ライフサイエンスコーパス: dC

1 alogous N-oxopropenyl derivatives of dA (4), dC (5), and N1-methyl-dG (6) were synthesized and their

2 in mitosis A (NIMA)-related kinase, by 5aza-dC is context-specific as NEK2 transcript levels were re

3 gene, illustrate that its repression by 5aza-dC is specific and associated with nucleosome reorganiza

4 Demethylation by 5aza-dC was associated with increased accessibility to microc

5 tion and ignores repression elicited by 5aza-dC.

6 ng agents (e.g. 5-aza-2'-deoxycytidine (5aza-dC)) to study epigenetic regulation often focuses on gen

7 ss-of-function (5-Aza-2'-deoxycytidine (5Aza-dC)-induced senescence bypass) screening system.

8 Expression of cytidine deaminase, a dC-catabolizing enzyme, in leukemia cells both in cell c

9 For example, a dC N3-QM adduct is made stable over the course of observ

10 that a 3' end of the primer terminating in a dC residue opposite a 5' dG provides the greatest degree

11 lex and another complex with Dpo4 bound to a dC.M1dG pair located in the postinsertion context.

12 s to be lost principally via transition to a dC:dG pair.

13 In addition to accepting dC and purine nucleosides (and their analogs) as phospho

14 Pol V played a major role in bypassing alpha-dC, alpha-dG and alpha-dT in vivo.

15 uncedly reduced the C-->A mutation for alpha-dC and triggered T-->A mutation for alpha-dT.

16 was error-free, replicative bypass of alpha-dC and alpha-dG yielded mainly C-->A and G-->A mutations

17 Irradiation of the dT-1 and dC-1 cross-linked products at 254 nm leads to a reversib

18 We report multiple annealing and dC-tailing-based quantitative single-cell RNA-seq (MATQ-

19 the substitutions of a dA with N(6)-CMdA and dC with N(4)-CMdC in a 12-mer duplex increased Gibbs fre

20 G, A, or C and reactions between dG, dA and dC and 8-mer peptides containing a single reactive targe

21 The N-oxopropenyl derivatives of dA and dC both exhibited pKa's of 10.5, whereas the N-oxopropen

22 inserted opposite an AP site whereas dA and dC were inserted at equal frequencies opposite F and L s

23 d by 4-OHEN oxidation react with dG, dA, and dC to form unusual stable cyclic bulky adducts, with fou

24 s of Lys, Cys, His, and Trp with dG, dA, and dC.

25 s of DNA polymerase beta with dG-dAMPCPP and dC-dAMPCPP mismatches in the active site.

26 structures with O(6)- MeG opposite dCTP and dC display sheared configuration of base pairs but to di

27 is the complementary base for both dFdC and dC.

28 on of dCTP with templating bases dA, dT, and dC over correct dNTPs.

29 e, two, or three nonadjacent modified dU and dC and of a single dU(8) in the Dickerson-Drew dodecamer

30 nd there is little difference between dU and dC.

31 resulting labeled nucleotides (dC(MBI)TP and dC(FBI)TP) were used for a facile enzymatic synthesis of

32 ivation, which included increased Draper and dCed-6 expression and extension of glial membranes to de

33 y (e.g., the engulfment receptor Draper, and dCed-6), respond morphologically to axon injury, and aut

34 erential RGYW/WRCY targeting by mutations at dC/dG.

35 reatment with 5'-aza-2-deoxycytidine (5'-aza-dC) (an inhibitor of DNA methylation) allowed TFAP2C to

36 5-AZA-dC and DNMT1 AS similarly depleted available DNMT1 prote

37 ere increased 5-fold by treatment with 5-aza-dC and were increased 100-1,000-fold by treatment with T

38 The cellular sensitivity to 5-aza-dC correlated well with the expression status of Dnmt3 i

39 The DNA demethylating agent 5-aza-dC did not increase NAG-1 expression, but TSA up-regulat

40 glioblastomas were exposed to 5 microM 5-aza-dC for 96 h followed by cRNA hybridization to an oligonu

41 As the therapeutic effects of 5-Aza-dC greatly depend on the presence of DNMT1, the expressi

42 prevent the anti-adipogenic effect of 5-Aza-dC in 3T3-L1 preadipocytes and block the osteoblastogeni

43 enografts resulted from treatment with 5-AZA-dC in combination with IFN-beta, an effect not resulting

44 ified the antiproliferative effects of 5-aza-dC in HCC cells, but failed to enhance senescence.

