ライフサイエンスコーパス: uracil

1 Hypoxanthine was a weaker inhibitor than uracil.

2 ious results that demonstrated inhibition by uracil.

3 responsible for the proton-driven uptake of uracil.

4 ansformants that grow on agar plates lacking uracil.

5 e to produce adenine, guanine, cytosine, and uracil.

6 cluding Drosophila, are incapable of binding uracil.

7 in incomplete conversion of intermediates to uracil.

8 te resonance form for residue bound 1-methyl-uracil.

9 he dynamic spatio-temporal nature of genomic uracil.

10 superfamily are essential for the removal of uracil.

11 (Vif) by deaminating viral cDNA cytosines to uracils.

12 infected individuals also contained abundant uracils.

13 elity by catalyzing the removal of mutagenic uracils.

14 hich converts cytosines in switch regions to uracils.

15 nduced APOBEC3A/APOBEC3B to increase genomic uracils.

16 id expressing APOBEC3A acquired more genomic uracils.

17 33%), which was not observed for cytosine to uracil (17.86%) editing.

18 ethylacetophenone (1), nicotinamide (2), and uracil (3) from palmyra palm syrup is described.

19 tyl side chain (-CHF-CO-) bearing nucleobase uracil (5-F/5-CF3-U).

20 Novel conjugates of ferrocene with uracil, 5-fluorouracil, tegafur, or acyclovir are report

21 ndings relating to the function of the human uracil-5 methyltransferase (U5MT), TRMT2A, and its inter

22 gnated as Endonulcease Q (EndoQ), recognizes uracil, abasic site and xanthine, as well as hypoxanthin

23 nucleosides did not affect maternal hepatic uracil accumulation in DNA but did affect plasma folate

24 obulin (Igh) gene deamination as measured by uracil accumulation occurs primarily in early G1 after c

25 howed that SMUG1 efficiently prevent genomic uracil accumulation, even in the presence of UNG, and id

26 e et al. (2015) reveal how pathogen-secreted uracil acts at two steps to induce ROS via the Hedgehog

27 By injecting a uracil analog, 4-thiouracil, into transgenic mice that e

28 nstrate that mammalian cells can incorporate uracil analogs and characterize the enzymatic pathways r

29 any ligands or additives to give 5-arylated uracil analogues.

30 the impact of SMUG1 deficiency, we measured uracil and 5-hydroxymethyluracil, another SMUG1 substrat

31 and -7-deazaguanine as well as 5-substituted uracil and cytosine 2'-deoxyribonucleosides and mono- an

32 Uracil and hypoxanthine slowed Afu Pol-D "in trans", tha

33 ylated H3K14 or H3K56 and measured repair of uracil and single-nucleotide gaps.

34 higher than 10(9) M(-1) s(-1), while in the uracil and tert-butyluracil analogues, k(q) was markedly

35 onship between the degree of polarization in uracil and the leaving group ability of uracilate.

36 egradation was observed at the hydroxymethyl uracil and tricyclic guanidine groups; uracil moiety cle

37 he error-prone or error-free repair of these uracils and by selection pressures.

38 rocesses non-helix distorting lesions (e.g., uracils and gaps) and is composed of two subpathways tha

39 ncrease of the choline derivative compounds, uracil, and free amino acids, and a large decrease of ta

40 ucleic acids, is highly specific for thymine/uracil, and maintains and slightly stabilises the canoni

41 to survive by exchanging histidine, leucine, uracil, and methionine.

42 converts cytosines in single-stranded DNA to uracil, and mutations in a variety of human cancers are

43 Its role is to bind to DNA, locate unwanted uracil, and remove it using a base flipping mechanism.

44 Simulations were performed in the absence of uracil, and resulted in a closed state of the transporte

45 n UNG-null cells causes a buildup of genomic uracil, and the ensuing lethality requires processing of

46 les, aminoisoxazole, aminoisothiazole, amino uracils, and aliphatic enamines has been developed in an

47 The rotational temperature of the trapped uracil anion is evaluated to be 35 K.

48 We propose that more uracils are created during B cell cancer development tha

49 The uracils are subsequently removed by two DNA-repair pathw

50 ines (fluorouracil, capecitabine, or tegafur-uracil as single agents, in combination with other antic

51 on the post-transcriptional modification of uracil at position 8 (U8) of tRNAs by the 4-thiouridine

52 tructural features such as the presence of a uracil at the first residue.

