ライフサイエンスコーパス: HPRT

1 oxanthine-guanine phosphoribosyltransferase (HPRT).

2 xanthine guanine phosphoribosyl transferase (HPRT).

3 and hypoxanthine phosphoribosyltransferase (HPRT).

4 hypoxanthine phosphoribosyltransferase gene (Hprt).

5 oxanthine-guanine phosphoribosyltransferase (HPRT).

6 us with Leu67, Lys68, and Gly69 in the human HPRT.

7 gene C-MOS, and housekeeping genes GAPDH and HPRT.

8 ogous to position 192 (Leu-192) of the human HPRT.

9 ite was placed within the repeated region of HPRT.

10 ins, and most mutants had a single change in HPRT.

11 In addition, IMPDH type I(-/-) HPRT(-/0) splenocytes showed reduced interleukin-4 produ

12 We conclude that both IMPDH and HPRT activities contribute to normal T-lymphocyte activa

13 ity despite the presence of IMPDH type I and HPRT activities.

14 Restoration of HPRT activity by homologous recombination with human/mou

15 region that are characteristic of the active HPRT allele.

16 Sox-3 is located on the X chromosome between Hprt and Dmd.

17 We recommend using Rplp0, Nono, Tbp, Hprt and Eef2 instead of common reference genes.

18 Finally, using both endogenous HPRT and exogenous reporters, we validate novel cell cyc

19 e high rates of 5aC-induced reactivation for HPRT and G6PD in this hybrid relative to other inactive

20 e demonstrate that the GTP synthesis enzymes HprT and Gmk bind with a high affinity, leading to an in

21 Hprt and Plp lie in a region of the X chromosome that ex

22 with two guide RNAs that target respectively HPRT and the gene of interest.

23 y a competitive RIA) and mutagenicity at the HPRT and TK loci (as assessed by cell-cloning assays) we

24 ation, mutation assays were performed on the HPRT and TK loci, and gene expression profiles were gene

25 ereas NO(*)-induced mutant fractions in both HPRT and TK1 genes were significantly lower in TK6 cells

26 xanthine quanine phosphoribosyl transferase (hprt) and the thymidine kinase loci.

27 the hypoxanthine phosphoribosyl transferase (HPRT) and Type I collagen (COL1A1) loci in normal human

28 cant decrease in frameshift mutation rate at HPRT, and (iii) the in vitro repair of looped substrates

29 xanthine guanine phosphoribosyl transferase (HPRT) as a test locus, it was determined that while no t

30 cI mutation assay is less sensitive than the hprt assay for detecting increases in Mf induced by ENU

31 The HPRT assay measures hypoxanthine phosphoribosyl transfer

32 monitoring DSB mis-repair using a sensitive HPRT assay, we found that depletion of HR proteins, incl

33 The gene maps 65 kb telomeric to HPRT at Xq26 and has been completely sequenced at the cD

34 nd contained a high proportion of unreported HPRT base substitutions, -1-bp deletions and multiple mu

35 f HPRT, with zero transposon integrations in HPRT by deep sequencing.

36 Hprt(CAG)146 mice are a useful model for studying polygl

37 Hprt(CAG)146 mice did not exhibit increased susceptibili

38 poxanthine phosphoribosyl transferase locus (Hprt(CAG)146), which does not normally contain polygluta

39 for the involvement of two metal ions in the HPRT-catalyzed reaction, and structural details further

40 oxanthine-guanine phosphoribosyltransferase (HPRT) cause the intractable neurodevelopmental Lesch-Nyh

41 d here show that the 5aCdr-induced change in HPRT chromatin structure precedes the appearance of thre

42 HPRT co-targeting thus provides a simple, efficient and

43 Reactivation of HPRT correlated with complete promoter demethylation.

44 r findings in SH-SY5Y cells demonstrate that HPRT deficiency is accompanied by dysregulation of some

45 in brain development, the mechanisms linking HPRT deficiency, purinergic pathways, and neural dysfunc

46 ed at characterizing purinergic signaling in HPRT deficiency, we used a lentivirus vector stably expr

