ライフサイエンスコーパス: hypoxanthine

1 e of the downstream metabolites (inosine and hypoxanthine).

2 e transformed into purine derivatives (e.g., hypoxanthine).

3 ed out at high concentrations of guanine and hypoxanthine.

4 hibitor, allopurinol, a structural isomer of hypoxanthine.

5 ountering the pro-mutagenic bases uracil and hypoxanthine.

6 the ability of the suppressors to metabolize hypoxanthine.

7 prevent polymerization opposite a templating hypoxanthine.

8 th defect at physiological concentrations of hypoxanthine.

9 ted enzymatically using xanthine oxidase and hypoxanthine.

10 N1-methylhypoxanthine and N1-(2-aminoethyl)-hypoxanthine.

11 ing both 5'-methylthioinosine and inosine to hypoxanthine.

12 t that is achieved by AAG in the excision of hypoxanthine.

13 7, also mediate the uptake of the nucleobase hypoxanthine.

14 ng step may be rate-limiting for excision of hypoxanthine.

15 elated purine metabolite 5'-AMP, inosine, or hypoxanthine.

16 ions for both prominent neutral tautomers of hypoxanthine.

17 mino group, present in guanine but absent in hypoxanthine.

18 catalyzed excision of the deaminated purine, hypoxanthine.

19 GVB when meiotic arrest was maintained with hypoxanthine, 8-AHA-cAMP, guanosine, or milrinone, but w

20 levels of the DNA nucleobase damage products hypoxanthine, 8-oxo-7,8-dihydroguanine, 1,N6-ethenoadeni

21 4 in vitro but have bypass activities across hypoxanthine, 8-oxoguanine, and either uracil or cis-syn

22 the xpt-pbuX operon of B. subtilis bound to hypoxanthine, a prevalent metabolite in the bacterial pu

23 Hypoxanthine, a transported substrate, protected L393C,

24 It is known that hypoxanthine acts as guanine when interacting with other

25 nt enhances the differences in acidity among hypoxanthine, adenine, and guanine.

26 classes that specifically recognize guanine/hypoxanthine, adenine, or 2'-deoxyguanosine (dG).

27 N(6) and, to a lesser extent, N1 help drive hypoxanthine:adenine base-pair formation by BF.

28 idine, they regained the ability to clone in hypoxanthine-aminopterin-thymidine medium and reexpresse

29 rous TK+ colonies that survived selection in hypoxanthine-aminopterin-thymidine medium.

30 Single-turnover excision of hypoxanthine and 1,N(6)-ethenoadenine follows bell-shape

31 Both Dpo2 and Dpo3, but not Dpo1, bypassed hypoxanthine and 8-oxoguanine.

32 The initial rates of uptake of hypoxanthine and adenine by spirochetes carrying bbb23 a

33 Combinations with hypoxanthine and adenine markedly potentiate the cytosta

34 ties of spirochetes carrying bbb22 alone for hypoxanthine and adenine were similar to those of spiroc

35 s (BF), an A family enzyme, generate adenine:hypoxanthine and adenine:8-oxo-7,8-dihydroguanine (8-oxo

36 and the associated interaction modes between hypoxanthine and all standard, non-glycyl/non-prolyl ami

37 nerated from AdoHcy is further hydrolyzed to hypoxanthine and ammonia by recombinant adenine deaminas

38 ed Appel reactions at C6 of trityl-protected hypoxanthine and guanine derivatives followed by detrity

39 ifetimes of the singly deprotonated forms of hypoxanthine and inosine show drastic differences, where

40 dynamics following electronic excitation of hypoxanthine and its nucleoside inosine were studied by

41 adenosine is more important than salvage of hypoxanthine and other purine nucleobases.

42 ent with theory for equilibrium formation of hypoxanthine and oxacarbenium ion at this level of theor

43 15, p < 0.01, Spearman's correlation) showed hypoxanthine and purine metabolism have association with

44 ining uracil 1.5-4.5-fold more strongly than hypoxanthine and site-directed mutagenesis suggested tha

45 n, a folate antagonist, co-administered with hypoxanthine and thymidine (HAT/Met).

