ライフサイエンスコーパス: dNTP

1 dNTP binding is rapid with Kd values of 20 and 476 mum f

2 ct with regulatory (i.e., allosteric) Mg(2+)-dNTP-binding sites of nucleos(t)ide-metabolizing enzymes

3 ibrating the insertion efficiencies of the 4 dNTPs.

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

5 drolysis of any dNTP only after binding of a dNTP to site 2.

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

7 SAMHD1, a dNTP triphosphohydrolase, contributes to interferon sign

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

9 ates its inhibitory effects on RNR activity, dNTP pool level, and DNA replication.

10 nce to nucleoside/nucleotide analogs, affect dNTP selection during replication.

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

12 by GTP alone but instead, the levels of all dNTPs and the generation of a persistent tetramer that i

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

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

15 e is sensitive to 2' modifications, although dNTPs can be incorporated, and mixed DNA-RNA templates c

16 lly exclusive functions of ssRNA binding and dNTP hydrolysis depending on dNTP pool levels and the pr

17 binding to the A1 sites generates dimer and dNTP binding to the A2 and catalytic sites generates act

18 mplex with different combinations of GTP and dNTP mixtures, which depict the full spectrum of GTP/dNT

19 me substitutions, nucleotide imbalances, and dNTP alterations in different tissues.

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

21 Combined activation by GTP and dNTPs results in a long-lived tetrameric form of SAMHD1

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

23 AMHD1 is activated for the hydrolysis of any dNTP only after binding of a dNTP to site 2.

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

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

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

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

28 Evidence supports a relationship between dNTP pools and microsatellite repeat instability.

29 distinct from the tetrameric form that binds dNTPs.

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

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

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

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

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

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

36 1 is a phosphohydrolase maintaining cellular dNTP homeostasis but also acts as a critical regulator i

37 ions of SAMHD1 in the regulation of cellular dNTP levels, as well as in HIV restriction and the patho

38 HIV-1 restriction and regulation of cellular dNTP levels.

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

40 ide reductase genes, which regulate cellular dNTP pools.

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

42 es, including HIV, by depleting the cellular dNTP pool available for viral reverse transcription.

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

44 ity role, possibly by affecting the cellular dNTP pool.

45 intact in their ability to deplete cellular dNTPs.

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

47 rocesses by changing the balance of cellular dNTPs.

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

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

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

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

52 of the transcriptional response controlling dNTP production and cellular survival after UV damage.

53 ion conformation is observed and the correct dNTP stabilizes this complex compared with the binary co

54 e fingers close after binding to the correct dNTP, but that there is a second conformational change a

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

58 ty by preferably binding and incorporating D-dNTPs over unnatural L-dNTPs during DNA synthesis.

59 Considering that all natural nucleotides (D-dNTPs) and the building blocks (D-dNMPs) of DNA chains p

60 dNTPs, enantiomers of natural nucleotides (D-dNTPs), by any DNA polymerase or reverse transcriptase h

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

62 merase by promoting dNTP binding (decreasing dNTP Km), polymerase stimulates the helicase by increasi

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

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

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

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

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

68 cific dNTP triphosphohydrolase that depletes dNTP pools in resting CD4+ T cells and macrophages and e

69 of myeloid and resting T cells by depleting dNTPs.

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

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

72 AP-DNA binary complex and the Phi29 DNAP-DNA-dNTP ternary complex, residues Tyr-226 and Tyr-390 in th

73 ral comparison of binary DNA and ternary DNA-dNTP complexes of DNA polymerase beta, several side chai

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

75 report crystal structures of ternary Pol.DNA.dNTP complexes between MeFapy-dG-adducted DNA template:p

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

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

78 lomere length, and were rescued by elevating dNTP pools.

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

80 creases the discrimination against 2'-fluoro-dNTPs during RNA synthesis.

81 of translocation, increased the affinity for dNTP in the post-translocation state by decreasing the d

82 gulation of SAMHD1 by siRNA expands all four dNTP pools, with dGTP undergoing the largest relative in

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

84 hpol eta inserted all four dNTPs in steady-state and pre-steady-state assays, prefe

85 d by the combined action of GTP and all four dNTPs.

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

87 tures, which depict the full spectrum of GTP/dNTP binding at the eight allosteric and four catalytic

88 eous cross-coupling reactions of halogenated dNTPs is discussed.

89 N1 pol2-M644G cells have constitutively high dNTP levels, consistent with checkpoint activation.

90 that Polzeta function does not require high dNTP levels.

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

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

93 T expression in HeLa cells causes imbalanced dNTP pools and altered cell cycle progression.

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

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

96 e for the maintenance of a proper balance in dNTP pools required for proliferation.

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

98 e HIV-1 V148I RT mutant that is defective in dNTP binding and has DNA synthesis delay promoted RT sta

99 leads to a checkpoint-dependent increase in dNTP levels and (ii) this increase mediates the hypermut

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

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

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

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

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

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

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

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

108 an additional hydrogen bond between incoming dNTP and templating base.

