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

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

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

25 is the complementary base for both dFdC and dC.

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

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

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

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

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

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

32 (histone deacetylase inhibitor) and/or 5-aza-dC (an inhibitor of DNA methylation).

33 5-Aza-dC activated demethylation of the MEG3-DMR and expressio

34 5-AZA-dC and DNMT1 AS similarly depleted available DNMT1 prote

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

64 However, 5-aza-dC treatment prevented that phenomenon.

65 5-aza-dC treatment restored PER3 expression in HCC cell lines,

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

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

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

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

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

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

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

73 5-Aza-2'-deoxycytidine (5-aza-dC) is a nucleoside analogue with cytotoxic and DNA deme

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

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

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

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

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

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

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

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

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

83 tion inhibitor 5-aza-2'-deoxycytidine (5-aza-dC), we investigated whether DNA methylation alters Thy1

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

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

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

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

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

89 nhibition with 5-Aza-2'-deoxycytidine (5-Aza-dC, decitabine) to demonstrate that DNA methylation pred

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

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

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

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

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

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

96 sion of 14q32 miRNAs and resistance to 5-Aza-dC-induced suppression of AIM.

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

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

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

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

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

102 e DNA hypomethylating drug decitabine (5-aza-dC; DAC) extended survival in the KPC-Brca1 mouse model

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

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

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

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

107 n when the modified nucleotide is opposed by dC.

108 5-Formyl-dC (fdC) and 5-carboxy-dC (cadC) are newly discovered bases in the mammalian ge

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

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

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

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

113 ics for the i-motif form of cytosine chains (dC)(10), using the ultrafast fluorescence up-conversion

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

115 The complementary dC is extruded into the major groove.

116 IQ quinoline nitrogen and the complementary dC.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

137 photogenerated benzyl cations alkylated dG, dC, and dA, ICL assay with variation of DNA sequences sh

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

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

140 2Tri4 combines with [poly(dA-dT)]2, [poly(dG-dC)]2, or salmon testes DNA.

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

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

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

144 t the ICL reaction occurred with opposing dG/dC but not with staggered dA/dA.

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

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

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

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

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

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

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

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

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

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

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

156 -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

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

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

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

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

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

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

163 5-Formyl-dC (fdC) and 5-carboxy-dC (cadC) are newly discovered ba

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

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

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

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

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

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

170 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

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

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

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

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

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

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

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

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

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

180 enetic marks 5-methyl-dC and 5-hydroxymethyl-dC in genomic DNA isolated from lungs of A/J mice expose

181 The lowest excitonic state in i-(dC)(10) is responsible for a 2 ps red-shifted emission a

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

183 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

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

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

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

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

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

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

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

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

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

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

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

195 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,

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

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

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

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

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

201 separately map DNA epigenetic marks 5-methyl-dC and 5-hydroxymethyl-dC in genomic DNA isolated from l

202 troduced via enzymatic oxidation of 5-methyl-dC in DNA.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

217 an explain the preferential incorporation of dC by Dpo4.

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

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

220 catalyzes mainly error-free incorporation of dC, with misincorporation of dA and dG in 5-10% of produ

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

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

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

224 4-Hydroxyequilenin (4-OHEN)-dC is a major, potentially mutagenic DNA adduct induced

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

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

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

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

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

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

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

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

233 iciency of beta-C-Fapy*dG insertion opposite dC.

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

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

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

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

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

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

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

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

242 8-oxoG bypass and that extension from 8-oxoG:dC over 8-oxoG:dA is favored by 15-fold.

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

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

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

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

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

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

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

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

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

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

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

254 dC, while AMV-RT incorporated predominantly dC.

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

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

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

258 6-Substituted pyrrolo-dC-pyrrolo-dC mismatches selectively capture silver ions to form ex

259 Placement of Pyrrolo-dC within the DNA recognition site results in a fluoresc

260 6-Substituted pyrrolo-dC-pyrrolo-dC mismatches selectively capture silver ions

261 This Pyrrolo-dC strand separation assay should be useful for the stud

262 a fluorescence-based assay by which Pyrrolo-dC tracks the strand separation event.

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

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

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

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

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

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

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

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

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

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

273 igher than incorporation opposite a template dC.

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

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

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

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

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

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

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

281 The dC derivative produces ICLs approximately 10x faster tha

282 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-

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

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

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

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

287 especially cadC react considerably faster to dC.

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

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

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

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

292 red to the hairpins containing an unmodified dC residue.

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

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

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

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

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

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

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

300 ](3+) resulted in exothermic isotherms with (dC-dG)(4) being more exothermic than (dm(5)C-dG)(4) by 7