45 d block the osteoblastogenic effect of 5-Aza-dC in ST2 mesenchymal stem cell line.

46 the latter accounted for inhibition of 5-Aza-dC incorporation into the cell genome, enabling them to

47 The molecular mechanism by which 5-aza-dC induces cancer cell death, however, is not fully unde

48 Thus, 5-aza-dC induces Dnmt1 degradation in wild-type mouse ES cells

49 ition to demethylation, treatment with 5-Aza-dC induces gamma-H2AX expression, a marker for DNA break

50 Here we show that 5-aza-dC induces the proteasomal degradation of free (non-chro

51 ypothesis that the mutagenic effect of 5-Aza-dC may be directly mediated through the DNA methyltransf

52 s suggest that the cytotoxic effect of 5-aza-dC may be mediated primarily through Dnmt3a and Dnmt3b d

53 that adducts formed between DNMT1 and 5-aza-dC molecules in DNA induce a ubiquitin-E3 ligase activit

54 ude that inhibiting DNA methylation by 5-Aza-dC mutual-exclusively regulates the lineage determinatio

55 Demethylation by 5-AZA-dC of the promoter of the prototypic, apoptosis-associat

56 ytotoxicity, we examined the effect of 5-aza-dC on cell growth and apoptosis in various Dnmt null mut

57 Either 5-AZA-dC or an antisense to DNA methyltransferase 1 (DNMT1) ov

58 comparable with treatment with either 5-aza-dC or RA.

59 esis and the targeting of incorporated 5-aza-dC residues by DNMT1 itself.

60 cells with the DNA demethylating agent 5-aza-dC reversed the silencing of Peg3 biallelically.

61 methylation in 3T3-L1 preadipocytes by 5-Aza-dC significantly inhibited adipogenesis whereas promoted

62 sults imply a therapeutic potential of 5-aza-dC to cancers expressing Dnmt3.

63 ression and acted synergistically with 5-aza-dC to induce NAG-1 expression.

64 ntage CpG methylation was decreased by 5-aza-dC treatment but was reduced considerably more by IL-1be

65 That is, 5-Aza-dC treatment did not significantly induce AID expression

66 ed 163 genes that were increased after 5-aza-dC treatment in at least two of three CRC cell lines.

67 m, reduction of GnT-V activity through 5-Aza-dC treatment might provide a new approach towards preven

68 Importantly, 5-aza-dC treatment of MDA-MB-231 cells restored TGF-beta induc

69 5-aza-dC treatment restored PER3 expression in HCC cell lines,

70 Of the 271 genes that were induced by 5-aza-dC treatment, 25 also displayed reduced expression in pr

71 prognostic factor for the efficacy of 5-Aza-dC treatment.

72 and that MBD2 binding was released by 5-Aza-dC treatment.

73 ith the promoter was reduced following 5-aza-dC treatment.

74 y restored heparanase expression after 5-Aza-dC treatment.

75 This dual effect of 5-Aza-dC was associated with up-regulation of Wnt10a, a key fa

76 uble null ES cells, the sensitivity to 5-aza-dC was partially restored.

77 null ES cells were highly resistant to 5-aza-dC when compared to wild type, Dnmt3a null, Dnmt3b null,

78 thylating agent 5 aza-2'deoxycytidine (5-Aza-dC) antagonizes the effects of AID knockdown on the expr

79 hylating agent 5-aza-2'-deoxycytidine (5-aza-dC) increased mRNA levels of TPM1 with no effect on TPM2

80 rase inhibitor 5-aza-2'-deoxycytidine (5-aza-dC) increases the expression of PTCH1 and other methylat

81 5-Aza-2'-deoxycytidine (5-aza-dC) is a nucleoside analogue with cytotoxic and DNA deme

82 ytidine analog 5-aza-2'-deoxycitidine (5-aza-dC) is a potent chemotherapeutic agent effective against

83 everse silencing, 5-AZA-deoxycytidine (5-AZA-dC) or selective depletion of DNA methyltransferase 1 (D

84 leoside analog 5-AZA-2'-deoxycytidine (5-AZA-dC) synergistically augmented antiproliferative effects

85 pression after 5-aza-2'-deoxycytidine (5-aza-dC) treatment, suggesting that aberrant methylation of t

86 er IFNgamma or 5-aza-2'-deoxycytidine (5-aza-dC) treatment.

