ライフサイエンスコーパス: dA

1 dA* was independently generated in DNA for the first tim

2 dA-AL-I was then measured in 10-mum thick tissue-section

3 otopologues (e.g. deoxyadenosine (dA) M + 1, dA M + 2, dA M + 3), as well as tumor cell proliferation

4 enine 10S-(+)-trans-anti-benzo[a]pyrene-N(2)-dA adduct.

5 s (e.g. deoxyadenosine (dA) M + 1, dA M + 2, dA M + 3), as well as tumor cell proliferation effects f

6 ort of lambs with exogenous adrenaline at 21 dA.

7 cting with the putative (*)Y99(Bs) and/or 5'-dA(*) intermediates to lower the energy barrier for the

8 s that use a 5'-deoxyadenosyl 5'-radical (5'-dA(*)) generated from a reductive cleavage of SAM to ini

9 AM to form a 5'-deoxyadenosyl 5'-radical (5'-dA(*)) intermediate.

10 ing a catalytic 5'-deoxyadenosyl radical (5'-dA(*)).

11 ylmethionine (SAM) to generate a reactive 5'-dA radical.

12 Since 5'-dA has been demonstrated to be an inhibitor of radical S

13 The 5'-dA radical is proposed to abstract one of the two H-atom

14 roR) atom of SP that is abstracted by the 5'-dA radical.

15 ious studies proved that SPL utilizes the 5'-dA* generated by the SAM cleavage reaction to abstract t

16 icance of DNA N(6)-methyladenine (6mA or m(6)dA) in eukaryotes had been underappreciated until recent

17 her an incorporated dA or dT opposite 1,N(6)-dA and 2'-deoxythymidine-5'-[(alpha,beta)-imido]triphosp

18 reference for purine pairing opposite 1,N(6)-dA and for -1 frameshifts.

19 ynucleotides containing a site-specific N(6)-dA dodecylpeptide cross-link were created and utilized f

20 DNA vectors containing a site-specific N(6)-dA dodecylpeptide cross-link were replicated in these st

21 In contrast, (+)-trans-anti-B[c]Ph-N(6)-dA dramatically reduces transcript production in cells p

22 cells lacking NER, (+)-trans-anti-B[a]P-N(6)-dA exhibited a deleterious effect on transcription that

23 a staggered configuration relative to 1,N(6)-dA in the anti conformation, thus opposite the 5'-T in t

24 The (+)-trans-anti-B[a]P-N(6)-dA lesion exhibited no detectable effect on transcriptio

25 1,N(6)-Ethenodeoxyadenosine (1,N(6)-dA) is the major etheno lesion formed in the reaction of

26 a the exocyclic amino group of adenine (N(6)-dA).

27 complex, dTTP was positioned opposite 1,N(6)-dA, and the adduct base was in the syn conformation, wit

28 ion in vitro, and (+)-trans-anti-B[c]Ph-N(6)-dA, which is a poor substrate for NER but also blocks tr

29 erived DNA adducts (+)-trans-anti-B[a]P-N(6)-dA, which is subject to NER and blocks transcription in

30 , Pol I can catalyze DNA synthesis past N(6)-dA-linked peptide cross-links and is likely to play an e

31 ntly and accurately synthesize DNA past N(6)-dA-linked peptides.

32 ency not to incorporate dTTP opposite 1,N(6)-dA.

33 oligonucleotide templates containing 1,N(6)-dA.

34 Orf2x binding site (O1) on attL as well as a dA+dT-rich upstream element that is required for Orf2x i

35 c studies showed that the substitutions of a dA with N(6)-CMdA and dC with N(4)-CMdC in a 12-mer dupl

36 When positioned opposite to a dA in a DNA duplex, the prototype arylamine-DNA adduct [

37 strand cross-links (ICLs) selectively with a dA opposite the 3'-adjacent nucleotide.

38 ional age (dGA) and lambs at 18 days of age (dA).

39 AL-dA adduct levels were elevated in cells deficient in GG-

40 ppear from the DNA of laboratory animals, AL-dA lesions has lasting persistence in the genome.

41 We determined the level of AL-dA adducts in human fibroblasts treated with AA to deter

42 However, placing AL-dA in mismatched sequences promotes XPC-RAD23B binding a

43 In vitro, plasmids containing a single AL-dA adduct were resistant to the early recognition and in

44 We conclude that AL-dA adducts are not recognized by GG-NER, explaining thei

45 ged at its center by the presence of an ALII-dA adduct.

