ライフサイエンスコーパス: p53 gene

1 d p53 in cell lines that contain a wild-type p53 gene.

2 f functional importance to repression of the p53 gene.

3 ch led us to test if it was regulated by the p53 gene.

4 tion mutation p53(R172H) and of deleting the p53 gene.

5 although mutations were not detected in the p53 gene.

6 kingly increased by cotransfection of the wt p53 gene.

7 ) oligonucleotide representing exon 7 of the p53 gene.

8 splice variants have been described for the p53 gene.

9 evels of p53 protein but no mutations in the p53 gene.

10 , docetaxel treatment, and overexpression of p53 gene.

11 nd pyrimidine-containing sequences along the p53 gene.

12 er of mutations within certain codons of the p53 gene.

13 t specific codons along exons 6 and 8 of the p53 gene.

14 ) versions of a 32 bp exon 7 fragment of the p53 gene.

15 ts of the synthetic templates related to the p53 gene.

16 ors acquire mutations in both alleles of the p53 gene.

17 was related to mutation or expression of the p53 gene.

18 euroblastoma has a low mutation rate for the p53 gene.

19 ferential formation of PAH adducts along the p53 gene.

20 racteristic for CpG dinucleotides within the p53 gene.

21 Xpc (Xpc(-/-)) and hemizygous mutant for the p53 gene.

22 frequently associated with mutations in the p53 gene.

23 tion, although these cells possess a mutated p53 gene.

24 nt mutations, deletions or insertions in the p53 gene.

25 ncer cells MIA PaCa-2 that possess a mutated p53 gene.

26 yclic aromatic hydrocarbon adducts along the p53 gene.

27 ed in wt mice or mice with a mutation in the p53 gene.

28 d NCI-H1703, have mutations and LOH in their p53 gene.

29 plasmid containing full-length cDNA from the p53 gene.

30 ted with transcriptional inactivation of the p53 gene.

31 , particularly those that harbor inactivated p53 gene.

32 is a relatively low rate of mutations in the p53 gene.

33 one null allele and one mutant allele of the p53 gene.

34 it is rescued by UB-specific deletion of the p53 gene.

35 tional coding polymorphism (codon 72) in the p53 gene.

36 e panel of point mutants in exons 5-9 of the p53 gene.

37 678-bp tract from exons 5 to 9 of the human P53 gene.

38 on for mapping of DNA adducts in the cII and p53 genes.

39 sformed cells with nonfunctioning p21WAF1 or p53 genes.

40 or-mediated cotransfer of wild-type FHIT and p53 genes.

41 dominant-negative or gain-of-function mutant p53 genes.

42 quently in human cancer involves the ARF and p53 genes.

43 use embryo fibroblasts wild-type or null for p53 genes.

44 nes that retain wild-type ARF and functional p53 genes.

45 ived from a frequently mutated region of the p53 gene (5'-CCCGGCACCC GC[(15)N(3),(13)C(1)-G]TCCGCG-3'

46 at the third base of codon 249 (AGG*) of the p53 gene, a mutational hot spot in human cancers, partic

47 is preferentially formed at codon 249 of the p53 gene, a mutational hotspot in human cancers.

48 Deletion of p53 gene accelerated tumor onset and induced transformat

49 Namely, cells harboring a wild-type p53 gene accumulate p53 protein that is conformationally

50 Recently, we demonstrated that p53 genes act to restrict retrotransposons in germline t

51 nce of methyl cytosines (MeC) on kinetics of p53 gene adduction by model metabolite benzo[a]pyrene-7,

52 P53: gene alterations correlate highly with advanced ova

53 strated upregulation of the tumor suppressor p53 gene and activation of the ataxia telangiectasia mut

54 ts containing exons 5, 7, and 8 of the human p53 gene and also determined the effect of C5 cytosine m

55 spots of G:C to T:A transversions along the p53 gene and also their increased abundance in lung tiss

56 tilaginous fishes, giving rise to a separate p53 gene and at least one ancestral p63/p73 gene.

57 es induced by adenovirus-delivered wild-type p53 gene and chemotherapy of U87 MG glioblastoma cells,

58 53 gene, or mice with both a mutation in the p53 gene and deletion in the Ink4A/Arf locus.