109 and Trp-483 hamper insertion of the incoming dNTP in the presence of Mg(2+) ions, a reaction highly i

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

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

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

113 cludes molecular recognition of the incoming dNTP.

114 fingers domain that coordinate the incoming dNTP.

115 k the alpha phosphorous atom of the incoming dNTP.

116 iate on both DNA and RNA and can incorporate dNTPs.

117 ly distinguish between correct and incorrect dNTP substrates.

118 20 and 476 mum for the correct and incorrect dNTP, respectively.

119 rs do not close in the presence of incorrect dNTP.

120 FRET studies with incorrect dNTP result in no changes in fluorescence, indicating th

121 DinB2 discrimination against incorrect dNTPs in magnesium is primarily at the level of substrat

122 catalytic pathways of correct and incorrect dNTPs differ from each other.

123 the presence of either correct or incorrect dNTPs.

124 d with the binary complex, whereas incorrect dNTPs destabilize it.

125 Dm-dNK expression led to increased dNTP pools and an increase in the catabolism of purine a

126 siRNA silencing of SAMHD1 increases dNTP pools, stops cycling human cells in G1, and blocks

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

128 al and biochemical data provide insight into dNTP promiscuity at the secondary allosteric site and ho

129 s provide the first mechanistic insight into dNTP-mediated regulation of dNTPase activity.

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

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

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

133 1 replication by depleting the intracellular dNTP pool.

134 dependent manner, reducing the intracellular dNTP pool.

135 p21 decreased the size of the intracellular dNTP pool.

136 ndings argue that Bcl2 reduces intracellular dNTPs by inhibiting ribonucleotide reductase activity, t

137 and especially tight nucleotide binding (Kd (dNTP) approximately 1.7 mum), compared with DNA polymera

138 activity cannot be associated with any known dNTP binding site.

139 ture of a polymerase, DNA, and an incoming L-dNTP.

140 tural basis for the discrimination against L-dNTPs by DNA polymerases or RTs has not been established

141 ural basis for D-stereoselectivity against L-dNTPs, enantiomers of natural nucleotides (D-dNTPs), by

142 g and incorporating D-dNTPs over unnatural L-dNTPs during DNA synthesis.

143 DinB2 efficiently scavenges limiting dNTP and rNTP substrates in the presence of manganese.

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

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

146 pared with wild type RT, particularly at low dNTP concentrations.

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

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

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

150 an S-phase checkpoint kinase that maintains dNTP levels during a normal cell cycle and up-regulates

151 oducts or of the incorporation of mismatched dNTPs into cDNA.

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

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

154 1 quiescent mutant fibroblasts manifested mt dNTP pool imbalance and mtDNA depletion.

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

156 ing blocks for reverse transcription, namely dNTPs.

157 closed was similar for all analog and native dNTPs (0.2 to 0.4 ms), indicating no kinetic impact on t

158 65% of the rate for the corresponding native dNTPs.

159 fic recognition and discrimination of native dNTPs.

160 t excursions that does not occur with native dNTPs.

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

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

163 e artificial BenziTP in favor of the natural dNTPs.

164 SAMHD1 is a GTP-activated nonspecific dNTP triphosphohydrolase that depletes dNTP pools in res

165 Notably, dNTP pool alterations lead to genomic instability and ha

166 ancer cells are dependent on RNR for de novo dNTP biosynthesis.

167 ith pharmacological perturbations of de novo dNTP biosynthetic pathways could eliminate acute lymphob

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

169 (SWCNT-FET) to investigate accommodation of dNTP analogs with single-molecule resolution.

170 The addition of dNTP depends on pairing of the cap guanine with an oppos

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

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

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

174 ucleotide reductase ensures tight control of dNTP concentration.

175 phase, thereby fine-tuning SAMHD1 control of dNTP levels during DNA replication.

176 on of DNA damage checkpoint and depletion of dNTP concentrations to levels lower than those seen upon

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

178 es S-phase checkpoint-dependent elevation of dNTP pools.

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

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

181 Accordingly, the average rates of dNTP analog incorporation were largely determined by dur

182 ents provide insight into the recognition of dNTP substrate molecules by the polymerase binary state.

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

184 tion in macrophages and a major regulator of dNTP concentrations in human cells.

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

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

187 ase (RR) catalyzes the rate-limiting step of dNTP synthesis and is an established cancer target.

188 concentrations are much higher than those of dNTP.

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

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

191 We find that in the absence of dNTPs, the binary complex shuttles between two different

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

193 uce the production of nonlimiting amounts of dNTPs.

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

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

196 llular dNTP levels through its hydrolysis of dNTPs.

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

198 -1 cells is suppressed by elevated levels of dNTPs in vivo, and the activity of Pol epsilon is compro

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

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

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

202 biting HIV infection, curtailing the pool of dNTPs available for reverse transcription of the viral g

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

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

205 on and thereby controlling the production of dNTPs.