46 s of its implications for the repair of ALII-dA adducts in mammalian cells.

47 The presence of the ALII-dA perturbs the conformation of the 5'-side flanking bas

48 lication and, while replication across alpha-dA was error-free, replicative bypass of alpha-dC and al

49 induction, all alpha-dN lesions except alpha-dA strongly blocked DNA replication and, while replicati

50 ith relevant levels of dA M+1 (0.25-20%) and dA M+5 (internal standard) were used for sample quantita

51 fit for calibration of dA M+1 (0.25-20%) and dA, demonstrated excellent accuracy and precision, and h

52 NA sequence and occurs favorably with dC and dA but not with dG or dT.

53 s of N7mdG or dG paired with dC, dT, dG, and dA.

54 exclusively directed incorporation of dT and dA.

55 ctures of polbeta complexed with dG*dTTP and dA*dCTP mismatches in the presence of Mg2+ or Mn2+.

56 ted efficiently by ADAR deaminase domains at dA-C mismatches and with E to Q mutations in the base fl

57 y A:T to T:A transversions with mutations at dA residues located almost exclusively on the non-transc

58 sincorporation of dCTP with templating bases dA, dT, and dC over correct dNTPs.

59 ifferent hydrogen-bonding properties between dA and dG and to the presence of substituent at the 2-po

60 In contrast, when dA* is flanked by dA, the increased dA(*+) pKa results in DNA damage arisi

61 pass the fact that DNA polymerase can bypass dA/abasic sites more efficiently than other dN/abasic si

62 C-nucleotide character of CdG, and (ii) CdG:dA base pairs may be less stable than OdG:dA base pairs,

63 on that is possible in OdG:dA but not in CdG:dA.

64 less stable than dG:dC base pairs, while CdG:dA base pairs are less stable than OdG:dA base pairs.

65 Calibration standards containing dA and fortified with relevant levels of dA M+1 (0.25-20

66 that, within the same base sequence context, dA-rU base pairs are less stable than dT-rA base pairs.

67 -dG) and 8,5'-cyclo-2'-deoxyadenosine (cyclo-dA) in five different strains of Escherichia coli cells.

68 xes with the two enantiomeric forms of dA (D-dA, or L-dA), with either UDP or ADP bound to the donor

69 trast, the complexes with ADP, with either D-dA or L-dA, adopted a closed and catalytically competent

70 ate of dCK in which the nucleoside, either D-dA or L-dA, is surprisingly bound in a manner not consis

71 The dA(*+)/dA* equilibrium, and consequently the reactivity in DNA,

72 horylation, dCK is capable of converting dC, dA, and dG into their monophosphate forms.

73 urred on only one strand (the non-degenerate dA residue of 5'-CrTCnAG-3' being methylated at the N6 p

74 as it is prone to mispair with deoxyadenine (dA).

75 een abasic (Ap) sites and 2'-deoxyadenosine (dA) residues was recently reported, but the chemical str

76 tion from the N6-amine of 2'-deoxyadenosine (dA*).

77 asure low levels of DNA base deoxyadenosine (dA) and its isotopologues (e.g., dA M+1) from limited mo

78 nd their isotopologues (e.g. deoxyadenosine (dA) M + 1, dA M + 2, dA M + 3), as well as tumor cell pr

79 onversion of the nucleosides deoxyadenosine (dA), deoxyguanosine (dG), and deoxycytidine (dC) into th

80 ls in vivo by deamination of deoxyadenosine (dA) and deoxyguanosine (dG), respectively, and can misco

81 et base G, A, or C and reactions between dG, dA and dC and 8-mer peptides containing a single reactiv

82 oss-links of Lys, Cys, His, and Trp with dG, dA, and dC.

83 > M(1)dG:dG > M(1)dG:dT approximately M(1)dG:dA, but neither hPol iota nor Rev1 extended M(1)dG-conta

84 genomic integrity, post-replicative 8-oxo-dG:dA mispairs are removed through DNA polymerase lambda (P

85 e opening and the stability of each rU-dA/dT-dA base pair in the two structures are characterized by

86 se results suggest that the central rU-dA/dT-dA base pairs in the adenine tract make the largest ener

87 s also suggest that the high stability of dT-dA base pairs in the DNA provides a signal for the pausi

88 In the template DNA-DNA duplex, the dT-dA base pairs are more stable than the corresponding rU-

89 ng the modified S-cdG.dC and 3'- neighbor dT.dA base pairs.