59 he second position of codon 273 of the human P53 gene and explored the mutagenic potential of this le

60 Ad-p53 allowed for exogenous transfer of the p53 gene and expression of functional p53 protein.

61 Rassf1a-knockout mice with mice lacking the p53 gene and generated a combination of single- and comp

62 locked both basal transcription of the human p53 gene and initiation of transcription from the human

63 ete loss of chromosome 11, which harbors the p53 gene and is thus the selected event.

64 es do not introduce foreign sequences to the p53 gene and maintain naturally occurring post-translati

65 Co-transfection into cells of the p53 gene and plasmid DNA containing the consensus DNA bi

66 Strategies targeting the p53 gene and protein may halt or reverse the process of

67 We show that evaluation of both the p53 gene and protein statuses provides information in as

68 The p53 gene and protein statuses show significant concordan

69 Combining the p53 gene and protein statuses stratifies patients into t

70 Both the p53 gene and protein statuses were significantly associa

71 y evaluated the clinical relationship of the p53 gene and protein statuses.

72 s show that MUC1 represses activation of the p53 gene and that MUC1-C occupies the PE21 element in th

73 tic DNA templates mimicking mutations in the p53 gene and two disease-associated SNPs in the human he

74 tified a large repertoire of tissue-specific p53 genes and a common p53 transcriptional signature of

75 mbinations of different polymorphisms in the p53 gene) and for p53-target genes are taken into accoun

76 the G.C to T.A mutation at codon 249 of the p53 gene, and may play an important role in carcinogenes

77 ancer has a mutation in the tumor suppressor p53 gene, and the mutational spectrum bears unique featu

78 tivate p53, but also induce mutations in the P53 gene, and thus select for p53-mutated cells.

79 EMAST has been related to alterations of the p53 gene, and to the nature of the repeat sequence.

80 2 is genetically intact and mutations in the p53 gene are extremely rare in APL.

81 Mutations in the p53 gene are identified frequently in breast carcinomas.

82 rate that methylated CG dinucleotides of the p53 gene are the preferred binding sites for the diol ep

83 or genes-most prominently the APC, KRAS, and p53 genes-are mutated in a sizeable fraction of CRCs, an

84 uch evidence has accumulated implicating the p53 gene as of importance in breast carcinogenesis.

85 on induces mutations in the tumor suppressor p53 gene as well as chronic inflammation, which are both

86 6 methylation with mutation of the K-ras and p53 genes, as well as with methylation at the DAP-kinase

87 ion was detected by sequence analysis of the p53 gene at codon 155: ACC [Thr] --> CCC [Pro].

88 A germ-line mutation in the p53 gene at nucleotide 13964 with a G to C base change (

89 cells among sputum cells and, in the case of p53 gene, at many codons.

90 utlin-3 (Nutlin) led to strikingly different p53 gene binding patterns based on chromatin immunopreci

91 ear factor of activated T cells (NF-AT), and p53 genes by E3L.

92 alyzed for the presence of chromosome 17 and p53 genes by fluorescent in situ hybridization, p53 muta

93 tosis pathway that included the p14(ARF) and p53 genes by hypermethylation and mutation, respectively

94 substitutions of the Harvey-ras, N-ras, and p53 genes by the Needle-in-a-Haystack mutation assay wit

95 that DNA damage and somatic mutations in the p53 gene can occur because of genotoxic stress in many t

96 Transcription of the p53 gene can regulate progression of apoptosis in a wide

97 in the bcl-6 and c-myc genes, but not in the p53 gene, consistent with aberrant somatic hypermutation

98 d in shuttle vector studies, where the human p53 gene-containing vector was treated with diazoacetate

99 The human p53 gene contains an alternative promoter and transcribe

100 ogenic action, constitutively active EGFR or p53 gene defects have been associated with proangiogenic

101 However, p53 gene deficiency did not confer complete protection f

102 y defined oxidative nucleobase adducts along p53 gene-derived DNA duplexes using a novel isotope labe

103 pecific O(6)-POB-dG adducts within K-ras and p53 gene-derived DNA sequences were incubated with recom

104 ts were produced nonrandomly along K-ras and p53 gene-derived DNA sequences, with over 5-fold differe

105 ng viruses to Alb-TVA mice lacking an intact p53 gene does not increase tumor incidence.