87 determined by 5-aza-2'-deoxycytidine (5-aza-dC) treatment.

88 statin M (OSM), or 5-azadeoxycytidine (5-aza-dC) was added twice weekly for 4-5 weeks to primary cult

89 hylating agent 5-aza-2'-deoxycytidine (5-Aza-dC) was sufficient to reactivate BAI1 expression.

90 ed the role of 5-aza-2'-deoxycytidine (5-Aza-dC), an inhibitor of DNA methylation, in the lineage det

91 methylating agent 5-aza-deoxycytidine (5-aza-dC), transgenic expression of macroH2A1 isoforms in HCC

92 t treatment of 5-aza-2'-deoxycytidine (5-aza-dC).

93 rase inhibitor 5-Aza-2'-deoxycytidine (5-aza-dC).

94 gents, such as 5-aza-2'-deoxycytidine (5-Aza-dC).

95 lating agents [5-aza-2'-deoxycytidine (5-aza-dC)] and histone deacetylase (HDAC) inhibitors (trichost

96 f ABCG2 was achieved by treatment with 5-aza-dC, a demethylating agent, concomitant with the release

97 Treatment of cells with 5-Aza-dC, an inhibitor of DNA methylation, resulted in decreas

98 esistance to the cytostatic effects of 5-Aza-dC, delayed onset of gamma-H2AX expression and a signifi

99 wing treatment with trichostatin A and 5-aza-dC, the formerly unresponsive ER-negative MDA-MB-231 bre

100 An alternative mechanism for 5-Aza-dC-induced demethylation and genome rearrangements via a

101 adducts is the prevalent mechanism of 5-Aza-dC-induced genome rearrangements, although hypomethylati

102 There was no effect on the 5-Aza-dC-induced point mutations.

103 Cells that escaped 5-Aza-dC-induced senescence were subjected to miR-microarray a

104 n the DNA methyltransferase (Dnmt) and 5-aza-dC-substituted DNA.

105 ferase 1 (DNMT1) covalently trapped in 5-Aza-dC-substituted DNA.

106 and reduces hypomethylation induced by 5-aza-dC.

107 ed more than 10 times in expression by 5-AZA-dC.

108 lation levels were markedly reduced by 5-Aza-dC.

109 ation inhibitor, 5-aza-2'-deoxycytidine (aza-dC) increases collagen gene expression with time in huma

110 sertion of 8-oxodGTP opposite template bases dC and dA.

111 and in mice reduced the competition between dC and [(18)F]CFA, leading to increased dCK-dependent pr

112 observed tendency of hpol eta to insert both dC and dT opposite the O(6)-MeG lesion with similar effi

113 X-ray crystal structures of both dC and dT paired with O(6)-MeG were solved in both inser

114 n when the modified nucleotide is opposed by dC.

115 5-Formyl-dC (fdC) and 5-carboxy-dC (cadC) are newly discovered bases in the mammalian ge

116 double-domained deaminases that can catalyze dC-->dU deamination in HIV-1 and MLV retroviral DNA repl

117 l perturbations involving the modified S-cdG.dC and 3'- neighbor dT.dA base pairs.

118 rick base pairing was conserved at the S-cdG.dC pair.

119 , the results of which indicate that (i) CdG:dC base pairs are likely destabilized relative to dG:dC

120 Melting studies revealed CdG:dC base pairs are less stable than dG:dC base pairs, whi

121 G lesion in the absence of the complementary dC correlates with the one-base deletion extension produ

122 The complementary dC is extruded into the major groove.

123 IQ quinoline nitrogen and the complementary dC.

124 hosphorylation, dCK is capable of converting dC, dA, and dG into their monophosphate forms.

125 The lesion counterbase dC is displaced in the minor groove of the duplex where

126 This loop is disordered in the dCK-dC structure, which lacks a ligand at the phosphoryl don

127 had either a dThymidine (dT) or a dCytidine (dC) at the 13th position of the probe sequence.

128 One antiviral mechanism involves deaminating dC residues in minus-strand DNA during reverse transcrip

129 troviral replication by inducing deleterious dC > dU hypermutation of replication intermediates.

130 Deoxycytidine (dC) triphosphate (dCTP) can be produced both by the de n

131 or more contiguous runs of 2'-deoxycytidine (dC) nucleotides have the potential to adopt i-motif fold

132 times more frequently than 2'-deoxycytidine (dC) opposite OxodI.

