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 exes built on a core (bm-Calpha-PNA-T(7))(2):dA(8) triplex.

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 s H-4' atom from (4'R)-5'-deoxyadenosine (5'-dA) to transiently generate 5'-deoxyadenos-4'-yl radical

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

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

10 d the common 5'-deoxyadenosyl 5'-radical (5'-dA(*)) intermediate.

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

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

13 ly generate 5'-deoxyadenos-4'-yl radical (5'-dA-C4'(*)) that is subsequently reduced stereospecifical

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

15 reduced stereospecifically to yield (4'S)-5'-dA.

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

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

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

19 the radical SAM cluster in generating the 5'-dA(*) is well understood, the detailed role of the auxil

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

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

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

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

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

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

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

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

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

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

30 1,N(6)-Ethenodeoxyadenosine (1,N(6)-dA) is the major etheno lesion formed in the reaction of

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

58 nerated benzyl cations alkylated dG, dC, and dA, ICL assay with variation of DNA sequences showed tha

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

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

61 wed a similar photoreactivity toward dGs and dAs.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

79 ion prone to mispair with 2'-deoxyadenosine (dA).

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

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

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

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

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

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

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

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

88 In the presence of complementary DNAs dA(8) and dG(6) at neutral pH, bm-Calpha-PNA 1 forms a h

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

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

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

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

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

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

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

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

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

98 fted toward the radical cation by a flanking dA.

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

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

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

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

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

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

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

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

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

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

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

110 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

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

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

113 19 amol for dG-gx-dC and 0.89 amol for dG-gx-dA, which is 400 and 80 times more sensitive, respective

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

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

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

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

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

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

120 3-diyl)-2'-deoxyadenosine (1,N(6)-gamma-HMHP-dA) adducts are formed upon bifunctional alkylation of a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

136 in vivo, as indicated by increased N6-methyl-dA DNA levels in embryos developed from MTH1 knock-out z

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

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

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

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

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

159 ncorporation of dC, with misincorporation of dA and dG in 5-10% of products.

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 ic leading to errors that are reminiscent of dA:8-oxodG base pairing.

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

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

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

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

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

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

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

171 100-fold more efficiently than that opposite dA, respectively, indicating that the 8-oxo moiety great

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

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

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

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

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

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

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

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

180 8-oxo-dG) and 8-oxo-2'-deoxyadenosine (8-oxo-dA) in diseased RPE could provide important insights int

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

244 [(2.7 +/- 0.3) x 10(8) M(-1)] of 2 with poly(dA).2poly(dT) was the highest, almost 1000-fold greater

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

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

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

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 rt of the oligo(T)-tract, promoting oligo(rU:dA) extension toward greater hybrid instability and RNA

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

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

260 d with opposing dG/dC but not with staggered dA/dA.

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

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

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

264 ween dtCoTP and dTTP when copying a template dA.

265 resistant to acid-catalyzed hydrolysis than dA.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 he syn conformation, 8-oxodG base pairs with dA.

301 determine the selectivity for reaction with dA.

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