46 gene, initiates removal of the base analogs hypoxanthine and xanthine from DNA, acting to prevent mu

47 e in Escherichia coli is proposed to prevent hypoxanthine and xanthine incorporation into DNA by inte

48 of nucleobase deamination: incorporation of hypoxanthine and xanthine into DNA and RNA caused by def

49 nsistently, superoxide radicals generated by hypoxanthine and xanthine oxidase also induced the activ

50 tic role in purine degradation, metabolizing hypoxanthine and xanthine to uric acid with concomitant

51 lytic residues to facilitate its excision of hypoxanthine and xanthine.

52 , that all exogenous purines are funneled to hypoxanthine and/or xanthine by L. donovani, and that th

53 rs containing mutagenic N1-beta-hydroxyalkyl-hypoxanthines and the availability of the rare base-modi

54 Specificity for hypoxanthine (and uracil) arises from a combination of p

55 denine, 2-chloroadenine, 3-deazaadenine, and hypoxanthine) and N-3 and the exocyclic group at C-4 of

56 zol-1-yl)purine, 2-(3,5-dimethylpyrazol-1-yl)hypoxanthine, and 2-(3,5-dimethylpyrazol-1-yl)adenine, f

57 lic acid, tryptophan, L-valine, cycloserine, hypoxanthine, and 4-O-Methylmelleolide concentrations on

58 constitutively synthesizes AMP and excretes hypoxanthine, and a GMP kinase mutant (guk1), which accu

59 purine bases including 1,N(6)-ethenoadenine, hypoxanthine, and alkylation adducts in DNA.

60 uracil, abasic site and xanthine, as well as hypoxanthine, and cuts the phosphodiester bond at their

61 lycosylase (hAAG) excises alkylated purines, hypoxanthine, and etheno bases from DNA to form abasic (

62 nzymatic activity was observed with adenine, hypoxanthine, and guanine as substrates.

63 ted, designated KC62, the uptake of adenine, hypoxanthine, and guanine was reduced by approximately 7

64 entration of extracellular purines (adenine, hypoxanthine, and guanine) but not cytosine.

65 t in a decreased ability to salvage adenine, hypoxanthine, and guaninine via phosphoribosylation.

66 nucleotide metabolites, including xanthine, hypoxanthine, and inosine are elevated.

67 m chloride, thiamine, iron, zinc, magnesium, hypoxanthine, and pyruvate.

68 Basal oxypurines (xanthine, hypoxanthine, and urate) rose with FA pretreatment but i

69 xoguanine, thymine glycol, 2-hydroxyadenine, hypoxanthine, and xanthine.

70 Damaged bases such as hypoxanthine are associated with carcinogenesis and cell

71 Uracil and hypoxanthine are removed from DNA by base excision repai

72 Full details of the specific recognition of hypoxanthine are revealed, allowing a comparison with pu

73 Most of the extracellular hypoxanthine arose from the metabolism of inosine by ect

74 m falciparum is a purine auxotroph requiring hypoxanthine as a key metabolic precursor.

75 a nonpolar environment to favor deprotonated hypoxanthine as a leaving group versus deprotonated aden

76 ons of these results, both in the context of hypoxanthine as a universal base and as a damaged base,

77 evealed an optimal k(cat) of 412 s(-1) using hypoxanthine as the hydroxylase substrate.

78 in complex with the physiological substrate hypoxanthine at 1.8 A resolution and the chemotherapeuti

79 We also bracket a less acidic site of hypoxanthine at 368 +/- 3 kcal mol-1.

80 The structure with hypoxanthine at position 2 explains the stimulation of t

81 tion of the primer serves to move the uracil/hypoxanthine away from the primer-template junction, res

82 of mean force indicates that the tendency of hypoxanthine base flipping follows the order of G/I > T/

83 interdependence during formation of adenine:hypoxanthine base pairs by pol alpha, and N3 of dATP aga

84 lectrodeposition technique to create ATP and hypoxanthine biosensors as examples of the methodology.

85 2+) stimulated the enzyme activity only with hypoxanthine but not ethenoadenine.

86 is effect is rescued by the reaction product hypoxanthine, but not the substrate inosine, indicating

87 otherapy reduced levels of hexose sugars and hypoxanthine by 1.3%, but no statistically different cha

88 reduces the single turnover excision rate of hypoxanthine by a factor of 4 when paired with thymine.

