ライフサイエンスコーパス: uracil

1 ious results that demonstrated inhibition by uracil.

2 responsible for the proton-driven uptake of uracil.

3 ansformants that grow on agar plates lacking uracil.

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

5 cluding Drosophila, are incapable of binding uracil.

6 in incomplete conversion of intermediates to uracil.

7 otic acid to form (1-beta-D-erythrofuranosyl)uracil.

8 and one molecule of 5-amino-6-(ribitylamino)uracil.

9 superfamily are essential for the removal of uracil.

10 Hypoxanthine was a weaker inhibitor than uracil.

11 elity by catalyzing the removal of mutagenic uracils.

12 hich converts cytosines in switch regions to uracils.

13 ingle base mismatches flanked by adenines or uracils.

14 DMF (100 degrees C, 2 h) to yield 5-arylated uracils.

15 old, on enzymatic removal of these quenching uracils.

16 here hUNG acts iteratively on densely spaced uracils.

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

18 infected individuals also contained abundant uracils.

19 33%), which was not observed for cytosine to uracil (17.86%) editing.

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

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

22 are hypersensitive to high concentrations of uracil, 5-fluorouracil, and 4-thiouracil in the growth m

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

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

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

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

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

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

29 vation that LdUPRT is substrate-inhibited by uracil and 4-thiouracil, but 5-fluorouracil toxicity tra

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 , combined treatment of 5-fluoro-1-propargyl-uracil and Pd(0)-functionalized resins exhibits comparab

34 of 20 and 99 muM for the natural substrates uracil and phosphoribosylpyrophosphate, respectively, as

35 We have measured the repair of site-specific uracil and single nucleotide gaps along the surface of t

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

37 e for pyrimidine nucleotides are funneled to uracil and then phosphoribosylated to UMP in the parasit

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

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

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

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

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

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

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

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

46 acils in ssDNA, and also, in a context where uracils are densely clustered in duplex DNA.

47 instead, depends on the context in which the uracils are located.

48 The resulting uracils are processed by uracil base excision and/or mis

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

50 up pathway to base excision repair to remove uracils arising from cytosine deamination.

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

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

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

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

55 ssed using cps, an avirulent, nonreplicating uracil auxotroph strain of the parasite Toxoplasma gondi

56 A live, nonreplicating avirulent uracil auxotroph vaccine strain (cps) of Toxoplasma trig

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

58 c cancer vaccine strategies using engineered uracil auxotrophs.

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

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

61 p of de novo pyrimidine biosynthesis induced uracil auxotrophy.

62 tically deficient DHODH gene alleles induced uracil auxotrophy.

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

64 cks, bearing a fluorine sensor at C-5 of the uracil base [viz.

65 The resulting uracils are processed by uracil base excision and/or mismatch repair enzymes that

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

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

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

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

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

71 is an exemplar that efficiently locates rare uracil bases in both double-stranded DNA and single-stra

72 They are strongly quenched by uracil bases incorporated into the sequence, and they yi

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

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

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

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

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

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

79 proposed that Pol D is able to interact with uracil by looping out the single-stranded template, allo

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

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

82 the initial and rate-limiting enzyme of the uracil catabolic pathway, being critically important for

83 sed wing blister formation, while removal of uracil catabolism alleles was synthetic lethal with eogt

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

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

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

87 from an iodide anion within a binary iodide-uracil complex using a UV pump pulse; the ensuing dynami

88 with strengths comparable to those formed by uracil compounds.

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

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

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

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

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

94 U2AF(65) for region-dependent cytosine- and uracil-containing RNA sites.

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

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

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

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

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

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

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

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

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

104 Uracil derivatives form strong complexes with complement

105 st elucidation of the structural features of uracil derivatives that are critical for AC inhibition a

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 ate backbone in sliding and hopping by human uracil DNA glycosylase (hUNG), which is an exemplar that

110 genic cell line that had no detectable human uracil DNA glycosylase (hUNG2) activity, establishing th

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

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

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

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

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

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

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

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

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

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

123 Uracil DNA glycosylase plays a key role in DNA maintenan

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

125 The uracil DNA glycosylase superfamily consists of several d

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

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

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

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

130 Near the dyad, uracil DNA glycosylase/APE1 removes an outwardly oriente

131 Uracil DNA glycosylases (UNG) are highly conserved prote

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

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

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

135 Uracil-DNA glycosylase (UDG) compromises the replication

136 the activity of both bacterial and mammalian uracil-DNA glycosylase (UDG) enzymes.