90 -acetylaminofluorene (FAAF), and N is either dA or dT.

91 tly restored TLS in pold3 mutants, enhancing dA incorporation opposite abasic sites.

92 dducts, 1,N(2)-epsilon-dG and 1,N(6)-epsilon-dA, underwent glycolytic cleavage in rat liver cytosol.

93 binds duplex DNA containing consecutive FdU-dA base pairs in the major groove with distorted trigona

94 fted toward the radical cation by a flanking dA.

95 Structure-activity relationships for dA pairing have been examined extensively using analogs

96 initially formed alkyl radical (8b) to form dA* and acetone.

97 Tandem lesions emanating from dA* are the major products when the reactive intermediat

98 bine to combine advantageous properties from dA (favorable hydrogen-bonding pattern) and dG (propensi

99 Furthermore, [dA(2)]GLP-1/GcG elicited a protracted glucose-lowering a

100 Furthermore, [dA(2)]GLP-1/GcG significantly improved glucose tolerance

101 yadenosine (dA) and its isotopologues (e.g., dA M+1) from limited mouse cell populations.

102 intermediates generated by the direct (e.g., dA(*+)) and indirect (e.g., dA*) effects of gamma-radiol

103 he direct (e.g., dA(*+)) and indirect (e.g., dA*) effects of gamma-radiolysis.

104 standards [(15)N5]dG-gx-dC and [(15)N5]dG-gx-dA as internal standards, enzyme hydrolysis to release t

105 urthermore, the levels of dG-gx-dC and dG-gx-dA correlated with HbA1c with statistical significance.

106 and quantification of the dG-gx-dC and dG-gx-dA cross-links based on stable isotope dilution (SID) na

107 s (n = 38), the levels of dG-gx-dC and dG-gx-dA in leukocyte DNA were 1.94 +/- 1.20 and 2.10 +/- 1.77

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

109 on was 94 and 90 amol for dG-gx-dC and dG-gx-dA, respectively, which is equivalent to 0.056 and 0.065

110 19 amol for dG-gx-dC and 0.89 amol for dG-gx-dA, which is 400 and 80 times more sensitive, respective

111 pan-1,3-diyl)-2'-deoxyadenosine (1,N(6)-HMHP-dA), in tissues of laboratory mice exposed to 6.25-625 p

112 MP, dAMP, or dGMP opposite 1,N(6)-gamma-HMHP-dA and detected large amounts of -1 and -2 deletion prod

113 ted a single base opposite 1,N(6)-gamma-HMHP-dA but was unable to extend beyond the damaged site, and

114 ed 1,N(6)-propano group on 1,N(6)-gamma-HMHP-dA is expected to block the Watson-Crick base pairing of

115 a and kappa enzymes bypass 1,N(6)-gamma-HMHP-dA lesions in an error-prone fashion, potentially contri

116 ication past site-specific 1,N(6)-gamma-HMHP-dA lesions in the presence of human DNA polymerases (hpo

117 3-diyl)-2'-deoxyadenosine (1,N(6)-gamma-HMHP-dA) adducts are formed upon bifunctional alkylation of a

118 trands, we constructed 40 hypothetical homo-(dA) anti-parallel duplexes and docked coralyne into the

119 ents predict that the coralyne-induced homo-(dA) duplex structure adopts the transWH geometry.

120 rmal stability of the coralyne-induced homo-(dA) structure.

121 itutions (dA-->7) were engineered into homo-(dA) sequences.

122 n: high transcription and long homopolymeric dA:dT tracts.

123 ct 7-(deoxyadenosin-N(6)-yl) aristolactam I (dA-AL-I).

124 misincorporation of dA, which leads to AL-II-dA-->T and AL-II-dG-->T transversions.

125 ion of a hydrogen bond for a halogen bond in dA:dT and dG:dC base pairs, which allows 1 or 2 hydrogen

126 me, with over 90% of TLS events resulting in dA incorporation.

