ライフサイエンスコーパス: ras gene

1 preferential DNA damage at codon 12 of the K-ras gene.

2 rity of sensitive cell lines had a wild-type ras gene.

3 of single nucleotide polymorphisms in the k-ras gene.

4 use mammary tumor virus promoter-driven ha-v-ras gene.

5 ht reflect an unusual vulnerability of the K-ras gene.

6 trated up to 40-fold amplification of the Ki-ras gene.

7 hereas only one of these contained a mutated ras gene.

8 when it occurs, is exclusively in the Harvey ras gene.

9 mouse skin is mutational activation of the H-ras gene.

10 Tumors were typed for mutations in the K-ras gene.

11 ine (R18) containing a zinc-inducible mutant ras gene.

12 in the 3'-untranslated region of the human H-ras gene.

13 I) within the promoter region of the mouse N-ras gene.

14 o longer contained the mutated copy of the N-ras gene.

15 oma cell line HCT116 harbors an oncogenic Ki-ras gene.

16 ession via targeted knockout of the mutant K-ras gene.

17 including the first two exons of the mouse H-ras gene.

18 by a gain-of-function mutation of the let-60 ras gene.

19 n harboring a constitutively active mutant N-ras gene.

20 mouse embryonic fibroblasts deficient in all Ras genes.

21 TRK tyrosine kinase receptors, as well as of RAS genes.

22 ng mutant H-ras, mutant K-ras, and wild-type ras genes.

23 are protected against G to A transitions at ras genes.

24 nal transduction cascade by mutations in the RAS genes.

25 and analysed for mutations in the lacI and K-ras genes.

26 arcinomas, and in combination with mutated K-ras genes.

27 y discernible increases in the expression of RAS genes.

28 isms independent of direct genetic damage to ras genes.

29 ld stimulate growth of a strain lacking both RAS genes.

30 transformed cell types that express mutated ras genes.

31 ed less than 20 times higher than native C3H ras genes.

32 ns, is blocked in cells expressing activated Ras genes.

33 ribution of the normal products of the other ras genes.

34 in cancers evoked by oncogenic mutations in Ras genes.

35 cancer cells, which frequently carry mutant RAS genes.

36 due to activating mutations in the BRAF and RAS genes.

37 d by local regulatory elements in the target ras genes.

38 smid pMIKcys, which encodes a mini human c-K-ras gene (15 kb) containing a cysteine mutation at codon

39 codons and their surrounding codons in the K-ras gene, (2) the chromatin structure, and/or (3) epigen

40 ning of transgenic mice overexpressing the H-ras gene, 45% had increased LV wall thickness (> 0.9 mm)

41 ity and co-expression of a dominant negative ras gene ablated receptor stimulation.

42 tein kinases because both mutated Ki- and Ha-ras genes activated this pathway and increased cell prol

43 e mechanisms responsible for tissue-specific ras gene activation are poorly understood.

44 rotein activity to the tissue-specificity of ras gene activation was investigated using the rat mamma

45 The let-60 ras gene acts in a signal transduction pathway to contro

46 ras (Ad.K-ras scAb), (2) an antisense (AS) K-ras gene (Ad.K-ras AS) or (3) both mda-7/IL-24 and a K-r

47 R to measure CldATP incorporation into the N-ras gene after incubation of cultured human leukemia cel

48 es with oncogenic mutations in their H- or K-ras genes after treatment with prenyltransferase inhibit

49 ines revealed mutations in either the VHL or Ras genes, although karyotype analysis and chromosome pa

50 cant mammary tumor growth associated with Ki-ras gene amplification and over-expression that occurs d

51 Tumors bearing Ki-ras gene amplification exhibited high levels of Ki-ras R

52 r results suggest that a mutation in a human ras gene analogous to ga89 might contribute to oncogenic

53 p in bitransgenic mice bearing both the v-Ha-ras gene and a heterozygous mutant p53 allele tend to re

54 umber of mutations, including those in the K-ras gene and CTNNB1, that codes for beta-catenin.