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 Complementary pathways, initiated by the uracil-DNA glycosylase (UNG) or the mismatch repair fact

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

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

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

143 ion for abasic site recognition, the rate of uracil-DNA glycosylase hydrolysis of the N-glycosidic bo

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 il residues are removed from DNA by specific uracil-DNA glycosylases in the base excision repair path

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

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

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

151 tidine deaminases, which convert cytosine to uracil during RNA editing and retrovirus or retrotranspo

152 ycosylase/APE1 removes an outwardly oriented uracil efficiently; however, polymerase beta activity is

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

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

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

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

157 minases in yeast where it largely depends on uracil excision, which generates an abasic site for stra

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

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

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

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

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

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

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

165 in alcohol-fed mice and decreased cytidine, uracil, fumarate, creatine phosphate, creatine, and chol

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

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

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

169 Uracil glycosylase 2 (UNG2) is required for CSR, most li

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

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

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

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

174 A polymerase is inhibited by the presence of uracil in DNA template strands.

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

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

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

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

179 bases and stall replication on encountering uracil in template strands, four bases ahead of the prim

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

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

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

183 To investigate and compare the uracil in U-A and U*U base pairs, we have decided to pro

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

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

186 n enhanced local search mode when it acts on uracils in ssDNA, and also, in a context where uracils a

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

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

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

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

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

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

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

194 l D appears to interact with template strand uracil irrespective of its distance ahead of the replica

195 Uracil is an unavoidable aberrant base in DNA, the repai

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

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

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

199 RNAs ((Se)U-RNAs), where the exo-4-oxygen of uracil is replaced by selenium.

200 , suggesting that APOBEC3B-catalyzed genomic uracil lesions are further processed by downstream DNA "

201 analyses is that APOBEC3B-catalyzed genomic uracil lesions are responsible for a large proportion of

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

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

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

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

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

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

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

209 naling perturbations that increase cytosolic uracil levels, thereby causing wing blister formation.

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

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

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

213 Uracil loss also does not compete with strand scission.

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

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

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

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

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

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

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

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

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

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

224 Outwardly oriented uracils near the nucleosome center are efficiently cleav

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

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

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

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

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

230 at is activated by two classes of molecules: uracil-nucleotides and cysteinyl-leukotrienes.

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

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

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

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

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

236 n-regulation during necrotrophy, whereas the uracil phosphoribosyl transferase gene involved in pyrim

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

238 netic analysis has authenticated L. donovani uracil phosphoribosyltransferase (LdUPRT), an enzyme not

239 Uracil phosphoribosyltransferase (UPRT) is a pyrimidine

240 Cre-induced expression of uracil phosphoribosyltransferase (UPRT) provides spatial

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

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

243 inding the photochemical pathways leading to uracil photodamage.

244 However, it is not completely clear how uracil plays the diversifing roles.

245 nd this model is based on the structure of a uracil-proton symporter.

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

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

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

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

250 s not stop at a defined location relative to uracil, rather a general decrease in DNA synthesis is ob

251 Significantly, the rate of uracil removal with outwardly oriented DNA backbones is

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

255 lternatively, in certain archaeal organisms, uracil residues are eliminated by apurinic/apyrimidinic

256 In the majority of species, uracil residues are removed from DNA by specific uracil-

257 If not repaired, these uracil residues give rise to C --> T transitions, which

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

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 Synthetic nontranslatable uracil-rich mRNAs were also demonstrated to colocalize w

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

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

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

267 Uracil sensing prevents copying of the deaminated base a

268 In contrast, sliding of hUNG between uracil sites embedded in duplex and single-stranded DNA

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

270 ully integrated proviruses lacked detectable uracil, suggesting that only nonuracilated viral DNA pro

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 isons of base-pair steps with thymine versus uracil, the thymine methyl group tends to enhance the st

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

275 ycosylase (TDG) excises the mismatched base, uracil, thymine or 5-hydroxymethyluracil (5hmU), as well

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

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

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

279 is required for CSR, most likely by removing uracils to generate abasic sites.

280 und that these cells express a high-affinity uracil transporter (designated TbU3) that is clearly dis

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

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

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

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

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

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

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

288 aneous hydrolytic deamination of cytosine to uracil (U) in DNA is a constant source of genome instabi

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

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

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

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

293 C) and conversion of the newly formed 5fC to uracil (under bisulfite conditions) means that 5hmC can

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

295 eals that although hydrogen bonding to O2 of uracil underlies the UDG activity in a dissociative fash

296 ed medium in vitro, unless supplemented with uracil, uridine, deoxyuridine or UMP.

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

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

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

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