89 stimulates the multiple-turnover excision of hypoxanthine by AAG but has no effect on single-turnover

90 ne (SAH), is converted into adenine and then hypoxanthine by the recombinant coupling enzymes SAH nuc

91 R-HsPNP is fully dissociative, N7-protonated hypoxanthine (C1'-N9 distance >or= 3.0 A) with partial p

92 t in its affinities for protein side chains, hypoxanthine closely matches guanine, much more so than

93 tylation, stabilized the binding of MPG with hypoxanthine-containing oligos, and enhanced MPG-catalyz

94 In vivo, exogenous XO plus the substrate hypoxanthine did not protect and instead worsened the ou

95 E(20:1/0:0), LysoPC(16:0), LysoPE(16:0/0:0), hypoxanthine, dihydroxyacetone, 4-O-Methylmelleolide, Ly

96 /U, T/U, C/U, and A/U base pairs, but also a hypoxanthine DNA glycosylase acting on G/I, T/I, and A/I

97 G/I > T/I, A/I > C/I, matching the trend of hypoxanthine DNA glycosylase activity observed in vitro.

98 karyotes as family 6 and designate it as the hypoxanthine-DNA glycosylase family.

99 Instead, these enzymes act as hypoxanthine-DNA glycosylases in vitro and in vivo.

100 able phosphoribosyltransferase activity with hypoxanthine even though the genome lacks a discernible

101 lude that both dominant neutral tautomers of hypoxanthine exhibit ultrashort excited state lifetimes

102 -D activity is slowed by the template strand hypoxanthine, extending previous results that demonstrat

103 aminase (ADA) a key enzyme in the pathway of hypoxanthine formation.

104 Inhibition of hypoxanthine-forming reactions in both erythrocytes and

105 f mechanisms and results in the formation of hypoxanthine from adenine, uracil from cytosine, and xan

106 (AAG) is the enzyme responsible for excising hypoxanthine from DNA in humans.

107 ligos, and enhanced MPG-catalyzed removal of hypoxanthine from DNA.

108 Hypoxanthine functions to stabilize this structure and t

109 acid, nicotinamide, 5-oxoproline, xanthine, hypoxanthine, glucose, malic acid, and adenine) form the

110 Utilizing the hypoxanthine guanine phosphoribosyl transferase (HPRT) a

111 d gene encoding the purine metabolic enzyme, hypoxanthine guanine phosphoribosyl transferase (HPRT).

112 ine permease, or the HPT1 gene, encoding the hypoxanthine guanine phosphoribosyl transferase, enhance

113 We here demonstrate that human hypoxanthine guanine phosphoribosyltransferase (HGPRT) c

114 city and induced mutation frequencies at the hypoxanthine guanine phosphoribosyltransferase (HPRT) lo

115 genetic disorder caused by mutations of the hypoxanthine guanine phosphoribosyltransferase (HPRT) pu

116 lpha) and two with 17alpha or Yalpha and the hypoxanthine guanine phosphoribosyltransferase locus (HP

117 reaction and 45.6, 35.9, and 12.3 microM for hypoxanthine, guanine, and adenine in the direction of n

118 erties were examined toward their substrates hypoxanthine, guanine, and phosphoribosylpyrophosphate.

119 4 acquires the ability to transport adenine, hypoxanthine, guanine, and xanthine with Km values in th

120 to replicate in medium containing 10 microM hypoxanthine, guanine, or xanthine and replicated slowly

121 efinitely without 2'-deoxycoformycin or with hypoxanthine, guanine, xanthine, guanosine, inosine, or

122 The gene encodes hypoxanthine-guanine phosphoribosyl transferase, an enzy

123 rate an L. donovani strain deficient in both hypoxanthine-guanine phosphoribosyl-transferase (HGPRT)

124 donovani salvages purines primarily through hypoxanthine-guanine phosphoribosyltransferase (HGPRT) a

125 ly been shown to be good inhibitors of human hypoxanthine-guanine phosphoribosyltransferase (HGPRT) a

126 thase (GMPS) or direct salvage of guanine by hypoxanthine-guanine phosphoribosyltransferase (HGPRT).

127 l deficiency of the purine recycling enzyme, hypoxanthine-guanine phosphoribosyltransferase (HGprt).