47 In conclusion, our data show that HPRT-deficiency alters cAMP/PKA signaling pathway, which

48 that deficiency of APRT in combination with HPRT-deficiency in mice may lead to self-mutilation beha

49 sms may play a role in the neuropathology of HPRT-deficiency LND and may point to potential molecular

50 ful hypoxanthine phosphoribosyl-transferase (HPRT)-deficient mouse ES cell lines, two different metho

51 e establishment of E14.1TG3B1, a spontaneous HPRT-deficient cell line with an insertional mutation of

52 ression of phosphodiesterase 10A (PDE10A) in HPRT-deficient cell lines and that the PDE10 inhibitor p

53 SH-SY5Y cells over-expressing miR181a and in HPRT-deficient cells.

54 We show that stable Hprt-deficient clones can be recovered following introdu

55 osphoribosyltransferase ( HPRT) minigenes in HPRT-deficient embryonic stem cells.

56 hen delivered by infection into both a human HPRT-deficient fibroblast cell line and a mouse primary

57 n shRNA targeted to the HPRT gene to produce HPRT-deficient human CVB induced pluripotent stem cells

58 reased expression of the microRNA miR181a in HPRT-deficient human dopaminergic SH-SY5Y neuroblastoma

59 c basis for the phenotypic disparity between HPRT-deficient humans and mice.

60 expression of miR181a is not as apparent in HPRT-deficient LND fibroblasts, the relevance of the SH-

61 adenine phosphoribosyltransferase (APRT) in HPRT-deficient mice has produced the suggestion that def

62 In the present studies, we find that HPRT-deficient neuronal cell lines have reduced CREB (cA

63 trate that these genes are down-regulated in HPRT-deficient SH-SY5Y cells and that over-expression of

64 The absence of large hprt deletions in DHR strains indicates that DHR does no

65 lso revealed that V(D)J recombinase-mediated HPRT deletions increased with decreasing gestational age

66 on analyses showed a significant increase in HPRT deletions mediated by V(D)J recombinase in preterm

67 lopmental and gender-specific differences in HPRT deletions mediated by V(D)J recombinase provide ins

68 h the construction of two counter selectable hprt-/- DT40 derived cell lines.

69 The hypoxanthine phosphoribosyltransferase (hprt) encoding region of man is considered rich in Alu s

70 Cdr-treated clones that failed to reactivate HPRT exhibited sporadic promoter demethylation.

71 me of the 335 bp of human DNA containing the HPRT exon 1 and a truncated promoter.

72 nly 20% of the recovered mutations in either hprt exon 3 (1 of 5) or lacI (5 of 26).

73 ion was observed in a run of six guanines in HPRT exon 3, where a total of 23 (27%) of all PhIP-induc

74 Multiplex PCR amplification of hprt exons from 113 Chinese hamster ovary cell clones se

75 Furthermore, reconstitution of HPRT expression in mutant cells partly increased cAMP si

76 stal structure of an asymmetric dimer of the HPRT from the protozoan parasite Trypanosoma cruzi was d

77 ns (K68D, K68E, K68N, K68P, and K68R) in the HPRT from Trypanosoma cruzi, etiologic agent of Chagas'

78 nalysis, and X-ray crystallography using the HPRT from Trypanosoma cruzi.

79 The hypoxanthine phosphoribosyltransferase (HPRT) from Trypanosoma cruzi, etiologic agent of Chagas'

80 letions in parallel by selecting for loss of HPRT function with 6-thioguanine.

81 mans and great apes, while a disorder in the HPRT gene (leading to the Lesch-Nyhan syndrome) is uniqu

82 events that lead to the reactivation of the HPRT gene after 5aCdr treatment: (a) hemi-demethylation

83 A mutations at the human p53 gene, the human hprt gene and both the rodent transgenic lacI and lacZ l

84 ine for modifying the mouse genome using the HPRT gene as a selection marker and for transmission at

85 NA led to selective isolations of the entire HPRT gene as yeast artificial chromosomes (YACs) that ex

86 analysis of these homologs revealed that the HPRT gene family expanded as the result of ancient verte

87 All members of the vertebrate HPRT gene family share a common intron-exon structure; h

88 he target loci, and targeted knockout of the HPRT gene in human cells.