53 ne conversion by converting DNA cytosines to uracils at specific genomic regions.

54 ccine strains, such as type I nonreplicating uracil auxotroph mutants, are highly effective in elicit

55 onreverting, nonreplicating, live attenuated uracil auxotroph vaccine strains in the type II Deltaku8

56 However, previous attempts to generate uracil auxotrophy by genetically deleting the mitochondr

57 Deletion of OMPDC induced a severe uracil auxotrophy with loss of replication, loss of viru

58 tically deficient DHODH gene alleles induced uracil auxotrophy.

59 p of de novo pyrimidine biosynthesis induced uracil auxotrophy.

60 The E/Z isomerization process of a uracil-azobenzene derivative in which the nucleobase is

61 ed, contrary to current ideas, that cellular uracil base excision repair (UBER) enzymes target and cl

62 lated viral DNA products are degraded by the uracil base excision repair (UBER) machinery with less t

63 ity were also observed with RNA pol II using uracil base excision repair (UBER)-deficient human cells

64 counteracted in an error-free manner by the uracil base excision repair pathway.

65 abasic site resulting from the cleavage of a uracil base.

66 gen bonds with the N3 and O4 moieties of the uracil base.

67 g between the engineered valine and a target uracil base.

68 on study on the ultrafast photorelaxation of uracil, based on a quantum description of the nuclei.

69 Here, we describe new 1-(omega-phenoxyalkyl)uracils bearing acetanilide fragment in 3 position of py

70 id, arginine, N1-acetylspermidine, xanthine, uracil, betaine, symmetric dimethylarginine, and asymmet

71 turbed in histidine, leucine, methionine and uracil biosynthesis.

72 ion of A-U pair-recognizing 5-benzothiophene uracil ((bt)U).

73 thase inhibitor (raltitrexed), which induces uracil but not 5-FU accumulation, thus indicating that g

74 guanine over adenine, cytosine, thymine and uracil, but this selectivity is extraordinarily amplifie

75 initiated through deamination of cytidine to uracil by activation-induced cytidine deaminase (AID).

76 o not significantly contribute to removal of uracils by uracil DNA glycosylase regardless of the tran

77 The RNA nucleobase uracil can suffer from photodamage when exposed to UV li

78 The resulting uracils cause mutations and strand breaks that inactivat

79 uble-stranded DNA, and copying the resulting uracils causes C to T mutations.

80 convert cytosines in single-stranded DNA to uracils, causing base substitutions and strand breaks.

81 s expressing AID at high levels have genomic uracils comparable to those seen with stimulated UNG(-/-

82 with strengths comparable to those formed by uracil compounds.

83 f-assembly and self-organization behavior of uracil-conjugated enantiopure (R)- or (S)-1,1'-binaphthy

84 cient enzyme that can remove uracil from any uracil-containing base pairs including the A/U base pair

85 Here, we transfected uracil-containing DNA duplexes into human cells and meas

86 n alkoxyamine to covalently tag and sequence uracil-containing DNA fragments (UPD-Seq).

87 acts on double-stranded and single-stranded uracil-containing DNA.

