ライフサイエンスコーパス: dNTP

1 d weak incorporation and rather behaved as a dNTP-competitive inhibitor.

2 SAMHD1 is a dNTP hydrolase, whose activity is required for maintaini

3 Here, we present a dNTP assay based on isothermal rolling circle amplificat

4 acid domain-containing protein 1 (SAMHD1), a dNTP triphosphohydrolase, regulates the levels of cellul

5 nfluence of the restriction factor SAMHD1, a dNTP hydrolase (dNTPase) and RNase, on HBV replication.

6 SAMHD1, a dNTP triphosphohydrolase, contributes to interferon sign

7 a different mechanism, one consistent with a dNTP-stabilized misalignment mechanism.

8 molecular switch that impacts RNR activity, dNTP synthesis, and DNA replication fork progression.

9 HEK293T cell extracts could add dNTPs to DNA primers hybridized to RNA, but lost this ab

10 XP-V cell extracts did not add dNTPs to DNA primers hybridized to RNA, but could when h

11 of RRM2 during S/G2 phase to ensure adequate dNTP supply for DNA replication.

12 mportance of SAMHD1 in the regulation of all dNTP pools and suggest that dGK inside mitochondria has

13 research was demonstrated by quantifying all dNTPs in CEM-SS leukemia cells with and without hydroxyu

14 on fidelity, yet the consequences of altered dNTP pools on replication fidelity have not previously b

15 g a collection of yeast strains with altered dNTP pools, we discovered an inverse relationship betwee

16 P assays, RT-qPCR and ChIP-qPCR methods, and dNTP analyses, we show that DDR activation in the buddin

17 certain combinations of loop 2 mutations and dNTP effectors perturbed ATP's role as an allosteric act

18 he O helix-to engage the primer-template and dNTP triphosphate.

19 '-dideoxy-terminated DNA primer-template and dNTP.

20 sion droplets in the presence of primers and dNTPs, followed by the recovery of the partner genes via

21 vanced tool for both fundamental and applied dNTP research.

22 We demonstrate that some conjugates act as dNTP analogues and HIV-1 reverse transcriptase (RT) cata

23 At dNTP concentrations that mimic those in cycling cells, t

24 Our studies were carried out at dNTP levels representative of those prevailing either in

25 NA replication and maintenance of a balanced dNTP pool, and is an established cancer target.

26 cell cycle and depend on the balance between dNTP biosynthesis and degradation.

27 d cellular concentration discrepancy between dNTPs and rNTPs present pharmacological and mechanistic

28 mpeting RT inhibitor (NcRTI) INDOPY-1 blocks dNTP binding to RT.

29 In rad53-1 cells stressed by dNTP depletion, the replicative DNA helicase, MCM, and t

30 e EC50(dNTP) values for SAMHD1 activation by dNTPs are in the 2-20 mum range, and the half-life of th

31 ch maintains low concentrations of canonical dNTPs in these cells.

32 ymes display broad activity toward canonical dNTPs, such as the dNTPase SAMHD1 that blocks reverse tr

33 he fundamental mechanism of SAMHD1-catalysed dNTP hydrolysis remained unknown.

34 volved in RNR substrate production can cause dNTP imbalances, which cannot be compensated by RNR or o

35 e from WT in its ability to deplete cellular dNTP pools and to restrict HIV replication.

36 terminal deletion mutant, increases cellular dNTP content and HIV-1 reverse transcription.

37 1 is a phosphohydrolase maintaining cellular dNTP homeostasis but also acts as a critical regulator i

38 ght to result from the depletion of cellular dNTP pools, but it remains controversial whether the dNT

39 n through the proper maintenance of cellular dNTP pools.

40 , reveals how SAMHD1 down-regulates cellular dNTP and modulates the efficacy of nucleoside-based anti

41 phosphohydrolase activity regulates cellular dNTP concentration, reducing levels below those required

42 s involved in the regulation of the cellular dNTP pool and has been linked to cancer progression.