89 ates minichromosomes in HT1080 cells and the HPRT gene is expressed.

90 le triplexes in vivo, and showed the highest HPRT gene knockout activity.

91 emical assays in vitro, and in stability and HPRT gene knockout assays in vivo.

92 rom a 175 kb PAC containing the intact human HPRT gene locus.

93 ates microsatellite instability, an elevated HPRT gene mutation rate, and resistance to the cytotoxic

94 mutations occurring in vivo in the X-linked HPRT gene of kidney tubular epithelial cells.

95 MFs in the hprt gene of NO-producing cells were 16.6 and 31.3 x 10(

96 t fraction (MF) in the endogenous, X-linked, hprt gene of the cells are associated with NO exposure.

97 f mutations induced by UV in the single copy HPRT gene of the derivative strains was significantly hi

98 ally active in only two tissues, whereas the Hprt gene region is ubiquitously active.

99 and one TALE-PB chimera demonstrated notable HPRT gene targeting.

100 r stably expressing an shRNA targeted to the HPRT gene to produce HPRT-deficient human CVB induced pl

101 ation and chromosomal mapping of the chicken hprt gene together with the construction of two counter

102 oid DNA onto a 156-kb BAC carrying the human HPRT gene using Red homologous recombination in the EL35

103 A total of 676 bp of the HPRT gene was scanned using constant denaturing capillar

104 for the major dA mutational hot spot in the HPRT gene when Chinese hamster V79 cells are given low d

105 ning the BRCA1 promoter driving a selectable HPRT gene, long-term silencing of the promoter was obser

106 ical for maintaining repression of the human HPRT gene, we treated human/hamster hybrid cells contain

107 HPRT gene-targeting frequencies (HPRT mutant colonies) w

108 target and mutagenize a site in the hamster HPRT gene.

109 ltiple transcription initiation sites of the HPRT gene.

110 s similar to the mutation frequencies of the hprt gene.

111 rent spectrum of mutations in the endogenous hprt gene.

112 chosen pseudoexon from intron 1 of the human hprt gene.

113 maintaining transcriptional silencing of the HPRT gene.

114 containing a target sequence from the human HPRT gene.

115 reagent psoralen, directed at a site in the Hprt gene.

116 mutation of 203 bp in the third exon of the HPRT gene.

117 e-specific deletions of exons 2 and 3 in the hprt gene.

118 found to be randomly located throughout the hprt gene.

119 increased proportion of deletions within the hprt gene.

120 nous hypoxanthine phosphoribosyltransferase (Hprt) gene and an integrated viral thymidine kinase (tk)

121 oxanthine-guanine-phosphoribosyltransferase (HPRT) gene and compared with HPRT mutations observed in

122 tant hypoxanthine phosphoribosyltransferase (Hprt) gene and grown on feeder cells.

123 the hypoxanthine phosphoribosyl transferase (HPRT) gene in a TOP2-dependent manner; and (iv) acidic p

124 ous hypoxanthine phosphoribosyl transferase (Hprt) gene in mouse embryonic fibroblasts.

125 oxanthine-guanine phosphoribosyltransferase (HPRT) gene in the mouse and human genomes.

126 the hypoxanthine phosphoribosyltransferase (HPRT) gene located on human chromosome X.

127 the hypoxanthine phosphoribosyltransferase (Hprt) gene locus.

128 uman hypoxanthine phosphoribosyltransferase (HPRT) gene on the inactive X chromosome, acquisition of

129 the hypoxanthine phosphoribosyltransferase (hprt) gene to produce substrates for gene-targeting (pla

130 the hypoxanthine phosphoribosyl transferase (HPRT) gene, is elevated in human cells either stably tra

131 the hypoxanthine phosphoribosyltransferase (HPRT) gene.