106 Consistent with the reduced p53 gene dosage because of the allelic loss and the func

107 Previous mouse studies show that p53 gene dosage determines susceptibility to GI syndrome

108 significantly decreased with a reduction of p53 gene dosage from 44% in Twsg1(-/-)p53(+/+) pups (N=6

109 se that expresses an extra copy of the mouse p53 gene driven by its endogenous promoter is utilized.

110 ion occurs within the promoter region of the p53 gene during multistage tumorigenesis.

111 The p53 gene encodes 12 isoforms, some of which can modulate

112 As a result, the mutated p53 gene encodes a full-length protein incapable of tran

113 The p53 gene encodes a transcription factor that is composed

114 Transgenic mice with an ectopic p53 gene encoding Delta40p53 developed hypoinsulinemia a

115 Cells carrying mutant or no p53 genes exhibited slow BER of MMS-induced DNA damage,

116 g analysis of the whole coding region of the p53 gene (exons 2-11) detected one or two mutations in 6

117 af) led to significant loss of MARE-mediated p53 gene expression but had no effect on the repression

118 s to AM, OT and PT triggered upregulation of p53 gene expression, post-translational modification of

119 n of Maf recognition element (MARE) mediated p53 gene expression.

120 l growth and survival is regulated by mutant p53, gene expression profiling analysis was performed an

121 notion that core ancestral functions of the p53 gene family are intimately coupled to cell death as

122 ounting evidence for a consensus scenario of p53 gene family evolution.

123 d sensitivity is due to up-regulation of the p53 gene family member p73 in response to DNA damage.

124 , we have further characterized DeltaNp63, a p53 gene family member, and shown that TAZ suppresses De

125 To understand the role of p53 gene family members during invertebrate embryonic de

126 genes (including cytokines, chemokines, and p53 gene family members) as bona fide downstream transcr

127 In bony vertebrates, all three p53 gene family paralogs, p53, p63, and p73 are distinct

128 The p53 gene family, comprising p53, p63, and p73, has overl

129 p63, a member of the p53 gene family, encodes multiple proteins that may eith

130 to investigate whether p73, a member of the p53 gene family, has a role in the regulation of the IGF

131 Trp73, a member of the p53 gene family, plays a crucial role in neural developm

132 p73 is a member of the p53 gene family, which also includes p53 and p63.

133 3 and p63, were identified as members of the p53 gene family.

134 We further demonstrate that the p53 gene from atrophic cells expressing TAg is wild type

135 genotyped 30 potential mutation sites in the p53 gene from Wilms' tumor, head and neck tumor, and col

136 Loss of p53 gene function, which occurs in most colon cancer cel

137 Throughout the animal kingdom, p53 genes govern stress response networks by specifying

138 n humans, the diversity of haplotypes of the p53 gene has decreased during evolution, because the arg

139 igenesis, the transcriptional control of the p53 gene has remained unclear.

140 Although somatic mutations in the p53 gene have been demonstrated in rheumatoid arthritis

141 Although mutations in the p53 gene have been found in a subset of MPNSTs and mouse

142 though mouse lines carrying mutations in the p53 gene have been generated, they die primarily of lymp

143 Although mutations in the K-ras and p53 genes have been reported to be significantly higher

144 cells-particularly those bearing inactivated p53 gene (Huh7, Hep3B, and Mahlavu)-to ultraviolet irrad

145 ly we showed that the transcription from the p53 gene in breast cancer cells was down regulated by OM

146 pothesized that the status of the endogenous p53 gene in cancer cells is a key determinant in the out

147 contrast with the mutational spectrum of the p53 gene in human bladder cancer.

148 at odds with the mutational spectrum of the p53 gene in human bladder cancer.

149 contribute to the mutational spectrum of the p53 gene in human bladder cancer.

150 This situation mirrors the one in the p53 gene in lung cancers from smokers where 236 of 465 (

151 is and was associated with activation of the p53 gene in mature mTECs.

152 Germline deletion of the p53 gene in mice gives rise to spontaneous thymic (T-cel

153 ix lysine residues (K6R) into the endogenous p53 gene in mouse embryonic stem (ES) cells.

154 ith an increase in G to A transitions in the p53 gene in non-small cell lung cancer (NSCLC).