43 ohydrolase activity by reducing the cellular dNTP pool to a level that cannot support productive reve

44 intact in their ability to deplete cellular dNTPs.

45 scription (RT) through depletion of cellular dNTPs but is naturally switched off by phosphorylation i

46 ohydrolase, regulates the levels of cellular dNTPs through their hydrolysis.

47 rocesses by changing the balance of cellular dNTPs.

48 or the bromo substituent in beta,gamma-CHBr-dNTP analogues.

49 e the corresponding homolog (SAMHD1) cleaves dNTPs.

50 rivatives through the depletion of competing dNTPs, we show here that SAMHD1 reduces Ara-C cytotoxici

51 centrations and in the presence of competing dNTPs.

52 Complementary dNTP binding is affected by Me(2+) identity, with Ca(2+)

53 r ternary complexes with a non-complementary dNTP confirmed the presence of a state corresponding to

54 In this context, dNTP triphosphohydrolase SAM domain and HD domain-contai

55 d lower than for inserting the corresponding dNTPs.

56 nt cells results in RRM2 reduction, critical dNTP depletion, S-phase arrest, and apoptosis.

57 n is mimicked by a CXY group (beta,gamma-CXY-dNTPs) have provided information about DNA polymerase ca

58 Furthermore, as cytosolic dNTP pool imbalances were transmitted equally well into

59 LincNMR silencing decreases dNTP levels, while exogenous dNTPs rescues the prolifera

60 phosphate triphosphohydrolase that decreases dNTP pools, is frequently mutated in colon cancers, that

61 acted in the absence of SAMHD1 degradation, dNTP pool elevation, or changes in SAMHD1 phosphorylatio

62 MHD1 has been reported to be able to degrade dNTPs and viral nucleic acids, which may both hamper HIV

63 catalyzed the addition of deoxynucleotides (dNTP) containing biotinlated 2'-deoxyadenosine 5'-tripho

64 ce and concentration of deoxyribonucleotide (dNTP) pools, which are strictly regulated by ribonucleot

65 SAMHD1-dependent dNTP depletion is thought to impair retroviral replicati

66 of myeloid and resting T cells by depleting dNTPs.

67 nhibited ribonucleotide reductase, depleting dNTPs, resulting in durable S phase arrest.

68 embryos synthesize DNA, maternally deposited dNTPs can generate less than half of the genomes needed

69 The goal of this study is to develop dNTP/NTP analogues directly from nucleotides.

70 lly active tetramer is affected by different dNTP ligands bound in the allosteric site.

71 The building blocks of DNA, dNTPs, can be produced de novo or can be salvaged from d

72 recatalytic ternary structures (hPolbeta.DNA.dNTP) for both extension contexts, wherein the incoming

73 omoles of and excellent specificity for each dNTP against the other dNTPs, rNTPs, and dUTP evidenced

74 The EC50(dNTP) values for SAMHD1 activation by dNTPs are in the 2

75 leotide incorporation and promotes efficient dNTP incorporation.

76 f one SAMHD1 allele is sufficient to elevate dNTP pools.

77 Elevated dNTP/nucleotide triphosphate (NTP) ratios in Deltalon ce

78 ite inositol hexakisphosphate (IP6) enhances dNTP import, while binding of synthesized molecules like

79 leading strand DNA polymerase, Pol epsilon, dNTP depletion, and chemical inhibition of DNA polymeras

80 We examined dNTP metabolism in the early Drosophila embryo, in which

81 ncing decreases dNTP levels, while exogenous dNTPs rescues the proliferation defect induced by lincNM

82 educed polymerase activity and higher Km for dNTP during gap-filling.

83 We have developed a method for dNTP detection based on an enzymatic two-stage reaction

84 muscle with deoxyribonucleosides needed for dNTP production by salvage.

