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1 oxanthine-guanine phosphoribosyltransferase (HPRT).
2 hypoxanthine phosphoribosyltransferase gene (Hprt).
3 xanthine guanine phosphoribosyl transferase (HPRT).
4  and hypoxanthine phosphoribosyltransferase (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         We recommend using Rplp0, Nono, Tbp, Hprt and Eef2 instead of common reference genes.
17               Finally, using both endogenous HPRT and exogenous reporters, we validate novel cell cyc
18 e demonstrate that the GTP synthesis enzymes HprT and Gmk bind with a high affinity, leading to an in
19                                              Hprt and Plp lie in a region of the X chromosome that ex
20 with two guide RNAs that target respectively HPRT and the gene of interest.
21 y a competitive RIA) and mutagenicity at the HPRT and TK loci (as assessed by cell-cloning assays) we
22 ation, mutation assays were performed on the HPRT and TK loci, and gene expression profiles were gene
23 ereas NO(*)-induced mutant fractions in both HPRT and TK1 genes were significantly lower in TK6 cells
24 xanthine quanine phosphoribosyl transferase (hprt) and the thymidine kinase loci.
25 the hypoxanthine phosphoribosyl transferase (HPRT) and Type I collagen (COL1A1) loci in normal human
26 cant decrease in frameshift mutation rate at HPRT, and (iii) the in vitro repair of looped substrates
27 xanthine guanine phosphoribosyl transferase (HPRT) as a test locus, it was determined that while no t
28 cI mutation assay is less sensitive than the hprt assay for detecting increases in Mf induced by ENU
29                                          The HPRT assay measures hypoxanthine phosphoribosyl transfer
30  monitoring DSB mis-repair using a sensitive HPRT assay, we found that depletion of HR proteins, incl
31             The gene maps 65 kb telomeric to HPRT at Xq26 and has been completely sequenced at the cD
32 nd contained a high proportion of unreported HPRT base substitutions, -1-bp deletions and multiple mu
33 f HPRT, with zero transposon integrations in HPRT by deep sequencing.
34  (p)ppGpp inhibits the purine salvage enzyme HPRT by sharing a conserved motif with its substrate PRP
35                                              Hprt(CAG)146 mice are a useful model for studying polygl
36                                              Hprt(CAG)146 mice did not exhibit increased susceptibili
37 poxanthine phosphoribosyl transferase locus (Hprt(CAG)146), which does not normally contain polygluta
38 for the involvement of two metal ions in the HPRT-catalyzed reaction, and structural details further
39 oxanthine-guanine phosphoribosyltransferase (HPRT) cause the intractable neurodevelopmental Lesch-Nyh
40 d here show that the 5aCdr-induced change in HPRT chromatin structure precedes the appearance of thre
41                                              HPRT co-targeting thus provides a simple, efficient and
42                              Reactivation of HPRT correlated with complete promoter demethylation.
43 r findings in SH-SY5Y cells demonstrate that HPRT deficiency is accompanied by dysregulation of some
44 in brain development, the mechanisms linking HPRT deficiency, purinergic pathways, and neural dysfunc
45 ed at characterizing purinergic signaling in HPRT deficiency, we used a lentivirus vector stably expr
46            In conclusion, our data show that HPRT-deficiency alters cAMP/PKA signaling pathway, which
47  that deficiency of APRT in combination with HPRT-deficiency in mice may lead to self-mutilation beha
48 sms may play a role in the neuropathology of HPRT-deficiency LND and may point to potential molecular
49 ful hypoxanthine phosphoribosyl-transferase (HPRT)-deficient mouse ES cell lines, two different metho
50 e establishment of E14.1TG3B1, a spontaneous HPRT-deficient cell line with an insertional mutation of
51 ression of phosphodiesterase 10A (PDE10A) in HPRT-deficient cell lines and that the PDE10 inhibitor p
52 SH-SY5Y cells over-expressing miR181a and in HPRT-deficient cells.
53                          We show that stable Hprt-deficient clones can be recovered following introdu
54 osphoribosyltransferase ( HPRT) minigenes in HPRT-deficient embryonic stem cells.