155 clobutane pyrimidine dimers within exon 8 of p53 gene in normal and Li-Fraumeni syndrome fibroblasts

156 tion sites in exons 5, 7, and 8 of the human p53 gene in one tube using the SPC-SBE method.

157 ines and abasic sites was established in the p53 gene in only UVA1-irradiated cells.

158 er transgenic mouse (HIP) that expresses the p53 gene in rod and cone photoreceptors driven by the hu

159 underlying CC tandem mutations found in the p53 gene in skin cancers.

160 the cII and lacI transgenes, as well as the p53 gene in skin tumors, shows that 5-methylcytosine is

161 Inactivation of the p53 gene in the Mdm2 mutant background effectively rever

162 Sequence analysis of the p53 gene in these five squamous cell carcinoma samples i

163 ternative mechanism for the silencing of the p53 gene in tumors that do not have p53 mutations.

164 t not identical, formation of CPDs along the p53 gene in UVB- and UVA1-irradiated cells.

165 and/or strand breaks along exons 5-8 of the p53 gene in UVB- and UVA1-irradiated cells.

166 Concurrent deletion of the p53 gene in vivo reversed the observed phenotype of cell

167 ns of alterations in the ras, Ink4a/Arf, and p53 genes in the two melanoma groups.

168 E-dG adducts at the GAGG*C/A sequence in the p53 gene including codon 249 (GAGG*C).

169 Thus, in the absence of p53, gene induction does not contribute to the G(2) arre

170 Reintroduction of the wild type Arf or p53 genes into Arf(-/-) or p53(-/-) cells reversed the P

171 Mutation of the p53 gene is a common event during tumor pathogenesis.

172 The p53 gene is a critical tumor suppressor that is inactiva

173 Codon 273 ((5)(')CGT) of the human P53 gene is a mutational hot spot for the environmental

174 The p53 gene is commonly mutated in human cancers, and a p53

175 LN-Z308 cells, in which p53 gene is deleted, were also used.

176 As such, the P53 gene is frequently altered in human cancers.

177 The p53 gene is frequently deleted or mutated in human cance

178 Whereas the tumor suppressor p53 gene is frequently mutated in most human cancers, th

179 netic instability caused by mutations in the p53 gene is generally thought to be due to a loss of the

180 genomic stability, and transcription of the p53 gene is induced prior to cells entering S phase, pos

181 s may be worth exploring in sPNET, where the p53 gene is intact but the pathway is inactive in the ma

182 The p53 gene is intact in human retinoblastoma but the pathw

183 Accordingly, the p53 gene is mutated in a large number of human cancers.

184 The tumor suppressor p53 gene is mutated in minimally half of all cancers.

185 The p53 gene is mutated in over half of all cancers, reflect

186 In approximately 50% of human cancers, the p53 gene is mutated, and in the remaining cancers, the p

187 ing that dG-N(2)-tam adduct formation in the p53 gene is not a prerequisite for endometrial cancer in

188 ate the DNA binding spectrum of 4-ABP in the p53 gene is not known due to the lack of methodology to

189 The p53 gene is polymorphic at codon 72 (Arg/Pro) of its pro

190 The p53 gene is somatically mutated in over half of all huma

191 Mutation of the p53 gene is the most common genetic alteration in human

192 In fact, the p53 gene is the most commonly mutated tumor suppressor g

193 In this context, the p53 gene is the most commonly mutated tumor suppressor g

194 The p53 gene is the most frequently mutated gene in human ca

195 is p53-dependent, but a null mutation of the p53 gene is unable to maintain cell survival.

196 MKK4, located in close proximity to p53 gene, is thought to be a tumor suppressor and a meta

197 ple mechanisms that include mutations of the p53 gene itself and increased levels of the p53 inhibito

198 genetic and epigenetic events affecting the p53 gene itself and/or its interacting partners occur wi

199 erm line via ES-cell rat chimaeras to create p53 gene knockout rats.

200 his protocol to generate Tp53 (also known as p53) gene knockout rats.

201 53, but not in isogenic variants lacking the p53 gene, led to apoptotic cell death.

202 drag-tagged primers simultaneously probe 16 p53 gene loci, with an abbreviated thermal cycling proto

203 ) have been identified, including a putative p53 gene (Map53) from the soft-shell clam (Mya arenaria)

204 obacco carcinogen benzo(a)pyrene, can induce p53 gene mutation, down-regulate retinoic acid receptor

205 for p53 pathway attenuation in cancers than p53 gene mutation.