85 y at or above a threshold level required for dNTPs synthesis.

86 nscriptase ribozyme can incorporate all four dNTPs and can generate products containing up to 32 deox

87 lute and relative concentrations of the four dNTPs are key determinants of DNA replication fidelity,

88 ngstrom cleft separates SAMHD1 residues from dNTP bases, abolishing nucleotide-type discrimination.

89 that Polzeta function does not require high dNTP levels.

90 To better understand how dNTP binding influences specificity, activity, and oligo

91 on of the DNA damage response and imbalanced dNTP pools.

92 These imbalanced dNTP pools promote replication errors in specific DNA se

93 iring, both in an unperturbed S phase and in dNTP limitation.

94 ssible reasons for the observed asymmetry in dNTP and NTP pools in WT hearts.

95 We show that minor changes in dNTP pools in combination with inactivated mismatch repa

96 subunit M2 (RRM2), a rate-limiting enzyme in dNTP synthesis, induced premature senescence with concom

97 allosteric regulation of enzymes involved in dNTP biosynthesis (e.g., RNR or dCMP deaminase).

98 that VEN4, like human SAMHD1, is involved in dNTP catabolism.

99 er data for mutations in enzymes involved in dNTP metabolism.

100 d suppression of several enzymes involved in dNTP synthesis (i.e., RNR2, TYMS, and TK-1).

101 ing this elevation by strategic mutations in dNTP metabolism genes eliminated the mutator effect of p

102 xpression of MCM2 and CDK1, and reduction in dNTP levels.

103 karyotic loop 2 is essential for its role in dNTP-induced dimerization.

104 Even small variations in dNTP concentrations decrease DNA replication fidelity, a

105 inhibit HIV-1 in differentiated cells low in dNTPs.

106 itiate DNA replication despite an inadequate dNTP supply.

107 on-P301R, complexed with DNA and an incoming dNTP.

108 te that the binding affinity of the incoming dNTP is controlled by the overall hydrophobicity of the

109 ses not only select the base of the incoming dNTP to form a Watson-Crick pair with the template base

110 emplate and the triphosphate of the incoming dNTP.

111 fingers domain that coordinate the incoming dNTP.

112 k the alpha phosphorous atom of the incoming dNTP.

113 he non-bridging oxygen atoms of the incoming dNTP.

114 h a defect in respiration failed to increase dNTP synthesis and exhibited reduced fitness in the pres

115 Increased dNTP production in Deltalon results from higher expressi

116 ase and exonuclease activities has increased dNTP concentrations and an increased mutation rate at th

117 ent in SAMHD1 (-/-) mice that have increased dNTP pools.

118 R and indicate that the benefit of increased dNTP synthesis in the face of DNA damage outweighs possi

119 eaction vessel that identifies an individual dNTP based on a robust fluorescence signal, with the det

120 ship between the concentration of individual dNTPs and the amount of the corresponding ribonucleotide

121 ive elongation in the presence of inhibitory dNTPs.

122 W, whereas restoration of high intracellular dNTP levels restored the mutator phenotype.

123 teasomal degradation, increase intracellular dNTP pools, and facilitate HIV cDNA synthesis.

124 mmalian protein that regulates intracellular dNTP levels through its hydrolysis of dNTPs.

125 p21 decreased the size of the intracellular dNTP pool.

126 and specific quantification of intracellular dNTPs and has the potential to become an advanced tool f

127 ators in lincNMR-depleted cells like the key dNTP synthesizing enzymes RRM2, TYMS and TK1, implicatin

128 Thus, under Rnr1 depletion, limited dNTP pools slow DNA synthesis by replicative Pols and pr

129 ed in absence of RER and presence of limited dNTP pools, Top1-mediated genome instability leads to se

130 We propose that linking dNTP production with availability of Lon allows Caulobac

131 Using reverse-transcription at low dNTP concentrations followed by quantitative-PCR, we fou

132 n lagging-strand polymerase Pol delta at low dNTP concentrations in vitro.