128 Purine nucleoside phosphorylase (PNP) and hypoxanthine-guanine phosphoribosyltransferase (HGPRTase

129 gene encoding the purine biosynthetic enzyme hypoxanthine-guanine phosphoribosyltransferase (HPRT) ca

130 e transcriptional promoter and exon 1 of the hypoxanthine-guanine phosphoribosyltransferase (HPRT) ge

131 junctions associated with cRSS sites at the hypoxanthine-guanine phosphoribosyltransferase (HPRT) lo

132 way salvages guanine through the activity of hypoxanthine-guanine phosphoribosyltransferase (HPRT) to

133 frequency of somatic mutations (Mfs) at the hypoxanthine-guanine phosphoribosyltransferase (HPRT)-re

134 d by deficiency of the purine salvage enzyme hypoxanthine-guanine phosphoribosyltransferase (HPRT).

135 These genes included those for hypoxanthine-guanine phosphoribosyltransferase (hpt), ad

136 One potential new target is hypoxanthine-guanine phosphoribosyltransferase (MtHGPRT)

137 pectrum of clinical features associated with hypoxanthine-guanine phosphoribosyltransferase deficienc

138 e pathogenesis and diagnosis of all forms of hypoxanthine-guanine phosphoribosyltransferase deficienc

139 o the relatively stable mutation rate of the hypoxanthine-guanine phosphoribosyltransferase gene.

140 and induced cell death and mutations at the hypoxanthine-guanine phosphoribosyltransferase gene.

141 single-copy transgene (Tg; inserted into the hypoxanthine-guanine phosphoribosyltransferase locus) th

142 ntitative explanation for the specificity of hypoxanthine-guanine phosphoribosyltransferase, a key en

143 disorder caused by deficiency of the enzyme hypoxanthine-guanine phosphoribosyltransferase.

144 e, which encodes the purine recycling enzyme hypoxanthine-guanine phosphoribosyltransferase.

145 Hypoxanthine-guanine-(xanthine) phosphoribosyltransferas

146 Hypoxanthine-guanine-[xanthine] phosphoribosyltransferas

147 d in human lymphoblastoid cells in the human hypoxanthine-guanine-phosphoribosyltransferase (HPRT) ge

148 erase (HGPRT) and Plasmodium falciparum (Pf) hypoxanthine-guanine-xanthine phosphoribosyltransferase

149 the cloning, expression and purification of hypoxanthine-guanine-xanthine phosphoribosyltransferase

150 O) maintained in meiotic arrest by dbcAMP or hypoxanthine, GVB was dose-dependently induced.

151 guanine (G), thymine (T), cytosine (C), and hypoxanthine (H), have been examined toward understandin

152 k, we establish that the most acidic site of hypoxanthine has a gas-phase acidity of 332 +/- 2 kcal m

153 g N1-methylhypoxanthine or N1-(2-aminoethyl)-hypoxanthine has a reduced thermostability with no parti

154 the gas phase versus solution indicates that hypoxanthine has much less of a destabilizing effect in

155 sted the role of N-terminal extension on MPG hypoxanthine (Hx) cleavage activity.

156 ntiometric enzyme electrode for detection of hypoxanthine (Hx) in fish meat is described.

157 ective electrode material in an amperometric hypoxanthine (Hx) sensor for meat freshness evaluation.

158 Hypoxanthine (Hx) with specific (15)N labels has been us

159 including 3-methyladenine, 7-methylguanine, hypoxanthine (Hx), and 1,N(6)-ethenoadenine (epsilonA).

160 osine monophosphate (IMP), inosine (Ino) and hypoxanthine (Hx), in fish tissue, based on hydrophilic

161 (GuaA) catalyse the multistep conversion of hypoxanthine (Hyp) to dGMP for DNA synthesis.

162 NA results in the formation of xanthine (X), hypoxanthine (I), oxanine, and uracil, all of which are

163 observed large increases (up to 600-fold) in hypoxanthine in both DNA and RNA in cells unable to conv

164 Traces of uracil and hypoxanthine in DNA can lead to inhibition of the PCR by

165 he PCNA-polymerase complex encounters uracil/hypoxanthine in DNA templates, base excision repair is s

166 eases in 5-chlorocytosine in DNA and RNA and hypoxanthine in DNA.

167 als ascribed to guanine/xanthine and adenine/hypoxanthine in human hepatoma (HepG2) cells were detect

168 d tightly to the deaminated bases uracil and hypoxanthine in single-stranded DNA, stalling replicatio

169 possibly also via high levels of the purine hypoxanthine in the follicular fluid.