132 0(6) bp in the human beta-globin, c-myc, and HPRT genes and in mitochondrial DNA, respectively.

133 he footprint patterns of the mouse and human HPRT genes demonstrated that the in vivo binding of regu

134 enetic diseases involving the LPL, ApoB, and HPRT genes.

135 amster P-glycoprotein class I homologue) and HPRT (human hypoxanthine phosphoribosyltransferase), was

136 se in mutation frequencies at the hemizygous HPRT (hypoxanthine phosphoribosyl transferase) locus, bu

137 Differentially expressed genes included HPRT, IMPDH, PAICS, and GART, all of which were expresse

138 uction in base substitution mutation rate at HPRT in HEC-1-B cells (hMSH6-defective but possessing wi

139 of shared hot spots comprise some 18% of the HPRT in vivo hot spot spectrum and strongly suggest that

140 ypoxanthine phosphoribosyl transferase gene; HPRT) in both MRL/+ and MRL/lpr mice of all ages.

141 opy APOA5 haplotypes at a targeted location (Hprt) in the mouse genome.

142 omatic mutational events in a reporter gene, HPRT, in cord blood T lymphocytes from newborns after tr

143 ulted in the encoding of a Thr in the mutant HPRT, instead of an Ile found in the wild-type enzyme, a

144 Most of the HPRT isolates were functional, demonstrating that TAR cl

145 Both CVB and HUES11 cells show >99% HPRT knockdown and demonstrate markedly decreased expres

146 ls, P2Y1 mRNA and protein down-regulation by HPRT knockdown is refractory to activation by the P2Y1 r

147 Moreover, HPRT-knockdown CVB cells also demonstrate marked reducti

148 The HPRT knockout frequencies with the most active TFOs were

149 is of three inherited mutations in the human HPRT leading to Lesch-Nyhan syndrome (D193N) or gout (S1

150 Mutagenesis by arsenite (at the TK and HPRT loci in TK6 cells) was observed only for ATF4-deple

151 four selected regions (within the c-myc and HPRT loci).

152 ed mutation at the TK (thymidine kinase) and HPRT loci, and gene expression profiling through microar

153 ing radiation-induced mutation at the TK and HPRT loci, impaired phosphorylation of H2AX (gamma-H2AX)

154 t a mutation rate of up to 1 in 1,200 at the Hprt locus (encoding hypoxanthine guanine phosphoribosyl

155 omosome, we inserted into the mouse X-linked Hprt locus a GFP transgene flanked with zero, one, or tw

156 cells also reduced the mutation rate at the HPRT locus and restored sensitivity to N-methyl-N'-nitro

157 Instead, the HPRT locus appeared to be protected from transposon inte

158 had a 65-fold elevated mutation rate at the HPRT locus as compared to 2008 cells, both of which are

159 n angiotensinogen gene upstream of the mouse HPRT locus by homologous recombination.

160 rian cancer cell line A2780, analyzed at the HPRT locus can be increased upon oxidative stress and de

161 of p53 on radiation-induced mutations at the hprt locus in murine B cell precursors that are normally

162 g joint processing at cryptic RSS within the HPRT locus in peripheral T cells from healthy children.

163 Recombination at the hprt locus is markedly increased following transfection

164 as a single copy into the partially deleted Hprt locus of embryonic stem cells.

165 also examined the mutagenic response at the HPRT locus of human cells that had greatly reduced level

166 e resulting cassette was introduced into the Hprt locus of mice by homologous recombination.

167 To that end, the Hprt locus of mice was targeted with a Robo4-LacZ transg

168 of vWF2 coupled to LacZ were targeted to the Hprt locus of mice, and the resulting animals were analy

169 When targeted to the Hprt locus of mice, mutations of the ELF-1 binding site

170 cLys) chromatin domain was inserted into the Hprt locus on the mouse X chromosome.