133 ose activity is required for maintaining low dNTP concentrations in non-cycling T cells, dendritic ce

134 t anti-HIV-1 agents, under conditions of low dNTPs.

135 oblems were further exacerbated at the lower dNTP concentrations present in resting cells.

136 f retroviruses in macrophages by maintaining dNTP pools at low levels, Escherichia coli (Ec)-dGTPase

137 We propose that SAMHD1-mediated dNTP balance regulates dNTP-sensitive DNA end-processing

138 nds to the closed state of the enzyme-DNA-Mg.dNTP complex (K(d) = 3.7 mM) to facilitate catalysis.

139 We show that Mg.dNTP binding induces an enzyme conformational change at

140 rt a view of the cytosolic and mitochondrial dNTP pools in frequent exchange.

141 extension assays in the presence of modified dNTPs on various telomeric substrates.

142 nisms for targeting telomerase with modified dNTPs in cancer therapy.

143 ibitors presumably as a result of modulating dNTP pools that compete for recruitment by viral polymer

144 siRNA transfection the composition of the mt dNTP pool approached that of the controls, and mtDNA cop

145 ing blocks for reverse transcription, namely dNTPs.

146 65% of the rate for the corresponding native dNTPs.

147 ion has been established by replacing native dNTPs with dNTPalphaSe.

148 of and distinguish between, the four natural dNTPs at the single-molecule level, with negligible cros

149 difficult DNA and incorporating non-natural dNTPs, due to their low fidelity and loose active site,

150 eraging 13-fold higher than those of natural dNTPs, and kcat values within 1.5-fold of those of nativ

151 der extended conditions when PCR with normal dNTPs fails.

152 wever, to what extent the absence of de novo dNTP production can be compensated for by the salvage pa

153 All other tissues had normal de novo dNTP synthesis and theoretically could supply heart and

154 t dNTP salvage cannot substitute for de novo dNTP synthesis in the heart and that cardiomyocytes and

155 Here, we eliminated de novo dNTP synthesis in the mouse heart and skeletal muscle by

156 t advocates the feasibility of designing NTP/dNTP analogues by chemical substitutions to nucleotide a

157 We conclude that HCMV can obtain dNTPs in the absence of Rb phosphorylation and that UL97

158 gh genetic changes that alter the balance of dNTP binding and dissociation from DNA polymerases.

159 Binding of dNTP effectors is coupled to the formation of active dim

160 iction factor, lowering the concentration of dNTP substrates to limit RT.

161 ucleotide reductase ensures tight control of dNTP concentration.

162 We propose that frugal control of dNTP synthesis contributes to the well-characterized dec

163 Determination of dNTP pools in mouse embryos revealed that inactivation o

164 -stimulated respiration drove enlargement of dNTP pools; cells with a defect in respiration failed to

165 zed "on the go." The rate-limiting enzyme of dNTP synthesis, ribonucleotide reductase, is inhibited b

166 t the level of RT that acts independently of dNTP concentrations and is specific to resting CD4 T cel

167 nalysis of these mutants paints a picture of dNTP regulation in whole animals quite different from th

168 is review, we discuss how a key regulator of dNTP biosynthesis in mammals, the enzyme ribonucleotide

169 in the absence of the negative regulators of dNTP synthesis.

170 cterization of an RTIC after three rounds of dNTP incorporation (+3), the first major pausing point d

171 To understand the significance of dNTP pools increase for Polzeta function, we studied the

172 concentrations are much higher than those of dNTP.

173 cytosolic compartment and the fine-tuning of dNTP levels for chloroplast translation and development.

174 Further, the use of dNTP concentrations present in pol3-R696W cells for in v

175 We find that in the absence of dNTPs, both adducts alter polymerase binding as measured

176 elicase to unwind DNA, but in the absence of dNTPs, this leads to excessive single-strand DNA that ex

177 g as measured by smFRET, but the addition of dNTPs induces the formation of a ternary complex having

178 uce the production of nonlimiting amounts of dNTPs.