55 hen delivered by infection into both a human HPRT-deficient fibroblast cell line and a mouse primary
56 n shRNA targeted to the HPRT gene to produce HPRT-deficient human CVB induced pluripotent stem cells
57 reased expression of the microRNA miR181a in HPRT-deficient human dopaminergic SH-SY5Y neuroblastoma
58 c basis for the phenotypic disparity between HPRT-deficient humans and mice.
59  expression of miR181a is not as apparent in HPRT-deficient LND fibroblasts, the relevance of the SH-
60  adenine phosphoribosyltransferase (APRT) in HPRT-deficient mice has produced the suggestion that def
61         In the present studies, we find that HPRT-deficient neuronal cell lines have reduced CREB (cA
62 trate that these genes are down-regulated in HPRT-deficient SH-SY5Y cells and that over-expression of
63                         The absence of large hprt deletions in DHR strains indicates that DHR does no
64 lso revealed that V(D)J recombinase-mediated HPRT deletions increased with decreasing gestational age
65 on analyses showed a significant increase in HPRT deletions mediated by V(D)J recombinase in preterm
66 lopmental and gender-specific differences in HPRT deletions mediated by V(D)J recombinase provide ins
67 h the construction of two counter selectable hprt-/- DT40 derived cell lines.
68  The hypoxanthine phosphoribosyltransferase (hprt) encoding region of man is considered rich in Alu s
69 Cdr-treated clones that failed to reactivate HPRT exhibited sporadic promoter demethylation.
70                           (p)ppGpp-sensitive HPRT exists as a PRPP-bound dimer or an apo- and (p)ppGp
71 me of the 335 bp of human DNA containing the HPRT exon 1 and a truncated promoter.
72 ion was observed in a run of six guanines in HPRT exon 3, where a total of 23 (27%) of all PhIP-induc
73               Multiplex PCR amplification of hprt exons from 113 Chinese hamster ovary cell clones se
74               Furthermore, reconstitution of HPRT expression in mutant cells partly increased cAMP si
75 stal structure of an asymmetric dimer of the HPRT from the protozoan parasite Trypanosoma cruzi was d
76 ns (K68D, K68E, K68N, K68P, and K68R) in the HPRT from Trypanosoma cruzi, etiologic agent of Chagas'
77 nalysis, and X-ray crystallography using the HPRT from Trypanosoma cruzi.
78  The hypoxanthine phosphoribosyltransferase (HPRT) from Trypanosoma cruzi, etiologic agent of Chagas'
79 letions in parallel by selecting for loss of HPRT function with 6-thioguanine.
80 mans and great apes, while a disorder in the HPRT gene (leading to the Lesch-Nyhan syndrome) is uniqu
81  events that lead to the reactivation of the HPRT gene after 5aCdr treatment: (a) hemi-demethylation
82 A mutations at the human p53 gene, the human hprt gene and both the rodent transgenic lacI and lacZ l
83 ine for modifying the mouse genome using the HPRT gene as a selection marker and for transmission at
84 NA led to selective isolations of the entire HPRT gene as yeast artificial chromosomes (YACs) that ex
85 analysis of these homologs revealed that the HPRT gene family expanded as the result of ancient verte
86                All members of the vertebrate HPRT gene family share a common intron-exon structure; h
87 he target loci, and targeted knockout of the HPRT gene in human cells.
88 ates minichromosomes in HT1080 cells and the HPRT gene is expressed.
89 le triplexes in vivo, and showed the highest HPRT gene knockout activity.
90 emical assays in vitro, and in stability and HPRT gene knockout assays in vivo.
91 rom a 175 kb PAC containing the intact human HPRT gene locus.
92 ates microsatellite instability, an elevated HPRT gene mutation rate, and resistance to the cytotoxic
93  mutations occurring in vivo in the X-linked HPRT gene of kidney tubular epithelial cells.
94                                   MFs in the hprt gene of NO-producing cells were 16.6 and 31.3 x 10(
95 t fraction (MF) in the endogenous, X-linked, hprt gene of the cells are associated with NO exposure.
96 f mutations induced by UV in the single copy HPRT gene of the derivative strains was significantly hi
97 ally active in only two tissues, whereas the Hprt gene region is ubiquitously active.
98 and one TALE-PB chimera demonstrated notable HPRT gene targeting.