133 imately 63% replacement of 2'-deoxycytidine (dC) with 5-hydroxymethyl-2'-deoxycytidine (5hmC) in the

134 dA), deoxyguanosine (dG), and deoxycytidine (dC) into their monophosphate forms, with subsequent phos

135 es to deoxythymidine (dT) and deoxycytidine (dC), we hypothesized that: (1) deoxynucleosides might be

136 es of BPQ-dG, BPQ-dA, and BPQ-deoxycytidine (dC) as standards.

137 8)F]CFA uptake was reduced by deoxycytidine (dC) competition, this inhibition required high dC concen

138 DNA polymerase kappa, insert deoxycytidine (dC) opposite N2-furfuryl-dG with 10-15-fold greater cata

139 ural analog of the nucleoside deoxycytidine (dC), derives its primary antitumor activity through inte

140 that catalyzes deamination of deoxycytidine (dC) on single-stranded DNA (ssDNA).

141 as wild type, in complex with deoxycytidine (dC) and UDP, and in the presence of dC but the absence o

142 by reaction of bisulfite with deoxycytidine (dC)) to uracil (dU).

143 s CSR and SHM by deaminating deoxycytidines (dCs) in switch (S) and V(D)J region DNA, respectively, t

144 emonstrated that a simple mass-weighted deta/dC response function is the incorrect equation to determ

145 mprised of just two base pairs (dA-dT and dG-dC), is conserved throughout all life, and its expansion

146 se pair, and when combined with dA-dT and dG-dC, it provides a fully functional six-letter genetic al

147 2Tri4 combines with [poly(dA-dT)]2, [poly(dG-dC)]2, or salmon testes DNA.

148 Extension from M(1)dG.dC was equally as efficient as from control primer-templ

149 ficient as from control primer-templates (dG.dC).

150 M(1)dG.dA was 20-fold less efficient than dG.dC.

151 xtended template-primers in the order M(1)dG:dC > M(1)dG:dG > M(1)dG:dT approximately M(1)dG:dA, but

152 ogen bond for a halogen bond in dA:dT and dG:dC base pairs, which allows 1 or 2 hydrogen bonds, respe

153 nt from the patterns joining the dA:T and dG:dC pairs.

154 and N7mdG:dG are very similar to those of dG:dC and dG:dG, respectively, indicating the involvement o

155 ed CdG:dC base pairs are less stable than dG:dC base pairs, while CdG:dA base pairs are less stable t

156 pairs are likely destabilized relative to dG:dC as a result of structural constraints imposed by the

157 eplaced with inosine [poly(dC-dG) vs poly(dI-dC)], and 10-100-fold slower catalytic rates with Dnmt1

158 essed two therapies in Tk2(-/-) mice: (1) dT+dC and (2) coadministration of the deaminase inhibitor,

159 ated into template-primers containing either dC or dT residues 5' to the adduct, and the template-pri

160 incorporated into DNA and paired with either dC or dA.

161 le inhibitor of the NSP rate-limiting enzyme dC kinase (dCK).

162 -purine, dF, 4-thio-dU, N(3)-Me-dC, N (4)-Et-dC, Psi-iso-dC, and arabinoC or 7-deaza-dG, 7-deaza-8-az

163 idues in the 5-position of pyrimidines ((eth)dC and (eth)dU) or the 7-position of 7-deazaguanine ((et

164 lore the TLS mechanism of a heptanone-etheno-dC (H-epsilondC) adduct, an endogenous lesion produced b

165 a functional vif gene by inducing extensive dC-to-dU editing, only the induced A3B protein inhibited

166 pathway, we established that the fluorescent dC analogs tC degrees and PdC can be used to monitor ind

167 The fluorescent dC-analog 6-methylpyrrolo[2,3-d]pyrimidine-2(3H) one deo

168 lts lay the foundation for using fluorescent dC analogs to follow structural changes during iM format

169 ver 1000-fold while eliminating activity for dC, dA, and dG under physiological conditions.

170 5-Formyl-dC (fdC) and 5-carboxy-dC (cadC) are newly discovered ba

171 posite the lesion, as well as extension from dC:8-oxo-dG base pairs.

172 -dG approximately 10-fold and extension from dC:8-oxo-dG by 2.4-fold.