206 More than 50% of human cancers contain p53 gene mutations and as a result accumulate altered fo

207 p53 gene mutations are among the most common alterations

208 The majority of the p53 gene mutations in human cancers are missense mutatio

209 hose tumors had normal p53 expression or had p53 gene mutations preventing presentation of this epito

210 In many cases, p53 gene mutations result in high levels of inactive, fu

211 The frequency of p53 gene mutations was 13% for pediatric patients with M

212 haracteristics significantly associated with p53 gene mutations were determined using logistic regres

213 No p53 gene mutations were found in MM28, MM50, or Mel270 c

214 BRCA1 and p53 gene mutations were screened for using single-strand

215 s (which comprise approximately 30% of human p53 gene mutations) are largely devoid of transcriptiona

216 lity (MSI-H) have an unexplained low rate of p53 gene mutations.

217 d prog nosis and MSI status and frequency of p53 gene mutations.

218 study demonstrates that inactivation of the p53 gene occurs at the post-transcriptional level by rap

219 ethylation and C-to-T mutations found in the p53 gene of basal and squamous cell cancers.

220 3-CMdT and O4-CMdT to the mutations found in p53 gene of human gastrointestinal cancers.

221 In the p53 gene of human sunlight-associated skin cancers, 35 %

222 Acr-DNA adducts at the sequence level in the p53 gene of lung cells using the UvrABC incision method

223 K317R) missense mutation into the endogenous p53 gene of mice.

224 uced a missense mutation into the endogenous p53 gene of mouse embryonic stem (ES) cells that changes

225 of mutations are frequently observed in the p53 gene of nonmelanoma skin tumors.

226 Mutations in the p53 gene, often resulting in loss of wild-type (WT) p53

227 rformed with animals deficient in either the p53 gene or the Ink4A/Arf locus, tumors arose more quick

228 mice with targeted disruptions in either the p53 gene or the MutL homologue MMR gene Pms2 were interb

229 gous deficiency, mice with a mutation in the p53 gene, or mice with both a mutation in the p53 gene a

230 Deletion of the p53 gene permits the accumulation of nondiploid cells su

231 The p53 gene plays an important role in cell cycle control,

232 Transcriptional regulation of the p53 gene plays an important role leading to elevated exp

233 estigate whether a germ-line mutation in the p53 gene predisposes for tumorigenesis in mice.

234 The p53 gene product is overexpressed by almost 50% of cance

235 The activity of the p53 gene product is regulated by a plethora of posttrans

236 K-ras mutation was present in 8% of HPs, p53 gene product overexpression in none, and microsatell

237 ed, but p53 protein, phosphorylated p53, and p53 gene products (i.e. p21 and PIDD) were increased.

238 s vector-mediated transduction of either the p53 gene (rAd-p53) or the p21(WAF1/CIP1) gene (rAd-p21)

239 ancer cell-lines and normal fibroblasts, the p53 gene region was found to be rapidly repaired relativ

240 upled repair (TCR), this rapid repair of the p53 gene region was not observed when compared to both t

241 ncing protocols has enabled the study of the p53 gene regulatory network (GRN) and underlying mechani

242 armacological induction of p53 and PPARgamma-p53 genes repaired damaged DNA utilizing genes from the

243 ntroduced, gain-of-function mutations in the p53 gene, reported by Caulin et al., and chemokine seque

244 5) of the nucleotide changes in the PTCH and p53 genes, respectively, were UV-specific C-->T and CC--

245 The absence of information about p53 gene responsiveness mediated by half-site REs led us

246 A mutation in codon 122 of the mouse p53 gene resulting in a T to L amino acid substitution (

247 nalysis within the individual strands of the p53 gene revealed decreased repair of adducts from the n

248 HPLC mutation screening of all exons of the p53 gene, sequencing the cDNA, and assessing the functio

249 om paraffin-embedded tissues and employing a p53 gene-sequencing chip.

250 7 and NCI-H838, both of which have wild-type p53 gene, showed near complete lysis at a multiplicity o

251 The p53 gene status (mutation) and protein alterations (nucl

252 We compared p53 gene status, mutation site, and protein status with

253 ene, p21, in cancers that retain a wild-type p53 gene status.