170 polymerase in complex with a DNA containing hypoxanthine in the single-stranded region of the templa

171 show that the multiple-turnover excision of hypoxanthine in vitro is limited by release of the abasi

172 The modified base, N1-(2,4-dinitrophenyl)-hypoxanthine, in synthesized oligomers, upon treatment w

173 converted into corresponding N1-substituted hypoxanthines, including N1-15N-hypoxanthine, N1-methylh

174 [3H]hypoxanthine incorporation assays demonstrated up to a 4

175 al supplementation of Mthfd1(gt/+) dams with hypoxanthine increased FGR frequency and caused occasion

176 tures were parsed, one feature identified as hypoxanthine increased with salbutamol (p < 0.001).

177 ucleoside transporter 1) are auxotrophic for hypoxanthine, inosine, and adenosine under physiological

178 B. hermsii incorporated radiolabeled hypoxanthine into RNA and DNA to a much greater extent t

179 tral role in purine catabolism by converting hypoxanthine into xanthine and then further into uric ac

180 hetic pathway, and its further metabolism to hypoxanthine involves PfPNP in purine recycling (in addi

181 Hypoxanthine is a mutagenic purine base that most common

182 g exonuclease activity and binding of uracil/hypoxanthine is addressed, using the family-B DNA polyme

183 in purine catabolism, the inosine nucleobase hypoxanthine is also one of the most abundant modified n

184 When uracil/hypoxanthine is bound four bases ahead of the primer-tem

185 restingly, when the base pairing partner for hypoxanthine is changed to difluorotoluene, which cannot

186 ernate mechanism involving preprotonation of hypoxanthine is energetically less attractive, because t

187 Kinetic experiments demonstrate that >98% of hypoxanthine is hydroxylated at C-2 rather than C-8, ind

188 In this reaction sequence, hypoxanthine is hydroxylated to xanthine by PH and then

189 t enzyme selectivity for the C-2 over C-8 of hypoxanthine is largely due to differences in the intrin

190 s attractive, because the proton affinity of hypoxanthine is less than that of adenine and guanine.

191 We find that the N9-H of hypoxanthine is more acidic than that of adenine and gua

192 Hypoxanthine is the key precursor for purine metabolism

193 tight complexes when uracil (K(d)=16 pM) or hypoxanthine (K(d)=65 pM) was present.

194 oxopropyl)-N-(2-phosphonoethyl)-2-aminoethyl]hypoxanthine (K(i) = 100 nM): no inhibition could be det

195 most adept at excising the deaminated lesion hypoxanthine (k(st)/k(non) = 10(8)), suggesting that enz

196 old more tightly to an abasic site than to a hypoxanthine lesion site.

197 le nor the details of its interaction with a hypoxanthine ligand.

198 Dual recognition of uracil and hypoxanthine may be facilitated by binding the bases wit

199 osydnonimine; NONOates plus xanthine oxidase/hypoxanthine, menadione, or mitomycin C) were examined.

200 r to promote oxygen-free radical generation, hypoxanthine (n=9) or xanthine (n=9), XO substrates, or

201 -substituted hypoxanthines, including N1-15N-hypoxanthine, N1-methylhypoxanthine and N1-(2-aminoethyl

202 tations because of a defect in the repair of hypoxanthine (nitrosatively deaminated adenine) in DNA.

203 Neither hypoxanthine nor xanthine infusion increased brain damag

204 , we report that adenine, diaminopurine, and hypoxanthine nucleoside phosphates and a noncanonical py

205 examined toward understanding the effect of hypoxanthine on DNA stability.

206 nted by the addition of the purine precursor hypoxanthine or by introduction of purMCDN in trans.

207 rate is 58-fold higher than that with either hypoxanthine or guanine, representing a distinct dispari

208 No measurable rescue is observed with either hypoxanthine or xanthine (250 microm), indicating that d

209 Larvae fed on hypoxanthine or xanthine showed a decreased JH sensitivi

210 sive riboswitch that directly binds guanine, hypoxanthine or xanthine to terminate transcription.

211 that contained the deaminated bases uracil, hypoxanthine, or xanthine in a similar manner to E. coli

212 kb) functional transgene cassettes into the hypoxanthine phosphoribosyl transferase (HPRT) and Type

213 c pH increases the mutation frequency of the hypoxanthine phosphoribosyl transferase (HPRT) gene in a

214 n to insert a single-copy transgene into the hypoxanthine phosphoribosyl transferase (hprt) locus, we

215 ssion cassette (neo) into the X-linked human hypoxanthine phosphoribosyl transferase (HPRT) locus.