55 ype of cultured cells expressing a mutated H-ras gene and induces dramatic regression of mammary and

56 to tumor formation include mutations in the ras gene and loss or inactivation of cell cycle inhibito

57 by PCR amplification and sequencing of the K-ras gene and microsatellite PCR analysis of proliferativ

58 cific allele-specific transcription of the K-ras gene and provide further support to the thesis that

59 bset of PILs that contain mutations of the K-ras gene and that these mutations might identify high-ri

60 tations affected known oncogenic hotspots of RAS genes and conferred variably enhanced RRAS function

61 Alterations of the bcl-1, bcl-2, or ras genes and evidence of Epstein-Barr virus infection w

62 ntains an endogenous mutated allele of the N-ras gene, and its derivative (MCH603c8), which lacks the

63 ed mutations of the APC, beta-catenin, and K-ras genes, and microsatellite instability (MSI) status i

64 Nine (69%) of these had wild-type K-ras genes, and one had microsatellite instability (MSI).

65 Mutations were found in p53 and ras genes, and one site showed microsatellite instabilit

66 Activating oncogenic mutations of the RAS gene are common in cancer, occurring in 30% of solid

67 Mutations in the K-ras gene are frequent in human cancer.

68 Mutations in the RAS gene are known to occur in human cancers and have be

69 Mutations of the K-ras gene are known to occur in PILs, but their high prev

70 Because mutations of the ras gene are most often found in tumors of epithelial or

71 Certain mutations in the mammalian ras gene are oncogenic and are often detected in human c

72 ore, DNA adducts formed at codon 12 of the K-ras gene are poorly repaired compared with those at othe

73 e residues in codons 12, 13, and 61 of the H-ras gene are strong syn-DMBADE binding sites.

74 RAS genes are commonly mutated in cancer; however, RAS m

75 Ras genes are commonly mutated in human cancers of the s

76 tumorigenic phenotypes, even when different ras genes are expressed from the same locus.

77 in cells transformed in vitro mutated human ras genes are expressed more than 100-fold than in the c

78 For example, activating point mutations in RAS genes are found in some patients with juvenile chron

79 Ras genes are frequently activated in human cancers, but

80 Activating mutations in ras genes are frequently associated with non-small cell

81 The products of the ras genes are known to regulate cell proliferation and d

82 RAS genes are mutated in 20% of human tumors, but these

83 RAS genes are mutated in approximately 30% of all human

84 part in cancer." The conclusion that mutated ras genes are not sufficient or dominant for cancer is d

85 Ras genes are the most common targets for somatic gain-o

86 The RAS genes are the most commonly mutated oncogenes in hum

87 Ras genes are the most frequently mutated oncogenes in h

88 Mammalian ras genes are thought to be critical in the regulation o

89 CKD associations with these RAS genes are uncertain in high-risk black populations.

90 Using the K- ras gene as a model system, multiplex PCR/LDR followed b

91 on 1-exon 1 region (rasI/E1) of the mouse Ki-ras gene as sufficient to reconstitute aldosterone respo

92 elements in the transcription of the human R-ras gene, as well as the transcription factors that inte

93 amined the mutational status of the N- and K-ras genes at codons 12, 13, and 61 in 160 newly diagnose

94 REF cells cotransfected with HCV core and H-ras genes became transformed and exhibited rapid prolife

95 atment, as well as mutation spectra in the H-ras gene between 6 h and 3 days after treatment.

96 ted keratinocytes possessing an activated Ha-ras gene, both in vitro and in vivo.

97 in the promoter sequences of the BCL-2 and k-RAS genes, both of which are dis-regulated in many human

98 he tumors did not present mutations in the H-ras gene, but Rasgrp1 transgene dosage correlated with t

99 HIV-1 nef and v-ras genes, but not the c-ras gene, were shown to substit

100 a mutation in either codon 12 or 13 of the K-ras gene by direct sequencing.

101 ration in transcriptional regulation of c-Ha-ras gene by estrogen may play an important role in progr

102 Expression of the oncogenic Ki-ras gene caused the altered beta1 integrin maturation be

103 Ha-ras gene codon 61 mutations were detected in 7 of 10 sta

104 The three RAS genes comprise the most frequently mutated oncogene

105 The 3'UTRs of the human RAS genes contain multiple LCSs, allowing let-7 to regul

106 ns in the genome and expression of the Mut H-ras gene could be detected as early as 1 d after DMBA ap

107 that dominant active mutation in the unique Ras gene (DARas) of the fungal phytopathogen Colletotric

108 lones which also expressed the activated c-K-ras gene displayed a transformed morphology, decreased d

109 s were conducted to examine the effect of Ki-ras gene dosage on tumor progression.