99 r stably expressing an shRNA targeted to the HPRT gene to produce HPRT-deficient human CVB induced pl
100 ation and chromosomal mapping of the chicken hprt gene together with the construction of two counter
101 oid DNA onto a 156-kb BAC carrying the human HPRT gene using Red homologous recombination in the EL35
102                     A total of 676 bp of the HPRT gene was scanned using constant denaturing capillar
103  for the major dA mutational hot spot in the HPRT gene when Chinese hamster V79 cells are given low d
104 ning the BRCA1 promoter driving a selectable HPRT gene, long-term silencing of the promoter was obser
105 ical for maintaining repression of the human HPRT gene, we treated human/hamster hybrid cells contain
106                                              HPRT gene-targeting frequencies (HPRT mutant colonies) w
107  target and mutagenize a site in the hamster HPRT gene.
108 ltiple transcription initiation sites of the HPRT gene.
109 s similar to the mutation frequencies of the hprt gene.
110 rent spectrum of mutations in the endogenous hprt gene.
111 chosen pseudoexon from intron 1 of the human hprt gene.
112 maintaining transcriptional silencing of the HPRT gene.
113  containing a target sequence from the human HPRT gene.
114  reagent psoralen, directed at a site in the Hprt gene.
115  mutation of 203 bp in the third exon of the HPRT gene.
116 e-specific deletions of exons 2 and 3 in the hprt gene.
117  found to be randomly located throughout the hprt gene.
118 increased proportion of deletions within the hprt gene.
119 nous hypoxanthine phosphoribosyltransferase (Hprt) gene and an integrated viral thymidine kinase (tk)
120 oxanthine-guanine-phosphoribosyltransferase (HPRT) gene and compared with HPRT mutations observed in
121 tant hypoxanthine phosphoribosyltransferase (Hprt) gene and grown on feeder cells.
122 the hypoxanthine phosphoribosyl transferase (HPRT) gene in a TOP2-dependent manner; and (iv) acidic p
123 ous hypoxanthine phosphoribosyl transferase (Hprt) gene in mouse embryonic fibroblasts.
124 oxanthine-guanine phosphoribosyltransferase (HPRT) gene in the mouse and human genomes.
125  the hypoxanthine phosphoribosyltransferase (HPRT) gene located on human chromosome X.
126  the hypoxanthine phosphoribosyltransferase (Hprt) gene locus.
127 uman hypoxanthine phosphoribosyltransferase (HPRT) gene on the inactive X chromosome, acquisition of
128  the hypoxanthine phosphoribosyltransferase (hprt) gene to produce substrates for gene-targeting (pla
129 the hypoxanthine phosphoribosyl transferase (HPRT) gene, is elevated in human cells either stably tra
130  the hypoxanthine phosphoribosyltransferase (HPRT) gene.
131 0(6) bp in the human beta-globin, c-myc, and HPRT genes and in mitochondrial DNA, respectively.
132 enetic diseases involving the LPL, ApoB, and HPRT genes.
133 amster P-glycoprotein class I homologue) and HPRT (human hypoxanthine phosphoribosyltransferase), was
134 se in mutation frequencies at the hemizygous HPRT (hypoxanthine phosphoribosyl transferase) locus, bu
135      Differentially expressed genes included HPRT, IMPDH, PAICS, and GART, all of which were expresse
136 uction in base substitution mutation rate at HPRT in HEC-1-B cells (hMSH6-defective but possessing wi
137 XPRT oligomeric interaction is distinct from HPRT in that XPRT forms a symmetric dimer with two (p)pp
138 of shared hot spots comprise some 18% of the HPRT in vivo hot spot spectrum and strongly suggest that
139 ypoxanthine phosphoribosyl transferase gene; HPRT) in both MRL/+ and MRL/lpr mice of all ages.
140 opy APOA5 haplotypes at a targeted location (Hprt) in the mouse genome.
141 omatic mutational events in a reporter gene, HPRT, in cord blood T lymphocytes from newborns after tr
142 ulted in the encoding of a Thr in the mutant HPRT, instead of an Ile found in the wild-type enzyme, a
143                                  Most of the HPRT isolates were functional, demonstrating that TAR cl
144          Both CVB and HUES11 cells show >99% HPRT knockdown and demonstrate markedly decreased expres
145 ls, P2Y1 mRNA and protein down-regulation by HPRT knockdown is refractory to activation by the P2Y1 r
146                                    Moreover, HPRT-knockdown CVB cells also demonstrate marked reducti
147                                          The HPRT knockout frequencies with the most active TFOs were
148 is of three inherited mutations in the human HPRT leading to Lesch-Nyhan syndrome (D193N) or gout (S1
149       Mutagenesis by arsenite (at the TK and HPRT loci in TK6 cells) was observed only for ATF4-deple
150  four selected regions (within the c-myc and HPRT loci).