216 also suppresses de novo genetic mutations of hypoxanthine phosphoribosyl transferase gene in CML and

217 insertion of 146 CAG repeats into the murine hypoxanthine phosphoribosyl transferase locus (Hprt(CAG)

218 ix metalloproteinase 1 (TIMP-1), TIMP-2, and hypoxanthine phosphoribosyl transferase-1 (HPRT1).

219 vided to cells using interfering RNA against hypoxanthine phosphoribosyl transferase.

220 sphoribosyl-1-pyrophosphate (consumed in the hypoxanthine phosphoribosyl transferase/adenine phosphor

221 e method with mouse ES cells having a mutant hypoxanthine phosphoribosyltransferase (Hprt) gene and g

222 he transposase enzyme designed to target the hypoxanthine phosphoribosyltransferase (HPRT) gene locat

223 cessfully targeted cells by co-targeting the hypoxanthine phosphoribosyltransferase (HPRT) gene.

224 The hypoxanthine phosphoribosyltransferase (Hprt) locus has

225 nd spectra of somatic mutation events at the hypoxanthine phosphoribosyltransferase (HPRT) locus in p

226 We found that hypoxanthine phosphoribosyltransferase (HPRT) mutation f

227 environment on the frequency of spontaneous hypoxanthine phosphoribosyltransferase (HPRT) mutations

228 ene, the X-chromosomal disease gene encoding hypoxanthine phosphoribosyltransferase (HPRT), we monito

229 uanine phosphoribosyltransferase (XGPRT) and hypoxanthine phosphoribosyltransferase (HPRT).

230 Hypoxanthine phosphoribosyltransferase (HPRT1) is a key

231 ns were quantified with the micronucleus and hypoxanthine phosphoribosyltransferase forward mutation

232 endent EGFP reporter gene 5' of the X-linked hypoxanthine phosphoribosyltransferase locus in mouse em

233 inhibition is needed for drugs targeting the hypoxanthine phosphoribosyltransferase of Trypanosoma cr

234 lity of the M. maripaludis hpt gene encoding hypoxanthine phosphoribosyltransferase to confer sensiti

235 of adenine phosphoribosyltransferase and of hypoxanthine phosphoribosyltransferase were the same in

236 successfully target HPRT1, the gene encoding hypoxanthine phosphoribosyltransferase-1 (HPRT1), and PO

237 Enzymes that salvage 6-oxopurines, including hypoxanthine phosphoribosyltransferases (HPRTs), are pot

238 Each mutant PurR-hypoxanthine-purF operator holo complex crystallizes iso

239 de incorporating 2-(3,5-dimethylpyrazol-1-yl)hypoxanthine readily accepted any of the natural nucleob

240 Infusion of hypoxanthine reduced cerebral injury suggesting that ano

241 o signal, FAD radical, and 2Fe-2S centers in hypoxanthine-reduced PH.

242 we report that both the NPPC/NPR2 system and hypoxanthine require the activity of inosine monophospha

243 ligodeoxyribonucleotides containing a unique hypoxanthine residue (Hx) and show that the steady-state

244 -hydrogen bonding shape mimics of uracil and hypoxanthine, respectively, is strongly diminished, sugg

245 and xanthine oxidase-catalyzed oxidation of hypoxanthine, respectively.

246 The appearance of hypoxanthine results in a decrease in absorbance at 265n

247 The ROC curve of hypoxanthine returned an AUC of 0.79 (p < 0.001).

248 studies of incorporated [3H]adenine and 3[H]hypoxanthine revealed a metabolic block at the level of

249 is 3.6 A from IMP, in the same plane as the hypoxanthine ring.

250 ld-type levels of adenine saturation but not hypoxanthine saturation, suggesting that maximal hypoxan

251 emains ultrafast but the singly deprotonated hypoxanthine shows a much longer lifetime of 19 ps.

252 However, administration of hypoxanthine significantly improved somatosensory evoked

253 fluorotoluene, which cannot hydrogen bond to hypoxanthine, single turnover excision rates increase by

254 Uracil and hypoxanthine slowed Afu Pol-D "in trans", that is, a cop

255 gle-turnover kinetics showed that uracil and hypoxanthine slowed the polymerase by factors of approxi

256 of damaged purine bases from DNA, including hypoxanthine that is formed by the oxidative deamination

257 of transporters for adenine, guanine, and/or hypoxanthine that remain unknown with respect to structu

258 B DNA polymerases bind tightly to uracil and hypoxanthine (the deamination products of cytosine and a

259 Upon ligand binding (hypoxanthine), the 3-fold fluorescence quench confirms c

260 sation was also inhibited by the presence of hypoxanthine, the deamination product of adenine.