110 tardation of tumor development by reduced Ki-ras gene dosage, overall survival was only modestly affe

111 s in Nf1(+/-) mast cells is decreased in a K-ras gene dose-dependent fashion in cells containing muta

112 In mammals, the three classical ras genes encode four highly homologous proteins, N-Ras,

113 Three Ras genes encode four proteins that differentially contr

114 The R-ras gene encodes a small GTPase of the ras family that i

115 The initial discovery that ras genes endowed retroviruses with potent carcinogenic

116 ly form adducts at codons 12 and 14 in the K-ras gene exon 1 in intact as well as in fragmented genom

117 o synthesized DNA fragments containing the K-ras gene exon 1 sequence with or without methylation of

118 PCR-amplified DNA fragments containing the K-ras gene exon 1 sequence.

119 On the other hand, Ad-36 increased Ras gene expression and protein abundance, and Ras siRNA

120 In this study, the contribution of ras gene expression and Ras protein activity to the tiss

121 soluble factors on the modulation of cardiac RAS gene expression in vivo; (ii) measure gene expressio

122 These data indicate that c-Ha-ras gene expression is modulated by BaP via a complex me

123 These data suggest that allograft-level RAS gene expression may be predictive of future graft fu

124 Differential ras gene expression was examined in mammary tissue from

125 growth, melanin synthesis, morphology and H-ras gene expression.

126 Strains carrying ras2(318S) as their sole RAS gene fail to elicit a transient increase in cAMP lev

127 Thus, K-ras is the only member of the ras gene family essential for mouse embryogenesis.

128 found between the independent members of the ras gene family is unlikely to fully account for the exc

129 as been widely studied in UCC, but all three Ras gene family members have not been screened for mutat

130 have identified an additional member of the Ras gene family which shows significant sequence similar

131 nctional overlap appears to occur within the ras gene family, but K-ras provides a unique and essenti

132 the effect of multiple mutations within the ras gene family.

133 ide metabolism, chromatin structure, and the Ras gene family.

134 de that the mutated, but normally expressed, ras genes found in human and animal cancers are not like

135 Oncogenic mutations in ras genes frequently occur in patients with myeloid diso

136 and we have also analyzed mutations in the H-ras gene from tumors induced by these compounds.

137 onserved sequence motif of the small GTPase, RAS GENES FROM RAT BRAINA1b.

138 olocalizes with microtubules and RabA2a (for RAS genes from rat brainA2a) GTPase-positive structures.

139 ammalian cells contain three closely related ras genes, H-ras, K-ras and N-ras.

140 r either of two wild-type sequences of the H-ras gene (H2/siRNA and H3/siRNA) and used these retrovir

141 isogenic counterparts in which the mutant K-Ras gene had been disrupted (DKS-8).

142 include mutations in the KIT, FLT3, JAK2 and RAS genes, haploinsufficiency of the putative tumor supp

143 In this case-control study, RAS gene haplotypes were not significantly associated wi

144 The expression of activated ras genes has been implicated as a contributing factor t

145 dent thyroid epithelial cell lines by mutant RAS genes has been widely studied as an experimental mod

146 Mutations in ras genes have been detected with high frequency in nons

147 Mutations in RAS genes have been found in approximately 25% of lung c

148 Activated ras genes have been frequently identified in both benign

149 Transforming proteins encoded by activated ras genes have been implicated in the etiology of many h

150 The RAS genes have emerged as important modulators of life-m

151 Although the ras genes have long been established as proto-oncogenes,

152 r a wild-type or a mutant codon 12 in the Ha-ras gene; however, the inhibitory effect was greater aga

153 Mutations in the three closely related RAS genes, HRAS, KRAS, and NRAS are among the most commo

154 The three closely related human Ras genes, Hras, Nras, and Kras, are all widely expresse

155 high mutation frequency at codon 12 of the K-ras gene in human cancers.