173 The distance between the 5' G-dC base pair and the 3' end of RNA fluctuates over a thr

174 We reveal that the G-dC base pair at the 5' end of the RNA-DNA hybrid interfe

175 Thus, the G-dC base pair can induce pausing in post-translocated, pr

176 nal pausing involves RNAP interaction with G-dC at the upstream end of the RNA-DNA hybrid, which inte

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

178 f the stable isotope standards [(15)N5]dG-gx-dC and [(15)N5]dG-gx-dA as internal standards, enzyme hy

179 Furthermore, the levels of dG-gx-dC and dG-gx-dA correlated with HbA1c with statistical s

180 us detection and quantification of the dG-gx-dC and dG-gx-dA cross-links based on stable isotope dilu

181 T2DM) patients (n = 38), the levels of dG-gx-dC and dG-gx-dA in leukocyte DNA were 1.94 +/- 1.20 and

182 quantification was 94 and 90 amol for dG-gx-dC and dG-gx-dA, respectively, which is equivalent to 0.

183 de adducts cross-linked by glyoxal are dG-gx-dC, dG-gx-dA, and dG-gx-dG.

184 dine derivatives examined [XdC, where X = H (dC), CH(3) (medC), CH(2)OH (hmdC), CHO (fmdC), COOH (cad

185 mely high outlier intensities contained high dC rich nucleotides, and low dA contents at other nucleo

186 ) competition, this inhibition required high dC concentrations present in murine, but not human, plas

187 erved DNA polymerase activity, which inserts dC, is much less well understood.

188 4-thio-dU, N(3)-Me-dC, N (4)-Et-dC, Psi-iso-dC, and arabinoC or 7-deaza-dG, 7-deaza-8-aza-dG, 9-deaz

189 ith a nicked substrate containing juxtaposed dC and 5'-phosphorylated dT deoxynucleotides (substrate

190 ry of a stable levuglandin-deoxycytidine (LG-dC) adduct that forms upon reaction of levuglandin with

191 Reaction of LG with DNA yielded a stable LG-dC adduct with a pyrrole structure.

192 xchange factor (GEF) Crk/myoblast city (Mbc)/dCed-12 has no effect on glial activation, but blocks in

193 We found that Crk/Mbc/dCed-12 and Rac1 functioned in a non-redundant fashion w

194 e nucleotide exchange factor complex Crk/Mbc/dCed-12 and the small GTPase Rac1 as modulators of glial

195 synaptic and neuronal debris and for Crk/Mbc/dCed-12 as a new glial pathway mediating pruning and rev

196 n of vCrz(+) neurites is mediated by Crk/Mbc/dCed-12 but not Draper.

197 In contrast, the Crk/Mbc/dCed-12 complex functioned at later phases, promoting gl

198 d by astrocytes using the Draper and Crk/Mbc/dCed-12 signaling pathways in a partially redundant mann

199 in a partially redundant manner with Crk/Mbc/dCed-12, with blockade of both complexes strongly suppre

200 eaza-8-methyl-purine, dF, 4-thio-dU, N(3)-Me-dC, N (4)-Et-dC, Psi-iso-dC, and arabinoC or 7-deaza-dG,

201 ytidine analogue 5-methyldeoxycytidine (5-Me-dC), an isostere of thymidine, can indeed be phosphoryla

202 rystal structure of dCK in complex with 5-Me-dC.

203 shown by lack of inhibition of AID-mediated dC deamination by other bivalent metal ions, such as Zn(

204 Rather, it inhibited AID-mediated dC deamination in a dose-dependent fashion.

205 ive site configurations with either O(6)-MeG:dC or O(6)-MeG:dT bound compared with the corresponding

206 ed with 2'-O-methylribonucleotides, 5-methyl-dC, or 2'-O-methyl-5-methyl-C and studied their immune s

207 ilin and equilenin, promotes 4-OHEN-modified dC, dA, and dG DNA adducts.

208 TCG1G2CG3*CNATC-3')(5'-GATNCGGCCGAG-3'), N = dC or dT] and -2 deletion [(5'-CTCG1G2CG3*CNATC-3')(5'-G

209 -CTCG1G2CG3*CNATC-3')(5'-GATNGCCGAG-3'), N = dC or dT] duplexes, in which G* was either AF [N-(2'-deo

210 The structures of N7mdG:dC and N7mdG:dG are very similar to those of dG:dC and d

211 highest (69-75%) at the G3 hot spot in NarI-dC duplexes.