179 een dN frequencies in RNA and the balance of dNTPs and ribonucleoside 5'-triphosphates (rNTPs) in the

180 back inhibition renders the concentration of dNTPs at gastrulation robust, with respect to large vari

181 d protease and that Lon-dependent control of dNTPs improves fitness during protein misfolding conditi

182 homeostasis by catalysing the hydrolysis of dNTPs into 2'-deoxynucleosides and triphosphate.

183 llular dNTP levels through its hydrolysis of dNTPs.

184 tiate DNA synthesis due to continued lack of dNTPs.

185 odel, we demonstrate that when the levels of dNTPs are abnormally high, nuclear cleavages fail to suf

186 High levels of dNTPs are associated with robust onset of oscillatory tw

187 The levels of dNTPs are tightly regulated during the cell cycle and de

188 -1 cells is suppressed by elevated levels of dNTPs in vivo, and the activity of Pol epsilon is compro

189 is disrupted in embryos with high levels of dNTPs, which have been recently shown to cause abnormall

190 hields them from hydroxyurea-induced loss of dNTPs.

191 equivalent of the alpha-phosphate oxygen of dNTPs and two oxygens of the phosphonate group of the al

192 by the beta- and gamma-phosphate oxygens of dNTPs.

193 plausible channel that allows the passage of dNTPs into assembled capsids.

194 DNA synthesis, thus requiring penetration of dNTPs into the viral capsid.

195 uction of p21 in MDDCs decreases the pool of dNTPs and increases the antiviral active isoform of SAMH

196 The reduction in the pool of dNTPs in MDDCs appears rather mostly due to a p21-mediat

197 in the presence of excess dCTP or a pool of dNTPs, implying that VEN4, like human SAMHD1, is involve

198 , a key enzyme for the de novo production of dNTPs, at embryonic day 13.

199 n part by inducing the de novo production of dNTPs.

200 on and thereby controlling the production of dNTPs.

201 itive to the relative concentration ratio of dNTPs specified by the RNA template slippage-prone seque

202 itive to the relative concentration ratio of dNTPs specified by the RNA template slippage-prone seque

203 Precise regulation of dNTPs within the cellular nucleotide pool is essential f

204 RRM2B), leading us to question the source of dNTPs in hypoxia.

205 vity and consequently decreased synthesis of dNTPs with concomitant inhibition of DNA replication, ar

206 able conditions for passive translocation of dNTPs into the HIV-1 capsid.

207 s cells from invading viruses that depend on dNTPs to replicate and is frequently mutated in cancers

208 specificity for each dNTP against the other dNTPs, rNTPs, and dUTP evidenced the strong performance

209 vivo data support a model where an oxidized dNTPs pool together with aberrant BER processing contrib

210 anisms by which naturally occurring oxidized dNTPs and therapeutic dNTPs inhibit telomerase-mediated

211 , mutations and drug treatments that perturb dNTP pool levels disproportionately influence the viabil

212 iphosphohydrolase that cleaves physiological dNTPs into deoxyribonucleosides and inorganic triphospha

213 blocker scaffolds, coupled to the polymerase/dNTP machinery, lead, in the presence of two primers P(1

214 blocker scaffolds, coupled to the polymerase/dNTP machinery, leads to the emergence of a CDN composed

215 /blocker scaffolds coupled to the polymerase/dNTP replication machinery leads, in the presence of a p

216 emplate/blocker scaffolds and the polymerase/dNTPs, the P(1)-guided emergence of a [3 x 3] CDN is dem

217 d their coupling to a nicking/polymerization/dNTP replication machinery, the amplified high-throughpu

218 e also arrest cells in S phase by preventing dNTP synthesis.