254 incidence for >20 years and evaluated their p53 gene status.

255 uman tumor cell lines, irrespective of their p53 gene status.

256 ar p53 contain a mix of wild-type and mutant p53 genes, suggesting that TAg may inactivate p53 in the

257 aCaT and SCC-13 cells, which encode inactive p53 genes, suggesting that the response is p53 independe

258 the presence of a wild-type (but not mutant) p53 gene suppressed 53BP2 steady-state levels in cell li

259 The p53 gene suppresses tumor cell growth by inducing cell c

260 Furthermore, the p53 gene-targeted mutation in the rat ES-cell genome can

261 p53 gene-targeted rat ES cells can be routinely generate

262 etion mutation in the first six exons of the p53 gene that express a truncated RNA capable of encodin

263 In the i.p. MidT2-1 tumor model p53 gene therapy enhanced the survival benefits of pacli

264 ne 20 is critical for apoptosis induction in p53 gene therapy for gliomas.

265 Tumor growth in vivo was inhibited by p53 gene therapy or by MMAC gene therapy.

266 ly, we undertook a phase I clinical trial of p53 gene therapy using an adenovirus vector (Ad-p53, ING

267 without p53 mutation are often resistant to p53 gene therapy.

268 te that OM inhibits the transcription of the p53 gene through the PE21 element.

269 n adenoviral vector containing the wild-type p53 gene to patients with advanced malignancies, charact

270 as well as cells from animals with a deleted p53 gene, to define groups of genes that require phospha

271 ratively activate ADD1 and CCND1 but repress p53 gene transcription by recruiting differential chroma

272 We here examine p53 gene transcription in such TI clones, with a focus o

273 Within T-cell-dependent germinal centers, p53 gene transcription is repressed by Bcl-6 and is thus

274 hat oncogenic signaling pathways inhibit the p53 gene transcription rate through a mechanism involvin

275 ion of p53R172H can be a surrogate marker of p53 gene transcription.

276 report that EP2 signaling triggers increased p53 gene transcriptional activity in AID(+) cycling blas

277 fy p53-responsive genes following adenoviral p53 gene transfer (Ad-p53) in PC3 prostate cancer cells.

278 Adenoviral-p53 gene transfer (Ad-p53) is currently being evaluated

279 ategy to assess gene expression following Ad-p53 gene transfer and to determine if the expression of

280 o identify p53-responsive genes following Ad-p53 gene transfer in control and bcl-2-overexpressing PC

281 and biologic activity of adenovirus-mediated p53 gene transfer in patients with locally advanced blad

282 ted the safety and maximum-tolerated dose of p53 gene transfer using an adenovirus vector (Ad-p53) de

283 1n) cell line was wild-type for p53, had two p53 genes, two copies of chromosome arm 17p and showed f

284 cells expressing a dominant negative mutant p53 gene underwent extensive apoptosis within 24 h after

285 Therapeutic replacement of the p53 gene using an adenovirus vector (Ad-p53) may be an e

286 ast tumors for mutations in exons 4-8 of the p53 gene, using single-strand conformational polymorphis

287 A mutation in exon 8 of the P53 gene was associated with loss of function of the p53

288 In addition, the p53 gene was mutated in 19 out of 85 (22%) samples as de

289 er, LPA failed to induce HIF-1alpha when the p53 gene was mutated.

290 The complete coding region of the p53 gene was queried using DNA from paraffin-embedded ti

291 The p53 gene was sequenced in three primary uveal melanoma c

292 0 bp of upstream DNA sequences of the murine p53 gene, we identified new positive and negative regula

293 the APC gene or with the tm1 mutation of the p53 gene were crossed with CD44 knockout mice.

294 Mutations of the p53 gene were detected by sequence analysis in 105 patie

295 Mutations in the beta-catenin and p53 genes were determined by DNA sequencing.

296 utations of clinical importance in the human p53 gene, were covalently conjugated to three unique pol

297 was then used to sequence exons 2-11 of the p53 gene where we identified 19 base substitutions.

298 where Tat inhibited the transcription of the p53 gene, which may aid in the development of AIDS-relat

299 lotting demonstrated the allelic loss of the p53 gene, which resides on mouse chromosome 11, in four

300 We engineered strains that replace the fly p53 gene with human alleles, producing a collection of s