171 into two defined chromosomal locations, the Hprt locus on the X-chromosome and the apolipoprotein (a

172 ken together, these results suggest that (1) Hprt locus targeting is a valuable tool for studying vas

173 lower mutation frequency as measured at the HPRT locus than CHOpcDNA3 cells treated with the same do

174 cells, HHUA cells have mutation rates at the HPRT locus that are elevated 500-fold for base substitut

175 tent analysis of the cRSS sites in the human HPRT locus to gain insight into the mechanisms mediating

176 e is targeted near the constitutively active HPRT locus under a tetracycline (tet)-regulatable promot

177 s induced by PhIP exposure at the endogenous HPRT locus was determined in cell lines defective in MMR

178 induced mutant frequencies at the endogenous HPRT locus were reduced up to 75% in cells with reduced

179 rns of the transcriptionally active X-linked HPRT locus, 323 bp of the endogenous human HPRT promoter

180 ch resulted in a 55-kb deletion of the mouse HPRT locus, demonstrating the feasibility of replacement

181 e markers revealed deletions of <3 cM at the Hprt locus, whereas results consistent with deletions co

182 ith the hCYP11B2 gene, targeted to the mouse HPRT locus, with either Hap-II or Hap-I variant are used

183 significant increase in mutation rate at the Hprt locus.

184 ity, and DNA methylation patterns across the HPRT locus.

185 l of the CaMKII alpha promoter into the safe HPRT locus.

186 ion and frameshift mutator phenotypes at the HPRT locus.

187 stant mutants and (ii) gene targeting of the HPRT locus.

188 utinin-tagged Ub minigene expressed from the Hprt locus.

189 and complementation of the partially deleted Hprt locus.

190 n (approximately 36 kb) at the 5' end of the HPRT locus.

191 gion (UTR) of a single copy transgene at the Hprt locus.

192 nked hypoxanthine phosphoribosyltransferase (Hprt) locus and at the neural cell adhesion molecule (Nc

193 uman hypoxanthine phosphoribosyltransferase (HPRT) locus contained within a 115-kilobase BAC insert w

194 The hypoxanthine phosphoribosyltransferase (Hprt) locus has been shown to have minimal influence on

195 oxanthine guanine phosphoribosyltransferase (HPRT) locus in diploid human fibroblasts.

196 xanthine-guanine phosphoribosyl transferase (Hprt) locus in Msh2-deficient cells.

197 opy hypoxanthine phosphoribosyl transferase (HPRT) locus in normal human cells.

198 oxanthine-guanine phosphoribosyltransferase (HPRT) locus in peripheral T cells from 111 children duri

199 the hypoxanthine phosphoribosyltransferase (HPRT) locus in peripheral T lymphocytes as well as the p

200 the hypoxanthine phosphoribosyl transferase (hprt) locus, we find that mice expressing a dominant-neg

201 man hypoxanthine phosphoribosyl transferase (HPRT) locus.

202 xanthine guanine phosphoribosyl transferase (hprt) locus.

203 the hypoxanthine phosphoribosyltransferase (HPRT) locus.

204 dium for expression of a randomly integrated HPRT marker lying 5' to an Oct4/ lacZ transgene.

205 We observed a significant increase in mean HPRT Mfs during each phase of therapy (diagnosis, 1.4 x

206 We measured HPRT Mfs from 130 peripheral blood samples from 45 child

207 ty of this approach by showing that the hAGT(hprt) mice have normal tissue- and cell-specific express

208 ouse primary hepatocyte culture derived from Hprt-/- mice.

209 The difference in the stability of HPRT minigene expression at the same target locus can be

210 erted into an intron in the APRT gene or the HPRT minigene, long tracts of CTG/CAG repeats (more than

211 Also, using an I-SceI-sensitive HPRT minigene, we show that gene correction is more effi

212 of hypoxanthine phosphoribosyltransferase ( HPRT) minigenes in HPRT-deficient embryonic stem cells.

213 he 5' region occurs before the appearance of HPRT mRNA.

214 The cytokine production profile of most HPRT mutant CD4+ T cell clones from both healthy and HIV

215 HPRT gene-targeting frequencies (HPRT mutant colonies) were lower with MVM vectors, and t

216 polymerase eta (pol eta) enhanced UV-induced Hprt mutant frequencies.