127 A*(+) found in (dA)6 at 150 K also deprotonates on thermal annealing.

128 tingly, locomotor activity was increased in [dA(2)]GLP-1/GcG mice, without appreciable changes in asp

129 extension stage, with either an incorporated dA or dT opposite 1,N(6)-dA and 2'-deoxythymidine-5'-[(a

130 st, when dA* is flanked by dA, the increased dA(*+) pKa results in DNA damage arising from hole trans

131 , pol beta showed a 2:1 preference to insert dA over dC, while AMV-RT incorporated predominantly dC.

132 the two enantiomeric forms of dA (D-dA, or L-dA), with either UDP or ADP bound to the donor site.

133 he complexes with ADP, with either D-dA or L-dA, adopted a closed and catalytically competent conform

134 CK in which the nucleoside, either D-dA or L-dA, is surprisingly bound in a manner not consistent wit

135 ite a benzo[a]pyrene-derived adenine lesion (dA*); while mainly error-free, the identity of misincorp

136 xcesses of N(2)-(1-MIM)-dG over N(6)-(1-MIM)-dA adducts were found in all cellular models independent

137 nt adducts, N(2)-(1-MIM)-dG and N(6)-(1-MIM)-dA, and developed an UPLC-ESI-MS/MS method for their spe

138 The nucleosides were converted to 5'-O-mono-(dA(SR)MP) or triphosphates (dA(SR)TP) by phosphorylation

139 tituted 7-deazapurine nucleotides (dA(BA)MP, dA(BA)TP, dG(BA)MP, and dG(BA)TP) were prepared by the d

140 ating from 1 is attributed to reaction at N1-dA, which requires local melting of the duplex.

141 In addition, N7mdG:dA adopts a novel shifted anti:syn base pair presumably

142 All 16 FAF-modified 12-mer NG*N/NAN dA mismatch duplexes (G* = FAF, N = G, A, C, T) exhibite

143 pyrazolo[1,5-a]-1,3,5-triazine C-nucleoside (dA(PT)), designed to form two hydrogen bonds with a comp

144 ferential adsorption of adenine nucleotides (dA) on gold, as previously demonstrated using a model sy

145 The 7-substituted 7-deazapurine nucleotides (dA(BA)MP, dA(BA)TP, dG(BA)MP, and dG(BA)TP) were prepare

146 spacer, a strand of k adenine nucleotides, (dA)(k).

147 that has additional m adenine nucleotides, (dA)(m), at the 5' end.

148 ng-range interaction that is possible in OdG:dA but not in CdG:dA.

149 dG:dA base pairs may be less stable than OdG:dA base pairs, at least in part, because of a third long

150 e CdG:dA base pairs are less stable than OdG:dA base pairs.

151 employed a quadratic fit for calibration of dA M+1 (0.25-20%) and dA, demonstrated excellent accurac

152 urs much faster, implying the consumption of dA* as it is formed.

153 The formation of dA* was followed by laser flash photolysis, which yields

154 lows the enzyme to minimize the formation of dA:8-oxo-dGMP at the expense of decreasing the insertion

155 complexes with the two enantiomeric forms of dA (D-dA, or L-dA), with either UDP or ADP bound to the

156 ensation of C4-AP with the N6-amino group of dA.

157 nnected to the exocyclic N(6)-amino group of dA.

158 olymerase eta, kappa, and iota, insertion of dA is catalyzed by an unidentified polymerase that canno

159 ing dA and fortified with relevant levels of dA M+1 (0.25-20%) and dA M+5 (internal standard) were us

160 , almost exclusively, to misincorporation of dA, which leads to AL-II-dA-->T and AL-II-dG-->T transve

161 to be useful for site-specific production of dA* in nucleic acid oligomers and/or polymers and also f

162 The limit of quantification of dA-AL-I was 3 adducts per 10(9) DNA bases per 2.5 mug of

163 ry of 3DA/dT is exactly the same as those of dA/dT, which makes 3DA an optimal analogue for probing m

164 us ion or thiophenol produces good yields of dA, whereas less reactive thiols afford lower yields pre

165 out mice confirmed the biological action of [dA(2)]GLP-1/GcG via multiple targets including GIP, GLP-

166 Twice daily administration of [dA(2)]GLP-1/GcG for 21 days decreased body weight and no

167 Acute administration of [dA(2)]GLP-1/GcG in combination with glucose significantl

168 ally decreases polymerase activity of gp5 on dA(350)/dT(25).

169 ncrease in 8-oxo-dGMP incorporation opposite dA.