88 AR9 is a giant Bacillus subtilis phage whose uracil-containing double-stranded DNA genome encodes dis

89 D4 binds weakly to nonspecific DNA and to uracil-containing substrates but binds abasic sites with

90 sured, including plasma nucleosides, hepatic uracil content, maternal plasma folate concentrations, a

91 east and discovered significant variation in uracil content, wherein uracil is excluded from the earl

92 Furthermore, this protein- and hence the uracils created by A3A- colocalize with replication prot

93 To directly map uracils created by AID/APOBEC enzymes, here we used urac

94 yzes the conversion of unpaired cytosines to uracils, creating permanent genetic tags for the positio

95 ubunit (APOBEC) enzymes convert cytosines to uracils, creating signature mutations that have been use

96 We examined the interplay between uracil creation by AID and its removal by UNG2 glycosyla

97 ing that UNG2 expression is coordinated with uracil creation by AID.

98 han are removed from the genome but that the uracil creation/excision balance is restored during esta

99 ance, such as the utility of the pyrimidine (uracil) degradation metabolites in predicting 5-fluorour

100 actions of free and hydrogen bonded 1-methyl-uracil demonstrate the relationship between the degree o

101 antiport mechanism and SLC25A36 cytosine and uracil (deoxy)nucleoside mono-, di-, and triphosphates b

102 The new trans-stilbene annulated uracil derivative "(ts)T" exhibits bright fluorescence e

103 ormation of unsymmetrical N,N'-disubstituted uracil derivatives can occur, the methodology demonstrat

104 t active compounds were the N(3)-substituted uracil derivatives containing 6-(4-bromophenoxy)hexyl or

105 Uracil derivatives form strong complexes with complement

106 A short and efficient one-pot synthesis of uracil derivatives with a high structural variability is

107 related substrates allows access to bicyclic uracil derivatives.

108 from Thermus thermophilus HB8 is not only a uracil DNA glycosyase acting on G/U, T/U, C/U, and A/U b

109 measured the probability that nuclear human uracil DNA glycosylase (hUNG2) excised two uracil lesion

110 Family 2 mismatch-specific uracil DNA glycosylase (MUG) from Escherichia coli is kn

111 or by single-strand selective monofunctional uracil DNA glycosylase (SMUG1).

112 y positioned 2'-deoxyuridine (dU) residue by uracil DNA glycosylase (UDG) and apurinic/apyrimidinic e

113 Enzymes like uracil DNA glycosylase (UDG) can achieve ground state de

114 Enzymes in Uracil DNA glycosylase (UDG) superfamily are essential f

115 UDGb belongs to family 5 of the uracil DNA glycosylase (UDG) superfamily.

116 ils in the Ig gene loci can be recognized by uracil DNA glycosylase (UNG) or mutS homologs 2 and 6 (M

117 We show that depletion of the uracil DNA glycosylase (UNG) sensitizes tumor cells to F

118 g uracil-guanine mismatches are processed by uracil DNA glycosylase (UNG)-mediated base-excision repa

119 nteractions with base excision repair enzyme uracil DNA glycosylase (UNG2) and crossover junction end

120 -excision repair pathway by antagonizing the uracil DNA glycosylase (Ung2) enzyme.

121 Uracil DNA Glycosylase (UNG2) is the primary enzyme in h

122 imilar to the recruitment of another target, uracil DNA glycosylase (UNG2), to the CRL4-DCAF1 E3 by V

123 ells can be selectively killed by inhibiting uracil DNA glycosylase 2 (UNG) and that this synthetic l

124 Uracil DNA glycosylase could hydrolyze deoxyuracils of t

125 time quantitative PCRs (qPCRs) targeting the uracil DNA glycosylase gene (udg) or the 23S rRNA gene a

126 ficantly contribute to removal of uracils by uracil DNA glycosylase regardless of the translational o

127 The uracil DNA glycosylase superfamily consists of several d

128 Family 4 UDGa is a robust uracil DNA glycosylase that only acts on double-stranded

129 ties of two model enzymes, exonuclease I and uracil DNA glycosylase with high sensitivity and selecti

130 We examined the role of the viral uracil DNA glycosylase, a protein conserved among all he

131 enine DNA glycosylase, MutY DNA glycosylase, uracil DNA glycosylase, and APE1 activity.