261 of the polymerase to read through uracil and hypoxanthine, the same kinetic parameters being observed

262 ylbenzoprim, this activity was unaffected by hypoxanthine/thymidine rescue.

263 he proton affinity of the most basic site of hypoxanthine to be 222 +/- 3 kcal mol-1.

264 concentrations of either adenine or guanine/hypoxanthine to control gene expression.

265 erize the binding of phosphate, guanine, and hypoxanthine to native, Leuko-, and Y249W-Leuko-PNPs, es

266 The enzyme catalyzes the oxidation of hypoxanthine to xanthine and also xanthine to uric acid

267 nthine oxidase (XO), an enzyme that converts hypoxanthine to xanthine and xanthine to uric acid, is t

268 -catalyzed conversion by xanthine oxidase of hypoxanthine to xanthine to uric acid.

269 eaminase was the major source of the inosine/hypoxanthine tone.

270 BBB22 and/or BBB23 is essential for hypoxanthine transport and contributes to the transport

271 bolic signature consisting of aconitic acid, hypoxanthine, trimethylamine N-oxide, and threonine diff

272 Biochemical studies further showed that hypoxanthine, unexpectedly, was an inefficient substrate

273 cross the PPM revealed a severe reduction in hypoxanthine uptake in the knockout, whereas adenosine a

274 chetes demonstrated a measurable increase in hypoxanthine uptake over a 30-min time course.

275 xanthine saturation, suggesting that maximal hypoxanthine uptake requires the presence of bbb23.

276 pathway for exogenous purine conversion into hypoxanthine using host enzymes followed by PfNT1-mediat

277 ated to the different deprotonation sites in hypoxanthine versus inosine, which gives rise to signifi

278 equential hydroxylation reactions to convert hypoxanthine via xanthine to urate.

279 Hypoxanthine was a competitive inhibitor of guanine resc

280 Hypoxanthine was a weaker inhibitor than uracil.

281 rt to understand the intrinsic properties of hypoxanthine, we examined the gas-phase acidity and prot

282 excited state dynamics of singly protonated hypoxanthine were also studied, showing biexponential de

283 codA orthologs, and a different response to hypoxanthine which increased cod expression in K. pneumo

284 atile basis nitrogen (TVB-N), histamine, and hypoxanthine, which were performed at scheduled times du

285 spectively, catalyzes adenine deamination to hypoxanthine with an apparent K(m) of 15.4 muM, and does

286 For the orientation of hypoxanthine with C-2 proximal to the molybdenum center,

287 increasing rates of mutation from adenine to hypoxanthine with D(ssH) appear to drive regional differ

288 ated by the reaction of xanthine oxidase and hypoxanthine with rates of 0.1-6.0 muM/min and trapped w

289 hat MPG lacking N-terminal extension excises hypoxanthine with significantly reduced efficiency, one-

290 o compare the acidic and basic properties of hypoxanthine with those of the normal bases adenine and

291 n act on all three purine deamination bases, hypoxanthine, xanthine, and oxanine.

292 The ROS donor hypoxanthine-xanthine oxidase (XO/HX) and the JNK activa

293 Using hypoxanthine-xanthine oxidase as the oxidizing method, X

294 way is the expression of two isoforms of the hypoxanthine-xanthine-guanine phosophoribosyltransferase

295 s for purine salvage, defined by the enzymes hypoxanthine-xanthine-guanine phosphoribosyltransferase

296 verification with a mutant parasite lacking hypoxanthine-xanthine-guanine phosphoribosyltransferase

297 ytic graphite (EPG) electrode to construct a hypoxanthine/xanthine biosensor that functions at physio

298 y to avoid chromosomal lesions is to prevent hypoxanthine/xanthine incorporation into DNA via interce

299 n of endonuclease V (gpnfi) specific for DNA-hypoxanthines/xanthines, suggesting that RdgB either int

300 ke of adenine (PurP and YicO) or guanine and hypoxanthine (YjcD and YgfQ).