217 ronmental exposure to cigarette smoke and 37 HPRT mutant isolates from 12 infants born to mothers exp

218 Analysis of 30 HPRT mutant isolates from 12 newborn infants born to mot

219 We find a high number of hprt mutants among X-irradiated p53 null cells, which re

220 of CD8+ clones was indistinguishable between HPRT mutants and wild type.

221 Eighty-six induced HPRT mutants from two different cell lines were isolated

222 Indeed, we observed an elevated frequency of HPRT mutants in the CD4+ T cells of most patients with <

223 Greater than 10% of hprt mutants proved to be a single 3 bp deletion located

224 Molecular analysis of hprt mutants resulting from both in vitro and an in vivo

225 Hprt mutation analysis demonstrates that Nfkb1(-/-) cell

226 effects of UV-irradiation, the incidence of Hprt mutation did not differ significantly between wild-

227 Amongst surviving clones, the Hprt mutation frequency was found to be dependent upon U

228 ly caused by hyperrecombination, we analyzed hprt mutation spectra.

229 The increased frequency of HPRT mutation was only modestly attributable to defects

230 yses of two signatures for mutant clonality, HPRT mutation, and T-cell receptor beta CDR3 region uniq

231 D1 cells exhibit a 12-fold-increased rate of hprt mutation, as well as 4- to 10-fold increased rates

232 that hypoxanthine phosphoribosyltransferase (HPRT) mutation frequencies were approximately 5-fold hig

233 smoke showed a significant difference in the HPRT mutational spectrum in those exposed in utero to ci

234 atory environment increased the frequency of HPRT mutations and down-regulated WEE1 (WEE1 homolog-S.

235 e induction of sister chromatid exchange and HPRT mutations by very low fluences of alpha particles (

236 d DNA sequencing revealed that NO-associated hprt mutations did not differ significantly from those a

237 s spectrum of somatic mutation differed from HPRT mutations identified in human peripheral blood T ly

238 heral blood T lymphocytes and from germ-line HPRT mutations identified in Lesch-Nyhan syndrome or hyp

239 ulfonate resulted in three- to fourfold more hprt mutations in splenic T lymphocytes from APNG ko mic

240 The types and proportion of hprt mutations induced under these conditions were strik

241 syltransferase (HPRT) gene and compared with HPRT mutations observed in somatic T lymphocytes from no

242 ority were compound, with an average of four hprt mutations per mutant.

243 Lastly, one third of hprt mutations proved to be transitions or transversions

244 tionships among the frequency and spectra of HPRT mutations with disease, duration of illness, durati

245 51d HR mutant has a greatly elevated rate of hprt mutations, >85% of which are deletions.

246 se in spontaneous chromosome aberrations and HPRT mutations, indicating a role in the maintenance of

247 to 2.5-fold) but normal levels of UV-induced hprt mutations.

248 SCD and 30-month HU exposure had equivalent hprt(-) mutations but significantly more VDJ mutations (

249 eous hypoxanthine phosphoribosyltransferase (HPRT) mutations that can be detected based on the resist

250 res hypoxanthine phosphoribosyl transferase (hprt) mutations, while the VDJ assay identifies "illegit

251 However, mice with an IMPDH II(+/-), HPRT(-/o) genotype demonstrate significantly decreased l

252 ned according to the N- and C-termini of the HPRT of Escherichia coli, were used in polymerase chain

253 /discover potent selective inhibitors of the HPRT of T. cruzi.

254 e prevalence of lysine at position 68 in the HPRT of the majority of eukaryotes is consistent with th

255 ibitor, trichostatin A, failed to reactivate HPRT on the inactive X chromosome, even when the promote

256 mutations at the reporter gene loci Aprt and Hprt, on the other hand, is significantly increased in b

257 ing techniques and bred to mice deficient in HPRT or heterozygous for IMPDH type II.

258 in large cell populations, by selecting for HPRT(+) or APRT(+) clones.