132 Uracil DNA glycosylases (UNG) are highly conserved prote

133 Although uracil DNA glycosylases limit APOBEC-induced mutation, i

134 ed Cas9 nickase, an Escherichia coli-derived uracil DNA N-glycosylase (eUNG) and a rat APOBEC1 cytidi

135 The present biosensor is able to detect both uracil DNA N-glycosylase (UNG) and AP-endonuclease 1 (AP

136 DNA repair enzymes such as human uracil-DNA glycosylase (hUNG) perform the initial step i

137 -induced cytidine deaminase are processed by uracil-DNA glycosylase (UNG) and mismatch repair (MMR) p

138 e excision repair (BER), either initiated by uracil-DNA glycosylase (UNG) or by single-strand selecti

139 f a Cas9 nickase, a cytidine deaminase and a uracil-DNA glycosylase (Ung).

140 roliferation depends on protective repair by uracil-DNA glycosylase (UNG).

141 no known enzymatic activity, D4 is an active uracil-DNA glycosylase (UNG).

142 created by AID/APOBEC enzymes, here we used uracil-DNA glycosylase and an alkoxyamine to covalently

143 us, and the VACV D4 protein serves both as a uracil-DNA glycosylase and as an essential component req

144 Coupled with a uracil-DNA glycosylase inhibitor, dCas9-AIDx converted t

145 6 exonuclease) and DNA repair enzymes (e.g., uracil-DNA glycosylase).

146 Unlike uracil-DNA glycosylases from diverse sources, where the

147 nockdown of SMUG1 or thymine-DNA glycosylase uracil-DNA glycosylases, proving that it is base excisio

148 moieties of Poly A nanocapsules and thymine/uracil does not affect the fluorescence of poly A nanoca

149 ion of bisulfite with deoxycytidine (dC)) to uracil (dU).

150 stly to a reduction in the rate constant for uracil elimination in the less polar solvent.

151 een with peripheral B cells and have nuclear uracil excision activity comparable to that seen with st

152 promoting activity of AID when it overwhelms uracil excision repair.

153 f-life of UNG2, reduces the rate of in vitro uracil excision, and slows UNG2 dissociation from chroma

154 o prevent this from happening in most cases, uracil exhibits an ultrafast relaxation mechanism from t

155 suggests that the C4-alkoxide (enol form of uracil) facilitates coupling by participation in the int

156 Thiol trapping competes with uracil fragmentation in less polar solvent conditions.

157 toethanol are unable to compete with loss of uracil from 1 in phosphate buffer.

158 n extremely efficient enzyme that can remove uracil from any uracil-containing base pairs including t

159 n in MUG not only accelerates the removal of uracil from mismatched base pairs but also enables the e

160 The removal of uracil from the genome requires a succession of intermed

161 In this study, we show that uracils generated in the G1 phase in B cells can generat

162 ted B cells, demonstrating a balance between uracil generation and removal.

163 he preferential access of mismatch repair or uracil glycosylase (UNG) to AID-initiated U:G mismatches

164 ctivator-like effector array proteins, and a uracil glycosylase inhibitor resulted in RNA-free DddA-d

165 and third-generation base editors that fuse uracil glycosylase inhibitor, and that use a Cas9 nickas

166 Finally, we demonstrate that uracil glycosylase initiates the bypass of DNA damage in

167 ults demonstrate that Pms2/Mlh1 and multiple uracil glycosylases act jointly, each one with a distinc

168 ations at A-T bases depend on two additional uracil glycosylases, thymine-DNA glycosylase and SMUG1.

169 Resulting uracil-guanine mismatches are processed by uracil DNA gl

170 biologically active dihydropyridinone-fused uracils have been developed.

171 ted enriched MTHFD1 in the nucleus, elevated uracil in DNA, lower rates of de novo dTMP synthesis, an

172 eaminase (AID), which deaminates cytosine to uracil in DNA.