219 ic pathways, de novo and salvage, to produce dNTPs for DNA replication.

220 bonucleoside diphosphates (dNDPs) to provide dNTP precursors for DNA synthesis.

221 cle and in quiescent cells where it provides dNTPs for mitochondrial DNA synthesis.

222 ave examined whether oxidation of the purine dNTPs in the dNTP pool provides a source of DNA damage t

223 und in cells (compared with micromolar range dNTP levels).

224 the suppressors identified here may regulate dNTP pool size, as well as similarities in phenotypes be

225 aminases, and SAMHD1 (a cell cycle-regulated dNTP triphosphohydrolase) dNTPase, which maintains low c

226 that SAMHD1-mediated dNTP balance regulates dNTP-sensitive DNA end-processing enzyme and promotes CS

227 ro at 'normal S-phase' and 'damage-response' dNTP concentrations.

228 he shift from 'S-phase' to 'damage-response' dNTP levels only minimally affected the activity, fideli

229 ifferent tissues and was defined by the rNTP/dNTP ratio of the tissue.

230 contrast, pol2-4 and POL2 cells have similar dNTP levels, which decline in the absence of Dun1 and ri

231 We show that similar dNTP elevation occurs in strains, in which intrinsic rep

232 ve, and alternative techniques that simplify dNTP quantification would present very useful complement

233 t instance of a Y-family-polymerase-specific dNTP, and this method could be used to probe the activit

234 ably more stable to hydrolysis than standard dNTPs.

235 y and is required for maintaining sufficient dNTPs during normal DNA replication.

236 Rrm2b is vital not only to supply dNTPs for DNA replication and repair, but also to mainta

237 verity, suggesting that treatments targeting dNTP pools could modulate mutator phenotypes for therapy

238 fter the addition of three and five template dNTPs, may serve as checkpoints to regulate the precise

239 We conclude that dNTP salvage cannot substitute for de novo dNTP synthesi

240 Previous reports have shown that dNTP pool imbalances can be caused by mutations altering

241 However, we found that dNTPs were limiting even in cells infected with wild-typ

242 The dNTP competing RT inhibitor retains activity against the

243 The dNTP metabolism machinery, including RNR, has been explo

244 Ca(2+) and Mn(2+) substantially decrease the dNTP dissociation rate relative to Mg(2+), while Ca(2+)

245 NSAH depresses dGTP and dATP levels in the dNTP pool causing S-phase arrest, providing evidence for

246 whether oxidation of the purine dNTPs in the dNTP pool provides a source of DNA damage that promotes

247 e to Mg(2+), while Ca(2+) also increases the dNTP association rate.

248 scriptase revealed that alpha-CNPs mimic the dNTP binding through a carboxylate oxygen, two phosphona

249 d other viral infections by depletion of the dNTP pool to a level that cannot support replication.

250 RRM2 at K95 results in the reduction of the dNTP pool, DNA replication fork stalling, and the suppre

251 Both pharmacological agents could reduce the dNTP production in a time- and dose-dependent manner.

252 We observed that the dNTP and NTP pools in WT postnatal hearts are unexpected

253 The rest of the dNTPs are synthesized "on the go." The rate-limiting enz

254 treating HCMV, knowing the provenance of the dNTPs incorporated into viral DNA may help inform antivi

255 gg is provided with at most one-third of the dNTPs needed to complete the thirteen rounds of DNA repl

256 lly occurring oxidized dNTPs and therapeutic dNTPs inhibit telomerase-mediated telomere elongation.