170 rising principally by incorporation of dC or dA opposite M1dG followed by partial or full-length exte

171 orated into DNA and paired with either dC or dA.

172 r reactivity was observed with dT than dC or dA.

173 tterns of the guanine when paired with dT or dA and suggest that N7 alkylation may alter the base pai

174 AMD donors averaged 0.54 and 0.96, and 8-oxo-dA averaged 0.04 and 0.05 adducts per 10(6) bases, respe

175 d AMD donors averaged 170 and 188, and 8-oxo-dA averaged 11 and 17 adducts per 10(6) bases, respectiv

176 athophysiological role of 8-oxo-dG and 8-oxo-dA in AMD and other oxidative damage-related diseases in

177 simultaneous analysis of 8-oxo-dG and 8-oxo-dA in human retinal DNA.

178 8-oxo-dG) and 8-oxo-2'-deoxyadenosine (8-oxo-dA) in diseased RPE could provide important insights int

179 hat extension from both 8-oxoG:dC and 8-oxoG:dA base pairs is 18- to 580-fold less efficient compared

180 , short-patch base excision repair of 8-oxoG:dA base pairs requires human DNA polymerase beta (hPolbe

181 d stability of the ternary complex of 8-oxoG:dA extension results in further loss of efficiency when

182 nd that extension from 8-oxoG:dC over 8-oxoG:dA is favored by 15-fold.

183 e that the inefficient extension from 8-oxoG:dA serves as a newly discovered fidelity checkpoint duri

184 steen base pairs with deoxyadenosine (8-oxoG:dA).

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

186 The most promising peptide, [dA(2)]GLP-1/GcG, stimulated cAMP production in GIP, GLP-

187 es not form these hydrogen bonds, permitting dA* to rotate around the glycosidic bond to syn and inco

188 anded DNA oligomers (poly dA 50-mer and poly dA 20-mer) through a protein ion channel (alpha-hemolysi

189 ation of single-stranded DNA oligomers (poly dA 50-mer and poly dA 20-mer) through a protein ion chan

190 Applying this combined approach to poly dA and poly dT, we find that the global properties of th

191 al production of IFN-beta triggered by poly (dA:dT) or HSV-1 requires IFNAR signaling.

192 The poly (dA-dT) tracts affect but do not deplete nucleosomes in S

193 Poly(dA) synthesis is dependent on both PRI1 protein and ATP

194 n complexes loaded onto the locus via a poly(dA:dT) tract in the gene promoter and mediated cohesion

195 s of the PHO5 promoter that introduce a poly(dA:dT) tract-stimulated gene expression under nonpermiss

196 lic B form double-stranded DNA, such as poly(dA-dT)*poly(dA-dT) [poly(dA-dT)], can also induce IFN-be

197 y expressed DNA sensor DDX41 attenuates poly(dA:dT)-triggered IFN-beta production and cGAS induction.

198 ing a closely knit relationship between poly(dA:dT) tracts, their capping patterns, and the central c

199 first small molecule discovered to bind poly(dA), binds with unexpectedly high affinity (K(a) >10(7)

200 nds, including lipid A, LPS, poly(I:C), poly(dA:dT), and cGAMP, induce cGAS expression in an IFN-I-de

201 model in which localized and G:C-capped poly(dA:dT) tracts initiate or facilitate the formation of NF

202 Here, we show that the cytosolic poly(dA-dT) DNA is converted into 5'-ppp RNA to induce IFN-be

203 Contrary to neomycin, 3 destabilizes poly(dA).2poly(dT) triplex but stabilizes poly(dA).poly(dT) d

204 hat selectively bind to the triplex DNA poly(dA)-[poly(dT)](2).

205 d DNA, such as poly(dA-dT)*poly(dA-dT) [poly(dA-dT)], can also induce IFN-beta, but the underlying me

206 ouble-stranded DNA, such as poly(dA-dT)*poly(dA-dT) [poly(dA-dT)], can also induce IFN-beta, but the

207 First, poly(dA:dT) tracts are localized in a strand-dependent manner

208 for poly(dG) and 1.2 x 10(9) s(-1) for poly(dA).

209 of intercalator-neomycin conjugates for poly(dA).2poly(dT) increases as a function of the surface are

210 stacking, we find that base-stacking in poly(dA) significantly enhances the polymer's rigidity.