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

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

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

209 RNA binding and dNTP hydrolysis depending on dNTP pool levels and the presence of viral ssRNA.

210 Most interestingly, on dNTP binding, only the insertion conformation is observe

211 hat is naturally adept at utilizing rNTPs or dNTPs as substrates.

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

213 amics of RT-template/primer (T/P) and RT-T/P-dNTP complexes.

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

215 iphosphohydrolase that cleaves physiological dNTPs into deoxyribonucleosides and inorganic triphospha

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

217 icase stimulates the polymerase by promoting dNTP binding (decreasing dNTP Km), polymerase stimulates

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

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

220 reduced pools of both purine and pyrimidine dNTPs in mitochondria, whereas cytosolic pools were unaf

221 motion of the enzyme on the T/P and reduces dNTP binding affinity.

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

223 ng key Dun1 targets that negatively regulate dNTP synthesis, suppress the dun1Delta pol2-M644G synthe

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

225 Because RNR-regulated dNTP production can influence DNA replication fidelity w

226 during a normal cell cycle and up-regulates dNTP synthesis upon checkpoint activation.

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 Adding deoxyribonucleosides to restore dNTP pools transiently protected cells from apoptosis.

230 on the ability of DNA polymerases to select dNTPs from a nucleotide pool dominated by NTPs.

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

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

233 es in the thumb/fingers opening, RT sliding, dNTP binding disruption and in vitro and in vivo RT inhi

234 during quiescence, contributing to the small dNTP pool sizes of these cells.

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

236 es (A1) as well as coactivation by substrate dNTP binding to a distinct set of nonspecific activator

237 tructures of DNA polymerase I with substrate dNTPs have revealed key structural states along the cata

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

239 26- to 78-fold lower affinity for rNTPs than dNTPs, but only a 2.6- to 6-fold differential in rates o

240 We found that dNTP pool changes caused by deficiencies in the ndk or d

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

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

243 The dNTP competing RT inhibitor retains activity against the

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

245 The dNTP triphosphohydrolase SAMHD1 is a nuclear antiviral h

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

247 e post-translocation state by decreasing the dNTP dissociation rate, and increased the affinity for p

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

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

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

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

252 ere, we report that SAMHD1 regulation of the dNTP concentrations influences HIV-1 template switching

253 e reacting alpha- and beta-phosphates of the dNTP, suggesting its role in stabilizing reaction interm

254 l, the findings suggest a model in which the dNTP alterations in the ndk and dcd strains interfere wi

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

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

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

260 oside triphosphate (dNTP) pool sizes through dNTP hydrolysis and modulates the innate immune response

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

262 ssion in the cell nucleus expanded the total dNTP pools to levels required for efficient mitochondria

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

264 he cellular deoxynucleoside 5'-triphosphate (dNTP) concentration to a level at which the viral revers

265 ich may affect deoxynucleoside triphosphate (dNTP) binding and polymerase activity.

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

267 d the cellular deoxynucleoside triphosphate (dNTP) pools.

268 hich increases deoxynucleoside triphosphate (dNTP) pools.

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

270 that alter the deoxynucleoside triphosphate (dNTP)-binding pocket, including those that confer resist

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

272 intracellular deoxynucleotide triphosphate (dNTP) pool, a limiting factor for retroviral reverse tra

273 f cellular deoxyribonucleoside triphosphate (dNTP) pool sizes through dNTP hydrolysis and modulates t

274 respect to deoxyribonucleoside triphosphate (dNTP) substrate, whereas a second compound is a competit

275 ppropriate deoxyribonucleoside triphosphate (dNTP).

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

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

278 onical deoxyribonucleoside 5'-triphosphates (dNTPs) at the replisome.

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

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

281 our different deoxynucleoside triphosphates (dNTPs).

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

283 nced pools of deoxynucleotide triphosphates (dNTPs) necessary for DNA replication and maintenance of

284 sis of 2'-deoxyribonucleoside triphosphates (dNTPs) either by classical triphosphorylation of nucleos

285 ecursors (deoxyribonucleoside triphosphates (dNTPs)).

286 nalogs of deoxyribonucleoside triphosphates (dNTPs), despite the enzymes' highly evolved mechanisms f

287 pools of deoxyribonucleoside triphosphates (dNTPs), the building blocks of DNA.

288 thesis of deoxyribonucleotide triphosphates (dNTPs).

289 requires deoxyribonucleotide triphosphates (dNTPs).

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

291 l and noncanonical nucleotide triphosphates (dNTPs).

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

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

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

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

296 llow for DNA repair with a 'ribo patch' when dNTPs are limiting.

297 e important in resting CD4(+) T cells, where dNTP pools are reduced to nanomolar levels to restrict i

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

299 ier and slowing polymerization compared with dNTP.

300 enzyme activated by guanine nucleotides with dNTP triphosphate hydrolase activity (dNTPase).

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