173 We applied the Excision-seq method to map uracil in E. coli and budding yeast and discovered signi

174 vidence for a direct transcription arrest by uracil in either of the two settings because the vectors

175 ontaneous deamination of cytosine, producing uracil in pyrimidine dimers, followed by monomerization

176 best known for deaminating cytosine bases to uracil in single-stranded DNA, with characteristic seque

177 mutations through deamination of cytosine to uracil in single-stranded HIV-1 (-) DNA is the dominant

178 late synthase and causes the accumulation of uracil in the genome, whereas FdUTP is incorporated by D

179 eatures shows that non-treated cells possess uracil in the late replicating constitutive heterochroma

180 ould cooperate with MMR by excising a second uracil in the vicinity of the U:G mismatch, but it faile

181 Smug1 (-/-) mice did not accumulate uracil in their genome and Ung (-/-) mice showed slightl

182 ed deaminase (AID) converts DNA cytosines to uracils in immunoglobulin genes, creating antibody diver

183 singly, there was little increase in genomic uracils in PMA-treated wild-type or uracil repair-defect

184 The presence of viral uracils in short-lived monocytes suggests their recent i

185 We show that UdgX strongly prefers uracils in ssDNA over those in U*G or U:A pairs, and loc

186 Strategically placed uracils in the DNA sequence trigger selective cleavage o

187 Uracils in the Ig gene loci can be recognized by uracil

188 d that AID generates few and mostly isolated uracils in the switch region, although processive AID de

189 Here we investigated the influence of uracil incorporated into a reporter vector on gene expre

190 y 5 UDGb can also act as an enzyme to remove uracil incorporated into DNA through the existence of dU

191 e pairs allows the MUG-K68N mutant to remove uracil incorporated into the genome during DNA replicati

192 thymidylate biosynthesis and lead to genomic uracil incorporation contributing to their antiprolifera

193 ication forks and the deleterious effects of uracil incorporation into DNA from thymidine-deficient n

194 Still, it is not yet characterized if uracil incorporations have any positional preference.

195 integrity by preventing misincorporation of uracil into DNA, which results in DNA toxicity and cell

196 hypermutation (SHM) of immunoglobulin genes, uracils introduced by activation-induced cytidine deamin

197 ificant variation in uracil content, wherein uracil is excluded from the earliest and latest replicat

198 and an intermediate for antibody maturation, uracil is primarily processed by base excision repair (B

199 Furthermore, a derivative of uracil is reduced under similar conditions to thymine.

200 anics (QM/MM) models of the UDG active site, uracil is strongly polarized when bound to UDG and resem

201 nes on the displaced strand of the D-loop to uracil, leaving a permanent signature for the displaced

202 the ensuing lethality requires processing of uracil lesions (likely U/G mispairs) by MSH2 and MLH1 (l

203 or genomes, the majority of APOBEC-catalyzed uracil lesions are probably counteracted in an error-fre

204 These uracil lesions base-pair with adenines during the comple

205 n uracil DNA glycosylase (hUNG2) excised two uracil lesions spaced 10-80 bp apart in a single encount

206 thesis in a dose-dependent manner, increased uracil levels in nuclear DNA, and increased genome insta

207 In stimulated UNG(-/-) cells, uracil levels increase by 11- to 60-fold during the firs

208 The genomic uracil levels remain unchanged in normal stimulated B ce

209 e in uracil levels with up to 25-fold higher uracil levels than wild type.

210 (-/-) mice showed a synergistic increase in uracil levels with up to 25-fold higher uracil levels th

211 and Ung (-/-) mice showed slightly elevated uracil levels.

212 ablishment of cell lines, fixing the genomic uracil load at high levels.

213 Initial studies with uracil located in nucleosome core DNA showed a distinct

214 Uracil loss also does not compete with strand scission.

215 his "tautomeric strain" raises the energy of uracil, making uracilate a better than expected leaving

216 A noncanonical base, uracil, may be also present in small quantities in DNA.

217 rget of arsenic trioxide (As2O3), leading to uracil misincorporation into DNA and genome instability.

218 ed nuclear de novo dTMP synthesis results in uracil misincorporation into DNA.