211 t S/MARs are preferentially enriched in poly(dA:dT) tracts, sequences that resist nucleosome formatio

212 ic cross-linking, we show that internal poly(dA:dT) tracts do not block the engagement of the ATPase

213 ich poly(dA).2poly(dT) dissociated into poly(dA).poly(dT) and poly(dT) increased dramatically (>12 de

214 The unstacking transition of poly(dA) at high force reveals that the intrinsic electrostat

215 njugates, the increment of T(m3-->2) of poly(dA).2poly(dT) induced by neomycin was negligible under t

216 characterized by positioned patterns of poly(dA:dT) tracts with several novel features.

217 By analyzing the dynamic expression of poly(dA:dT)-induced IFN-beta and cGAS transcripts, we have fo

218 pletion at promoters is maintained over poly(dA:dT) tracts, whereas internucleosome spacing and all o

219 fect is particularly strong at repeated poly(dA:dT) and poly(dC:dG) tracts.

220 Second, poly(dA:dT) tracts are preferentially "capped" by G:C residue

221 owing deserves to be singled-out: short poly(dA:dT) tracts are reported in the literature as fundamen

222 at all four conjugates (1-4) stabilized poly(dA).2poly(dT) much more than its parent compound, neomyc

223 ly(dA).2poly(dT) triplex but stabilizes poly(dA).poly(dT) duplex, suggesting the major groove as the

224 the elastic response of highly stacked poly(dA) and that of a polypyrimidine sequence with minimal s

225 free energy difference between stacked poly(dA) and unstacked polypyrimidine, finding it to be appro

226 Hud's laboratory has shown that poly(dA) in the presence of coralyne forms an anti-parallel d

227 Biochemical analyses showed that poly(dA-dT)-activated AIM2 inflammasomes induce autophagy and

228 c and equilibrium experiments show that poly(dA:dT) tracts perturb remodeling reactions if within one

229 ly(dA).poly(dT) DNA duplex than for the poly(dA).2poly(dT) DNA triplex.

230 ow that 3 has a higher affinity for the poly(dA).poly(dT) DNA duplex than for the poly(dA).2poly(dT)

231 le for synthesizing 5'-ppp RNA from the poly(dA-dT) template.

232 tercalator-neomycin conjugates (1-4) to poly(dA).2poly(dT) was also confirmed by competition dialysis

233 oly(dA-dT)(2) is enthalpy-driven and to poly(dA)poly(dT) is entropy-driven.

234 affinity where the binding of HMGA2 to poly(dA-dT)(2) is enthalpy-driven and to poly(dA)poly(dT) is

235 st, RSC clears promoters by translating poly(dA:dT) into directional nucleosome removal.

236 gates and a DNA polynucleotide triplex [poly(dA).2poly(dT)] were conducted.

237 denine hydrogen bonding between the two poly(dA) strands, we constructed 40 hypothetical homo-(dA) an

238 at the temperature (T(m3-->2)) at which poly(dA).2poly(dT) dissociated into poly(dA).poly(dT) and pol

239 ized in a strand-dependent manner, with poly(dA) tracts lying proximal to transcriptional start sites

240 g site size ( approximately 7-7.5) with poly(dA).2poly(dT) as compared to neomycin ( approximately 6.

241 ing affinity of all tested ligands with poly(dA).2poly(dT) increased in the following order: neomycin

242 The binding of compounds 1-4 with poly(dA).2poly(dT) was mostly enthalpy-driven and gave negati

243 [(2.7 +/- 0.3) x 10(8) M(-1)] of 2 with poly(dA).2poly(dT) was the highest, almost 1000-fold greater

244 e intercalator-neomycin conjugates with poly(dA).2poly(dT) were derived from an integrated van't Hoff

245 le internal mismatches is rG.dG > rU.dT > rA.dA > rC.dC.

246 The thermodynamic contributions of rA.dA, rC.dC, rG.dG and rU.dT single internal mismatches we

247 cannot catalyze extension from the resulting dA terminus.

248 ablished a method to quantitatively retrieve dA-AL-I from FFPE tissue.

249 s reveal concerted opening of the central rU-dA base pairs in the RNA-DNA hybrid.