151 ed mutation at the TK (thymidine kinase) and HPRT loci, and gene expression profiling through microar
152 ing radiation-induced mutation at the TK and HPRT loci, impaired phosphorylation of H2AX (gamma-H2AX)
153 t a mutation rate of up to 1 in 1,200 at the Hprt locus (encoding hypoxanthine guanine phosphoribosyl
154 omosome, we inserted into the mouse X-linked Hprt locus a GFP transgene flanked with zero, one, or tw
155  cells also reduced the mutation rate at the HPRT locus and restored sensitivity to N-methyl-N'-nitro
156                                 Instead, the HPRT locus appeared to be protected from transposon inte
157  had a 65-fold elevated mutation rate at the HPRT locus as compared to 2008 cells, both of which are
158 n angiotensinogen gene upstream of the mouse HPRT locus by homologous recombination.
159 rian cancer cell line A2780, analyzed at the HPRT locus can be increased upon oxidative stress and de
160 of p53 on radiation-induced mutations at the hprt locus in murine B cell precursors that are normally
161 g joint processing at cryptic RSS within the HPRT locus in peripheral T cells from healthy children.
162                         Recombination at the hprt locus is markedly increased following transfection
163  as a single copy into the partially deleted Hprt locus of embryonic stem cells.
164  also examined the mutagenic response at the HPRT locus of human cells that had greatly reduced level
165 e resulting cassette was introduced into the Hprt locus of mice by homologous recombination.
166                             To that end, the Hprt locus of mice was targeted with a Robo4-LacZ transg
167 of vWF2 coupled to LacZ were targeted to the Hprt locus of mice, and the resulting animals were analy
168                         When targeted to the Hprt locus of mice, mutations of the ELF-1 binding site
169 cLys) chromatin domain was inserted into the Hprt locus on the mouse X chromosome.
170  into two defined chromosomal locations, the Hprt locus on the X-chromosome and the apolipoprotein (a
171 ken together, these results suggest that (1) Hprt locus targeting is a valuable tool for studying vas
172  lower mutation frequency as measured at the HPRT locus than CHOpcDNA3 cells treated with the same do
173 cells, HHUA cells have mutation rates at the HPRT locus that are elevated 500-fold for base substitut
174 tent analysis of the cRSS sites in the human HPRT locus to gain insight into the mechanisms mediating
175 e is targeted near the constitutively active HPRT locus under a tetracycline (tet)-regulatable promot
176 s induced by PhIP exposure at the endogenous HPRT locus was determined in cell lines defective in MMR
177 induced mutant frequencies at the endogenous HPRT locus were reduced up to 75% in cells with reduced
178 rns of the transcriptionally active X-linked HPRT locus, 323 bp of the endogenous human HPRT promoter
179 ch resulted in a 55-kb deletion of the mouse HPRT locus, demonstrating the feasibility of replacement
180 e markers revealed deletions of <3 cM at the Hprt locus, whereas results consistent with deletions co
181 ith the hCYP11B2 gene, targeted to the mouse HPRT locus, with either Hap-II or Hap-I variant are used
182 gion (UTR) of a single copy transgene at the Hprt locus.
183 significant increase in mutation rate at the Hprt locus.
184 ity, and DNA methylation patterns across the HPRT locus.
185 ion and frameshift mutator phenotypes at the HPRT locus.
186 l of the CaMKII alpha promoter into the safe 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 nked hypoxanthine phosphoribosyltransferase (Hprt) locus and at the neural cell adhesion molecule (Nc
192 uman hypoxanthine phosphoribosyltransferase (HPRT) locus contained within a 115-kilobase BAC insert w
193  The hypoxanthine phosphoribosyltransferase (Hprt) locus has been shown to have minimal influence on
194 oxanthine guanine phosphoribosyltransferase (HPRT) locus in diploid human fibroblasts.
195 xanthine-guanine phosphoribosyl transferase (Hprt) locus in Msh2-deficient cells.