219 ARP inhibitors, methyl-methanesulfonate, and uracil misincorporation, which reflects the need to remo

220 Whereas the uracil moieties of the donors are observed to maintain a

221 ethyl uracil and tricyclic guanidine groups; uracil moiety cleavage/fragmentation and further ring-op

222 ht the importance of the substitution of the uracil moiety for potency and selectivity.

223 Participation of the uracil moiety in the cyclization step is proposed.

224 DA heterozygotes (AID+/-), and patients with uracil N-glycosylase (UNG) deficiency, which impairs CSR

225 Family 1 uracil N-glycosylase (UNG) from E. coli is an extremely

226 Uracil N-glycosylase 2 (UNG2), the nuclear isoform of UN

227 r engages CRL4 to trigger the degradation of uracil-N-glycosylase 2 (UNG2).

228 ere explained by the stronger acidity of the uracil N3 atom.

229 In comparison, the introduction of uracil nucleobase 3 had a minimal effect on DNA affinity

230 s of 5-(2-furyl, or 2-thienyl, or 2-pyrrolyl)uracil nucleosides, which are used as important RNA and

231 pan-agonist fluorescent probe of a subset of uracil nucleotide-activated hP2YRs.

232 eceptor characterized by some as a dualistic uracil nucleotide/cysteinyl leukotriene receptor and by

233 Herein we report that uracil nucleotides and cysteinyl leukotrienes do not act

234 d broad regions with elevated probability of uracil occurrence both in treated and non-treated cells.

235 s mostly through deaminating cytosine (C) to uracil on single-stranded DNA/RNA.

236 The expression constructs contained a single uracil opposite an adenine (to mimic dUTP misincorporati

237 ear isoform of UNG, catalyzes the removal of uracil or 5-fluorouracil lesions that accumulate in DNA

238 of strand breaks arising during excision of uracils or ribonucleotides from DNA.

239 aimed to uncover genome-wide alterations in uracil pattern upon drug treatments in human cancer cell

240 ) stress, a defect in the trafficking of the uracil permease, alpha-syn accumulation and foci, and a

241 tional yeast fusion gene, cytosine deaminase/uracil phosphoribosyltransferase (FCU).

242 Uracil phosphoribosyltransferase (UPP) catalyzes the ini

243 Uracil phosphoribosyltransferase (UPRT) is a pyrimidine

244 iouracil (TU) in cells expressing transgenic uracil phosphoribosyltransferase (UPRT), a method known

245 nsgenic mice that express cell-type-specific uracil phosphoribosyltransferase (UPRT), an enzyme requi

246 TK(SR39) mutants), yeast cytosine deaminase:uracil phosphoribosyltransferase (yCD:UPRT) and nitrored

247 inding the photochemical pathways leading to uracil photodamage.

248 frequencies for 21 vibrational modes of the uracil radical are reported.

249 The electron affinity of the uracil radical is measured accurately to be 3.4810+/-0.0

250 brational spectroscopy of the dehydrogenated uracil radical is obtained by a dipole-bound state with

251 The AR9 nvRNAP requires uracils rather than thymines at specific conserved posit

252 d in an Escherichia coli strain defective in uracil repair (ung mutant), and the mutations that accum

253 electrochemical sensing of 8-oxoguanine and uracil repair glycosylase activity within DNA monolayers

254 genomic uracils in PMA-treated wild-type or uracil repair-defective cells.

255 ngineered switch region in cells ablated for uracil repair.