212 d UV melting results indicated that the NarI-dC/-2 deletion duplex adopts exclusively an intercalated

213 cking at the lesion site and the 5'-neighbor dC.dG base pair.

214 (X = 1,N(2)-epsilondG), in which there is no dC opposite the lesion.

215 nker, and the resulting labeled nucleotides (dC(MBI)TP and dC(FBI)TP) were used for a facile enzymati

216 Analysis of dC homo-oligonucleotide strands ranging in length from 1

217 d cytidine deaminase-mediated deamination of dC residues, thereby promoting S-S region synapses and i

218 A3G mutates the HIV genome by deamination of dC to dU, leading to accumulation of virus-inactivating

219 ons initiated by AID-mediated deamination of dC to yield dU:dG mismatches.

220 an explain the preferential incorporation of dC by Dpo4.

221 ns necessary for error-free incorporation of dC opposite the lesion.

222 ucts arising principally by incorporation of dC or dA opposite M1dG followed by partial or full-lengt

223 These derivatives are designed as mimics of dC and dU, and in that respect, each can form two hydrog

224 ytidine (dC) and UDP, and in the presence of dC but the absence of UDP or ADP.

225 tuted C or G of a CpG dinucleotide with 5-OH-dC, 5-propyne-dC, furano-dT, 1-(2'-deoxy-beta- d-ribofur

226 4-Hydroxyequilenin (4-OHEN)-dC is a major, potentially mutagenic DNA adduct induced

227 The 4-OHEN-dC adducts are most predominant.

228 To study the miscoding property of 4-OHEN-dC and the involvement of Y-family human DNA polymerases

229 We have recently found that the 4-OHEN-dC DNA adduct is a highly miscoding lesion generating C

230 iota in that process, we incorporated 4-OHEN-dC into oligodeoxynucleotides and used them as templates

231 The miscoding potency of 4-OHEN-dC may be associated with the development of reproductiv

232 ctures and thermodynamics of the four 4-OHEN-dC stereoisomeric adducts in DNA duplexes.

233 Pol eta inserted dAMP opposite 4-OHEN-dC, accompanied by lesser amounts of dCMP and dTMP incor

234 As revealed by CD, DNA oligomers, (dC-dG)(4) and (dm(5)C-dG)(4), both form right-handed dou

235 The 8-oxodGTP was incorporated opposite dC in the template with a specificity constant of 0.005

236 f (R)- and (S)-CEdGTP only occurred opposite dC and was catalyzed by Kf(-) with equal efficiencies.

237 a site-specific S-cdG lesion placed opposite dC in the complementary strand was obtained by molecular

238 ducts contained incorporation of dA (52%) or dC (16%) opposite M(1)dG or -1 frameshifts at the lesion

239 and forming Watson-Crick pairs with dCTP or dC.

240 glia, in contrast, do not express Draper or dCed-6, fail to respond morphologically to axon injury,

241 ta showed a 2:1 preference to insert dA over dC, while AMV-RT incorporated predominantly dC.

242 demonstrate that extension from both 8-oxoG:dC and 8-oxoG:dA base pairs is 18- to 580-fold less effi

243 r loss of efficiency when compared to 8-oxoG:dC extension.

244 8-oxoG bypass and that extension from 8-oxoG:dC over 8-oxoG:dA is favored by 15-fold.

245 -Crick base pairs with deoxycytidine (8-oxoG:dC) and Hoogsteen base pairs with deoxyadenosine (8-oxoG

246 es (FB) 2-aminopurine (AP) and pyrrolo-dC (P-dC) as fluorophores.

247 to double strand for AP and vice versa for P-dC.

248 denaturation profiles monitored at 450 nm (P-dC emission) show a cooperative denaturation of the MB-F

249 nce increase (the fluorescence emission of P-dC over that of AP in the presence and absence of comple

250 rges, with protonation of the lesion partner dC and possible formation of a Hoogsteen base pair.

251 The lesion partner dC is extrahelical and is located in the minor groove of

252 We compare the alpha-OH-PdG.dC duplex structure with that of duplexes containing the

253 ower for substrates with a 5'-phosphorylated dC or dG residue on the 3' side of the ligation junction

254 arly strong at repeated poly(dA:dT) and poly(dC:dG) tracts.