196 opy hypoxanthine phosphoribosyl transferase (HPRT) locus in normal human cells.
197 oxanthine-guanine phosphoribosyltransferase (HPRT) locus in peripheral T cells from 111 children duri
198  the hypoxanthine phosphoribosyltransferase (HPRT) locus in peripheral T lymphocytes as well as the p
199 the hypoxanthine phosphoribosyl transferase (hprt) locus, we find that mice expressing a dominant-neg
200 man hypoxanthine phosphoribosyl transferase (HPRT) locus.
201 xanthine guanine phosphoribosyl transferase (hprt) locus.
202  the hypoxanthine phosphoribosyltransferase (HPRT) locus.
203 dium for expression of a randomly integrated HPRT marker lying 5' to an Oct4/ lacZ transgene.
204   We observed a significant increase in mean HPRT Mfs during each phase of therapy (diagnosis, 1.4 x
205                                  We measured HPRT Mfs from 130 peripheral blood samples from 45 child
206 ty of this approach by showing that the hAGT(hprt) mice have normal tissue- and cell-specific express
207 ouse primary hepatocyte culture derived from Hprt-/- mice.
208           The difference in the stability of HPRT minigene expression at the same target locus can be
209 erted into an intron in the APRT gene or the HPRT minigene, long tracts of CTG/CAG repeats (more than
210              Also, using an I-SceI-sensitive HPRT minigene, we show that gene correction is more effi
211  of hypoxanthine phosphoribosyltransferase ( HPRT) minigenes in HPRT-deficient embryonic stem cells.
212 he 5' region occurs before the appearance of HPRT mRNA.
213      The cytokine production profile of most HPRT mutant CD4+ T cell clones from both healthy and HIV
214             HPRT gene-targeting frequencies (HPRT mutant colonies) were lower with MVM vectors, and t
215 polymerase eta (pol eta) enhanced UV-induced Hprt mutant frequencies.
216 ronmental exposure to cigarette smoke and 37 HPRT mutant isolates from 12 infants born to mothers exp
217                               Analysis of 30 HPRT mutant isolates from 12 newborn infants born to mot
218                     We find a high number of hprt mutants among X-irradiated p53 null cells, which re
219 of CD8+ clones was indistinguishable between HPRT mutants and wild type.
220                           Eighty-six induced HPRT mutants from two different cell lines were isolated
221 Indeed, we observed an elevated frequency of HPRT mutants in the CD4+ T cells of most patients with <
222                                              Hprt mutation analysis demonstrates that Nfkb1(-/-) cell
223  effects of UV-irradiation, the incidence of Hprt mutation did not differ significantly between wild-
224                Amongst surviving clones, the Hprt mutation frequency was found to be dependent upon U
225 ly caused by hyperrecombination, we analyzed hprt mutation spectra.
226                   The increased frequency of HPRT mutation was only modestly attributable to defects
227 yses of two signatures for mutant clonality, HPRT mutation, and T-cell receptor beta CDR3 region uniq
228 D1 cells exhibit a 12-fold-increased rate of hprt mutation, as well as 4- to 10-fold increased rates
229 that hypoxanthine phosphoribosyltransferase (HPRT) mutation frequencies were approximately 5-fold hig
230 smoke showed a significant difference in the HPRT mutational spectrum in those exposed in utero to ci
231 atory environment increased the frequency of HPRT mutations and down-regulated WEE1 (WEE1 homolog-S.
232 e induction of sister chromatid exchange and HPRT mutations by very low fluences of alpha particles (
233 d DNA sequencing revealed that NO-associated hprt mutations did not differ significantly from those a
234 s spectrum of somatic mutation differed from HPRT mutations identified in human peripheral blood T ly
235 heral blood T lymphocytes and from germ-line HPRT mutations identified in Lesch-Nyhan syndrome or hyp
236 ulfonate resulted in three- to fourfold more hprt mutations in splenic T lymphocytes from APNG ko mic
237                  The types and proportion of hprt mutations induced under these conditions were strik
238 syltransferase (HPRT) gene and compared with HPRT mutations observed in somatic T lymphocytes from no
239 ority were compound, with an average of four hprt mutations per mutant.
240 tionships among the frequency and spectra of HPRT mutations with disease, duration of illness, durati
241 51d HR mutant has a greatly elevated rate of hprt mutations, >85% of which are deletions.