259 enerate sufficient gene product to yield the HPRT+ phenotype, and that recombination between the conc

260 Introns of four X-linked genes (Hprt, Plp, Glra2, and Amg) were sequenced to provide an

261 d HPRT locus, 323 bp of the endogenous human HPRT promoter (from position -222 to +102 relative to th

262 ent minigene, under the control of the mouse HPRT promoter and embedded in its natural CpG-rich islan

263 uggest a model in which the silencing of the HPRT promoter during X chromosome inactivation involves

264 e high resolution methylation pattern of the HPRT promoter in single cell-derived lines.

265 In contrast, analysis of the inactive HPRT promoter reveals no hypersensitivity to either DNas

266 romatin structure of the active and inactive HPRT promoters.

267 xport (NES) signals to versions of the mouse Hprt protein containing expanded polyglutamine (HprtQ150

268 Mutant mice express a form of the HPRT protein that contains a long polyglutamine repeat.

269 oxanthine guanine phosphoribosyltransferase (HPRT) purine biosynthesis gene and characterized by aber

270 gressive oligoclonal T-cell expansion (Vbeta/HPRT ratio) and gradually enhanced anti-cytomegalovirus

271 d of 5aCdr did not increase the frequency of HPRT reactivation.

272 order of markers within this segment of the Hprt region as: Agtr2-Pem-Ant2-DXMit50-Lamp2-DXMit49.

273 show that the order of gene loci within this Hprt region is conserved in mice and human.

274 insertions of Alu sequences are seen at the hprt region.

275 he mouse X chromosome, placing it within the Hprt region.

276 ere in the genome, before insertion into the hprt region.

277 poly(A) tract of an existing sequence at the hprt region; while another result from an Alu/Alu cross-

278 results indicate that the housekeeping gene HPRT regulates purinergic signaling in pluripotent human

279 the hypoxanthine phosphoribosyltransferase (HPRT) reporter gene in cord blood T lymphocytes from pre

280 oxanthine-guanine phosphoribosyltransferase (HPRT) reporter gene in independently isolated mutant T c

281 oxanthine-guanine phosphoribosyltransferase (HPRT) reporter gene mutational spectra analysis for 60 T

282 oxanthine-guanine phosphoribosyltransferase (HPRT)-reporter gene in children treated for acute lympho

283 transcription complex, and (e) synthesis of HPRT RNA.

284 Hypoxanthine phosphoribosyltransferase (HPRT) salvages 6-oxopurine bases in the nucleotide metab

285 f 3' hypoxanthine phosphoribosyltransferase (HPRT) sequence at one end and an 189-bp Alu repeat at th

286 yrimidone photoproducts from both strands of hprt suggests that global-genomic nucleotide excision re

287 Mf determinations were made by using the HPRT T cell cloning assay on cord blood samples from 52

288 HPRT targeted cells are selected by resistance to 6-thio

289 In Hprt-targeted mice, mutation of the ETS consensus motif

290 taining the neo(R) gene flanked by exon 3 of HPRT: The enzymes BamHI, BglII and EcoRI increased the i

291 hypoxanthine phosphoribosyltransferase gene (HPRT), this difference in chromatin structure is evident

292 ve contributions of IMPDH types I and II and HPRT to normal biological function, a mouse deficient in

293 oxanthine-guanine phosphoribosyltransferase (HPRT) to supply the cell with guanine nucleotides.

294 e targeted cells, which showed no detectable HPRT transcription, were then assayed for effects on DNa

295 nate amino acid at position 192 in the human HPRT was investigated using site-directed mutagenesis.

296 ding hypoxanthine phosphoribosyltransferase (HPRT), we monitor the relative utilization of three DSBR

297 vation mosaicism for the purine salvage gene Hprt, we found that reduced ENS precursor proliferation

298 repeat DNA locus and a protein-coding gene (hprt) were significantly elevated in both the germline (

299 ied hypoxanthine phosphoribosyl-transferase (HPRT) with enhanced substrate specificity for guanine.

300 cient isolation of Cas9-mediated knockout of HPRT, with zero transposon integrations in HPRT by deep