256 We found a group of purine-uracil repeat RNA secondary structure motifs plus other

257 he ability to synthesize the 5-amino-ribityl-uracil riboflavin precursor and to activate polyclonal a

258 of PcUP1 in ligand-free and in complex with uracil/ribose-1-phosphate, 2'-deoxyuridine/phosphate and

259 ne tract and closely associated Cytosine and Uracil-rich (CU-rich) sequences, upstream of the mini-ex

260 ds a subpopulation of mRNAs characterized by uracil-rich 3'-untranslated regions under normoxic condi

261 Higher expression in NGS was discovered for uracil-rich miRNAs (p = 7 x 10(-37)), while high express

262 During hypoxia, UBP1C association with non-uracil-rich mRNAs is enhanced concomitant with its aggre

263 natural hosts, expresses seven small nuclear uracil-rich non-coding RNAs (called HSURs) in latently i

264 N-propargylation of the N3 position of its uracil ring resulted in a vast reduction of its biologic

265 In addition, the chloroplast has an active uracil salvage pathway.

266 of Cid1 that provides detailed evidence for uracil selection via the dynamic flipping of a single hi

267 n in complex with a PAN RNA MRE, revealing a uracil specific binding site that is also conserved in K

268 construction based on DNA assembly and USER (Uracil-Specific Excision Reagent) cloning.

269 sulting path reveals an extensive network of uracil-specific interactions spanning the first 12 nucle

270 Uracil substitution with N(3)-methyl, but not larger gro

271 The Escherichia coli UraA H+-uracil symporter is a member of the nucleobase/ascorbate

272 ne in viral (-)DNA, which forms promutagenic uracils that inactivate the virus.

273 OBEC3A by PMA causes genomic accumulation of uracils that may lead to such mutations.

274 Unmethylated cytosines may be converted to uracil through the addition of sodium bisulphite, allowi

275 ameters demonstrate that SLC25A33 transports uracil, thymine, and cytosine (deoxy)nucleoside di- and

276 idine deaminase (AID) converts cytosine into uracil to initiate somatic hypermutation (SHM) and class

277 hway enzyme that catalyzes the conversion of uracil to uridine monophosphate (UMP).

278 ug treatment induced a shift of incorporated uracil towards segments that are normally more active/fu

279 ture with a substrate-bound structure of the uracil transporter UraA in an inward-facing conformation

280 ate domain, similar to the previously solved uracil transporter UraA, which belongs to the same famil

281 l importance is a bifurcation point at which uracil triphosphate is partitioned towards either nucleo

282 (mC) deamination and other lesions including uracil (U) and 5-hydroxymethyluracil (hmU).

283 se APOBEC3F (A3F) deaminates cytosine (C) to uracil (U) and is a known restriction factor of HIV-1.

284 esis of C-4'-spiro-oxetanoribonucleosides of uracil (U) and thymine (T) in 37 and 45% overall yields,

285 guanine (G), cytosine (C), thymine (T), and uracil (U) are investigated.

286 proteins that can deaminate cytosine (C) to uracil (U) on nucleic acids.

287 This approach was used to detect a uracil (U) or 8-oxo-7,8-dihydroguanine (OG) in codon 12

288 f the main OPV attenuating mutations such as uracil (U) to cytosine (C) at nucleotide 472 in the 5' n

289 ffect of three thymine (T) analogs including uracil (U), 5-fluorouracil (5FU) and 5-hydroxymethylurac

290 other deamination-derived lesions including uracil (U).

291 ed a protein that covalently links to DNA at uracils, UdgX, for mammalian expression and immunohistoc

292 The 1-N-benzyl-5-iodo(or bromo)uracil undergoes Pd-catalyzed [Pd2(dba)3] direct arylati

293 = 6.3 mum, and H = 7.7 mum were obtained for uracil (unretained), butyrophenone (k = 0.85), and valer

294 equent glycosylation reaction with activated uracil via C-1 phosphate and installation of the cyclic

295 During culture experiments, a xanthine/uracil/vitamin C permease (XUV) was upregulated approxim

296 in direct evidence for the presence of these uracils, we engineered a protein that covalently links t

297 terize its ability to convert cytosines into uracils, we tested several derivatives of APOBEC3B gene

298 alous X-ray diffraction label (5-selenophene uracil), which enables the correlation of RNA conformati

299 First, the copper-catalyzed coupling of uracil with aryl iodides, employing picolinamide 16 as t

300 deaminase (AID), which converts cytidine to uracil within the Ig variable (IgV) regions.