242 se in spontaneous chromosome aberrations and HPRT mutations, indicating a role in the maintenance of
243 to 2.5-fold) but normal levels of UV-induced hprt mutations.
244  SCD and 30-month HU exposure had equivalent hprt(-) mutations but significantly more VDJ mutations (
245 eous hypoxanthine phosphoribosyltransferase (HPRT) mutations that can be detected based on the resist
246 res hypoxanthine phosphoribosyl transferase (hprt) mutations, while the VDJ assay identifies "illegit
247         However, mice with an IMPDH II(+/-), HPRT(-/o) genotype demonstrate significantly decreased l
248 ned according to the N- and C-termini of the HPRT of Escherichia coli, were used in polymerase chain
249 /discover potent selective inhibitors of the HPRT of T. cruzi.
250 e prevalence of lysine at position 68 in the HPRT of the majority of eukaryotes is consistent with th
251  varies across organisms and correlates with HPRT oligomeric forms.
252 ibitor, trichostatin A, failed to reactivate HPRT on the inactive X chromosome, even when the promote
253 mutations at the reporter gene loci Aprt and Hprt, on the other hand, is significantly increased in b
254 ing techniques and bred to mice deficient in HPRT or heterozygous for IMPDH type II.
255  in large cell populations, by selecting for HPRT(+) or APRT(+) clones.
256 enerate sufficient gene product to yield the HPRT+ phenotype, and that recombination between the conc
257              Introns of four X-linked genes (Hprt, Plp, Glra2, and Amg) were sequenced to provide an
258 d HPRT locus, 323 bp of the endogenous human HPRT promoter (from position -222 to +102 relative to th
259 ent minigene, under the control of the mouse HPRT promoter and embedded in its natural CpG-rich islan
260 uggest a model in which the silencing of the HPRT promoter during X chromosome inactivation involves
261 e high resolution methylation pattern of the HPRT promoter in single cell-derived lines.
262        In contrast, analysis of the inactive HPRT promoter reveals no hypersensitivity to either DNas
263 romatin structure of the active and inactive HPRT promoters.
264 xport (NES) signals to versions of the mouse Hprt protein containing expanded polyglutamine (HprtQ150
265            Mutant mice express a form of the HPRT protein that contains a long polyglutamine repeat.
266 oxanthine guanine phosphoribosyltransferase (HPRT) purine biosynthesis gene and characterized by aber
267 gressive oligoclonal T-cell expansion (Vbeta/HPRT ratio) and gradually enhanced anti-cytomegalovirus
268 d of 5aCdr did not increase the frequency of HPRT reactivation.
269  order of markers within this segment of the Hprt region as: Agtr2-Pem-Ant2-DXMit50-Lamp2-DXMit49.
270 show that the order of gene loci within this Hprt region is conserved in mice and human.
271  insertions of Alu sequences are seen at the hprt region.
272 he mouse X chromosome, placing it within the Hprt region.
273 ere in the genome, before insertion into the hprt region.
274 poly(A) tract of an existing sequence at the hprt region; while another result from an Alu/Alu cross-
275  results indicate that the housekeeping gene HPRT regulates purinergic signaling in pluripotent human
276                                Intriguingly, HPRT regulation by (p)ppGpp varies across organisms and
277  the hypoxanthine phosphoribosyltransferase (HPRT) reporter gene in cord blood T lymphocytes from pre
278 oxanthine-guanine phosphoribosyltransferase (HPRT) reporter gene in independently isolated mutant T c
279 oxanthine-guanine phosphoribosyltransferase (HPRT) reporter gene mutational spectra analysis for 60 T
280 oxanthine-guanine phosphoribosyltransferase (HPRT)-reporter gene in children treated for acute lympho
281  transcription complex, and (e) synthesis of HPRT RNA.
282      Hypoxanthine phosphoribosyltransferase (HPRT) salvages 6-oxopurine bases in the nucleotide metab
283 f 3' hypoxanthine phosphoribosyltransferase (HPRT) sequence at one end and an 189-bp Alu repeat at th
284 use line by crossing insulin1(Dre) mice with HPRT-SMAD7/RosaGFP mice.
285 r (p)ppGpp target, the purine salvage enzyme HPRT, suggesting evolutionary conservation in different
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

 
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