for the unsubstituted adduct 8-phenoxy-dG (Ph-O-dG).

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

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

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

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

242 del pyridyloxobutylating agent, and O(6)-POB-dG adduct repair over time was monitored by HPLC-ESI(+)-

243 If not repaired, O(6)-POB-dG adducts induce large numbers of G --> A and G --> T m

244 e duplexes containing site-specific O(6)-POB-dG adducts within K-ras and p53 gene-derived DNA sequenc

245 and that inefficient AGT repair of O(6)-POB-dG at a specific sequences contributes to mutational spe

246 Previous studies have shown that O(6)-POB-dG can be directly repaired by O(6)-alkylguanine-DNA alk

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

248 HBEC cells were capable of removing O(6)-POB-dG lesions, and the repair rates were significantly redu

249 ution HPLC-ESI(+)-MS/MS analysis of O(6)-POB-dG remaining in DNA over time.

250 evaluate the contribution of AGT to O(6)-POB-dG repair in human lung, normal human bronchial epitheli

251 Overall, AGT-mediated repair of O(6)-POB-dG was 2-7 times slower than that of O(6)-Me-dG adducts.

252 (3-pyridyl)but-1-yl]deoxyguanosine (O(6)-POB-dG) lesions.

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

254 onsisting of furyl ((Fur)dG), pyrrolyl ((Pyr)dG), thienyl ((Th)dG), benzofuryl ((Bfur)dG), indolyl ((

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

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

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

258 , 4-cyanophenyl ((CNPh)dG), and quinolyl ((Q)dG).

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

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

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

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

263 nce context, in which G* is a C8-substituted dG adduct derived from fluorinated analogs of 4-aminobip

264 lymerase incorporates dZTP opposite template dG in the absence of dCTP.

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

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

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

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

269 ((Fur)dG), pyrrolyl ((Pyr)dG), thienyl ((Th)dG), benzofuryl ((Bfur)dG), indolyl ((Ind)dG), and benzo

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

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

272 AAF adduct is a better substrate of NER than dG-C8-AF in all three NarI sequence contexts.

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

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

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

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

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

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

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

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

281 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

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

283 Furthermore, the dG-C8-AAF adduct is a better substrate of NER than dG-C8

284 In a single nucleotide gap, the dG-FAF adduct adopts both a major-groove- oriented and b

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

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

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

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

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

290 Waals stacking interactions relative to the dG-C8-AF case.

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

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

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

294 deazapurine nucleotides (dA(BA)MP, dA(BA)TP, dG(BA)MP, and dG(BA)TP) were prepared by the direct Heck

295 being essentially the same as for undamaged dG on the template.

296 te-modified DNA by primer extension, whereas dG(BA)TP was an inhibitor of polymerases.

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

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

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

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

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

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