257 Importantly, these dNTP imbalances are strongly mutagenic in genetic backgr

258 All alpha-thio-dNTPs were incorporated more slowly, at 40 to 65% of the

259 This dNTP-stabilized misalignment reduced base substitution a

260 , SAMHD1 blocks HIV-1 infection through this dNTP triphosphohydrolase activity by reducing the cellul

261 Thus, dNTP pool levels correlate with Pol epsilon mutator seve

262 We examined their effects on translocation, dNTP binding, and primer strand transfer between the pol

263 Nucleoside 5'-triphosphate (dNTP) analogues in which the beta,gamma-oxygen is mimick

264 cellular 2'-deoxynucleoside-5'-triphosphate (dNTP) homeostasis by catalysing the hydrolysis of dNTPs

265 which supports deoxynucleoside triphosphate (dNTP) binding but not catalysis.

266 y due to lower deoxynucleoside triphosphate (dNTP) levels and the presence of multiple restriction fa

267 hich increases deoxynucleoside triphosphate (dNTP) pools.

268 d the cellular deoxynucleoside triphosphate (dNTP) pools.

269 SAMHD1 is a deoxynucleoside triphosphate (dNTP) triphosphohydrolase that cleaves physiological dNT

270 x and incoming deoxynucleotide triphosphate (dNTP) at 3.0-A resolution.

271 f cellular deoxyribonucleoside triphosphate (dNTP) levels is important for studying pathologies, geno

272 n controls deoxyribonucleoside triphosphate (dNTP) pools during stress through degradation of the tra

273 ppropriate deoxyribonucleoside triphosphate (dNTP).

274 that uses step-wise nucleotide triphosphate (dNTP) release, capture and detection in microdroplets fr

275 de triphosphate/ribonucleoside triphosphate (dNTP/rNTP) ratios, by the ability of DNA polymerases to

276 ailability of deoxynucleoside triphosphates (dNTP) and thus HIV-1 reverse transcription.

277 nst 2'-deoxyribonucleoside 5'-triphosphates (dNTPs).

278 intracellular deoxynucleoside triphosphates (dNTPs) to a lower level that restricts viral DNA synthes

279 ailability of deoxynucleoside triphosphates (dNTPs), which are needed for HIV-1 reverse transcription

280 Deoxynucleotide triphosphates (dNTPs) are essential for efficient hepatitis B virus (HB

281 cle, requires deoxynucleotide triphosphates (dNTPs) to fuel DNA synthesis, thus requiring penetration

282 thesis of deoxyribonucleoside triphosphates (dNTPs) and essential for both DNA replication and the re

283 rate both deoxyribonucleoside triphosphates (dNTPs) and ribonucleoside triphosphates (rNTPs) and can

284 thesis of deoxyribonucleoside triphosphates (dNTPs) that are essential for DNA replication and DNA da

285 ecursors (deoxyribonucleoside triphosphates (dNTPs)).

286 those of deoxyribonucleoside triphosphates (dNTPs), thereby influencing the frequency of incorporati

287 thesis of deoxyribonucleotide triphosphates (dNTPs) building blocks for DNA synthesis, and is a well-

288 thesis of deoxyribonucleotide triphosphates (dNTPs).

289 requires deoxyribonucleotide triphosphates (dNTPs).

290 ural and unnatural nucleoside triphosphates (dNTPs and xNTPs) using protocols that are efficient, ine

291 l and noncanonical nucleoside triphosphates (dNTPs) and has been associated with cancer progression a

292 l and noncanonical nucleotide triphosphates (dNTPs).

293 of approximately 0.1-5-fold for xNTP versus dNTP.

294 ries from minutes to hours depending on what dNTP is bound in the A2 allosteric site.

295 V irradiation in vivo was not decreased when dNTP synthesis was suppressed by hydroxyurea, indicating

296 chanism of rescuing stalled replication when dNTP supply is low.

297 The results support a model wherein dNTP elevation is needed to facilitate non-mutagenic tol

298 h to single-molecule DNA sequencing in which dNTPs, released by pyrophosphorolysis from the strand to

299 ier and slowing polymerization compared with dNTP.

300 nario of DNA polymerase enzyme kinetics with dNTP levels that can vastly change, depending on cell pr

301 In yeast, dNTP pools expand drastically during DNA damage response