255 which guanine is replaced with inosine [poly(dC-dG) vs poly(dI-dC)], and 10-100-fold slower catalytic

256 dC, while AMV-RT incorporated predominantly dC.

257 f a CpG dinucleotide with 5-OH-dC, 5-propyne-dC, furano-dT, 1-(2'-deoxy-beta- d-ribofuranosyl)-2-oxo-

258 resenting a puADD pattern), while protonated dC (presenting a pyDDA pattern) complements dP (presenti

259 idine-2(3H) one deoxyribonucleoside (pyrrolo dC), which pairs with G, was positioned opposite G, O6-M

260 escence changes were observed with G:pyrrolo dC or T:2-aminopurine pairs.

261 nt bases (FB) 2-aminopurine (AP) and pyrrolo-dC (P-dC) as fluorophores.

262 6-Substituted pyrrolo-dC-pyrrolo-dC mismatches selectively capture silver ions to form ex

263 6-Substituted pyrrolo-dC-pyrrolo-dC mismatches selectively capture silver ions

264 The thermodynamic contributions of rA.dA, rC.dC, rG.dG and rU.dT single internal mismatches were meas

265 nal mismatches is rG.dG > rU.dT > rA.dA > rC.dC.

266 mispair, with WT RT preferentially resolving dC-rC pairs either by excising the mismatched base or sw

267 f the single internal mismatch is rC.dG > rG.dC >> rA.dT > rU.dA.

268 irs 5' of the single internal mismatch is rG.dC > rC.dG > rA.dT > rU.dA.

269 tream portion of the PPT and a downstream rG:dC tract.

270 nus of the (+)-strand primer, whereas the rG:dC tract serves as the primary determinant of initiation

271 Adding a second dC residue at the 3' penultimate position opposite anoth

272 AID activity converts several dC bases to dU bases in each S region, and the dU bases

273 the selectivity of hTDG toward 5-substituted dC derivatives.

274 igher than incorporation opposite a template dC.

275 but instead with the 5'-neighboring template dC, utilizing Watson-Crick geometry.

276 matic copying of a DNA homopolymer template (dC(15)) encapsulated within fatty acid vesicles using 2'

277 r (NIR) product with an abortive 3'-terminal dC close to the scissile position in the enzyme active s

278 -Crick base pairing with the primer terminus dC and the incoming dCTP, providing the structural basis

279 higher reactivity was observed with dT than dC or dA.

280 (dm(5)C-dG)(4) being more endothermic than (dC-dG)(4) by 700 cal/mol basepair.

281 We observed that dC+dT delayed disease onset, prolonged life span of Tk2-

282 The dC derivative produces ICLs approximately 10x faster tha

283 e was only 2.3 times lower than that for the dC x dG-N2-TAM pair, indicating that dG-N2-TAM in the K-

284 in the structure with dC opposite M1dG, the dC residue moved out of the Dpo4 active site, into the m

285 kappa deltaC, the bypass frequency past the dC x dG-N2-TAM pair was higher than that of the dT x dG-

286 polymerase beta (Polbeta) would replace the dC deaminated by AID, leading to correct repair of the s

287 When placed complementary to dC in this duplex, both adducts open to the correspondin

288 especially cadC react considerably faster to dC.

289 heno-2'-deoxyguanosine (epsilonG), paired to dC.

290 ine destabilizes (dm(5)C-dG)(4) relative to (dC-dG)(4).

291 structure (Z-DNA), whereas the unmethylated (dC-dG)(4) analog remains right-handed under those condit

292 n which does not occur for the unmethylated (dC-dG)(4).

293 red to the hairpins containing an unmodified dC residue.

294 A homohexamers, relative exchange rates were dC(6) approximately dA(6) > dG(6) > dT(6), correlating w

295 es C higher than that of the duplex in which dC is present opposite the 1,N(2)-epsilondG lesion and 8

296 nding DNA sequence and occurs favorably with dC and dA but not with dG or dT.

297 dG), CdG should form a stable base pair with dC, but similar to OdG, CdG contains an N7-hydrogen that

298 rystal structures of N7mdG or dG paired with dC, dT, dG, and dA.

299 eric form of N7mdG in the base pairings with dC and dG.

300 n both structures, and in the structure with dC opposite M1dG, the dC residue moved out of the Dpo4 a

301 ](3+) resulted in exothermic isotherms with (dC-dG)(4) being more exothermic than (dm(5)C-dG)(4) by 7