250 These results suggest that the central rU-dA/dT-dA base pairs in the adenine tract make the larges

251 rs are more stable than the corresponding rU-dA base pairs in the hybrid by 0.9 to 4.6 kcal/mol and,

252 The opening and the stability of each rU-dA/dT-dA base pair in the two structures are characteriz

253 In the RNA-DNA hybrid, the stabilities of rU-dA base pairs range from 4.3 to 6.5 kcal/mol (at 10 degr

254 rnal mismatch is rC.dG > rG.dC >> rA.dT > rU.dA.

255 ernal mismatch is rG.dC > rC.dG > rA.dT > rU.dA.

256 flecting inherent sensitivity to an oligo(rU.dA) hybrid that is the termination signal proper.

257 promotes destabilization via a weak oligo(rU:dA) hybrid, the non-template strand provides distinct se

258 e-stranded DNA conjugates with the sequence (dA)10.(dT)10 and hexaethylene glycol linkers at one end

259 excited states observed in single-stranded (dA)n sequences.

260 ilities, 7-deaza adenine base substitutions (dA-->7) were engineered into homo-(dA) sequences.

261 With syn dA*, there is also an opportunity for increased misincor

262 ween dtCoTP and dTTP when copying a template dA.

263 resistant to acid-catalyzed hydrolysis than dA.

264 e in its anti conformation), suggesting that dA analogues with a substituent at the 2-position are li

265 The dA adduct is significantly more mutagenic than the dG ad

266 The dA(*+)/dA* equilibrium, and consequently the reactivity

267 pon cell division, which was detected as the dA M+1 isotopologue.

268 matic digestion of duplex DNA containing the dA-Ap cross-link.

269 its of detection of 100 fg on-column for the dA isotopologues.

270 escribe the total synthesis, de novo, of the dA and dG adducts derived from AA-II, their incorporatio

271 melting as a function of the location of the dA-->7 mutations, these results are consistent with the

272 ings establish the chemical structure of the dA-Ap cross-link released from duplex DNA and may provid

273 of the base sequence is the proximity of the dA-rU base pair, which destabilizes the G-C base pair wh

274 lock combined with the poor extension of the dA.rA mispair reduce transcriptional mutagenesis.

275 -bound ground-state structures show that the dA*dCTP-Mg2+ complex adopts an 'intermediate' protein co

276 re-chemistry-state' structures show that the dA*dCTP-Mn2+ complex is structurally very similar to the

277 t pH 7 and 37 degrees C, suggesting that the dA-Ap cross-link could be a persistent lesion with the p

278 complex is structurally very similar to the dA*dCTP-Mg2+ complex, whereas the dG*dTTP-Mn2+ complex u

279 oops by using Tel22 derivatives in which the dA residues were serially substituted with the fluoresce

280 the length or relative concentration of the (dA)(k) spacers added during probe immobilization control

281 ization for these probes indicates that the (dA)(m) block preferentially adsorbs on gold, forcing the

282 This dA nucleoside analogue is more resistant to acid-catalyz

283 Oligonucleotides including this dA nucleoside analogue possess base-pairing properties s

284 he crystal structure of the variant bound to dA:dCTP, the fingers domain closes around the mismatched

285 titutions (mostly M(1)dG to dT and M(1)dG to dA) and frameshift mutations.

286 d 8-aza-7-deazapurine nucleosides related to dA and dG bearing 7-octadiynyl or 7-tripropargylamine si

287 The triphosphates dA(SR)TP were good substrates for DNA polymerases useful

288 ed to 5'-O-mono-(dA(SR)MP) or triphosphates (dA(SR)TP) by phosphorylation.

289 fferences in stability are enhanced when two dA-rU base pairs are located next to each other in the h

290 ed structures that form readily in unlinked (dA)n.(dT)n sequences, allowing the excited-state dynamic

291 In contrast, when dA* is flanked by dA, the increased dA(*+) pKa results i

292 nd (1-MIM glucosinolate or alcohol), whereas dA adducts predominated in the cell-free system.

293 a natural base pair, and when combined with dA-dT and dG-dC, it provides a fully functional six-lett

294 the level of incorporation of 8-oxo-dG with dA in the template strand was reduced 500-fold.

295 ds and forms reversibly and exclusively with dA.

296 -digested material reveals that the ICL with dA is a cyclic adduct.

297 while such phenomena were not observed with dA-1 adducts.

298 also form a relatively stable base pair with dA.

299 d elongate an oxidized rGMP when paired with dA.

300 determine the selectivity for reaction with dA.

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