156 iscriminate single base differences in the K-ras gene in less than 5 min at a frequency of 1 mutant D

157 ctivating mutations in the endogenous Harvey ras gene in mammary carcinomas from the HrHr, HrKr trans

158 G to A point mutations in codon 12 of the K-ras gene in many tumors.

159 rototypic ras genes, the disruption of the R-ras gene in mice results in enhanced angiogenesis in tum

160 ducts at codons 12 and 14 (-CGTAG-) in the K-ras gene in normal human bronchial epithelial (NHBE) cel

161 it (hTERT), and an oncogenic allele of the H-ras gene in normal human fibroblast, kidney epithelial,

162 lysis of the 3' untranslated region of the K-ras gene in normal lung, spleen, liver and kidney from (

163 To investigate the role of an activated K-Ras gene in the initiation and maintenance of lung adeno

164 s (Flt-1, KDR [kinase domain receptor]), and ras genes in a group of 91 pediatric patients with AML t

165 epithelial cells, the occurrence of mutated ras genes in breast tumors is infrequent.

166 ell-validated role of mutationally activated RAS genes in driving cancer development and growth has s

167 omatic cell knockout of mutant and wild-type ras genes in human cancer cell lines.

168 mutations occurring throughout the p53 and K-ras genes in sputum of lung cancer patients.

169 r of mutation of only one of the three major RAS genes in tumors of different cellular origins.

170 Sequence analysis of the K-ras gene indicated that the mutations had occurred at ei

171 is of 16 cancer cell lines carrying mutant K-ras genes indicated that 50% of cancer cells harbor nono

172 Similarly, expression of a dominant negative ras gene inhibits phenylephrine-stimulated calcineurin a

173 Reintroduction of the activated N-ras gene into the HT1080 line, having lost its mutant al

174 t amplification and overexpression of the Ki-ras gene is associated with mammary tumor progression in

175 The Ras gene is frequently mutated in cancer, and mutant Ras

176 breast cancer, overexpression of normal c-Ha-ras gene is frequently observed.

177 vation of either the Harvey-, Kirsten-, or N-ras gene is often found in human and rodent cancers, alt

178 Although mutation of ras gene is rare in human breast cancer, overexpression

179 ene superfamily, codon 12 (-TGGTG-) of the K-ras gene is the most frequently mutated codon in human c

180 s not clear whether observed upregulation of RAS genes is a direct effect of hemodynamic stress or is

181 Dergulation of c-myc and mutation of ras genes is commonly found in many human tumors.

182 n of the second A of 5'-CAA (codon 61 of the ras gene), is mutagenic in human cells, inducing A-->T,

183 ce heterozygous for a null mutation of the K-ras gene (K-ras+/-) show normal hippocampal mitogen-acti

184 METHODS AND We used H- and K-Ras gene knockout mice and subjected them to pressure ov

185 in tumours that do not carry mutations in a RAS gene known as KRAS, and that BRAF mutation is linked

186 rmation of the mouse C3H cell line only with ras genes linked to viral promoters.

187 Our observations suggest that mutated RAS genes may mediate autocrine IL-1beta production in s

188 FTIs, it should be noted that Ki-ras is the ras gene most frequently mutated in human cancers.

189 cancers, and small molecule agents targeting RAS gene mutant cancers.

190 All of them had the K-ras gene mutated.

191 on and are largely ineffective in those with RAS gene mutation because of resistance.

192 Among the 16 cases with a K-ras gene mutation in the tumor, the same mutation was de

193 his mutual exclusion suggests that FGFR3 and Ras gene mutation may represent alternative means to con

194 PCO update addresses the utility of extended RAS gene mutation testing in patients with metastatic co

195 ras gene mutation, which perpetually turns on the growth

196 ships between microsatellite instability and ras gene mutations and p53 overexpression were shown to

197 Ras gene mutations are also found in UCC.

198 Moreover, tumors bearing RAS gene mutations are more vascular than tumors without

199 K-ras gene mutations have been reported as early events in

200 umours (55%) and three cell lines (10%), and Ras gene mutations in 13 tumours (13%) and four cell lin

201 Genomic analyses failed to detect N-ras gene mutations in any of the 35 leukemias.

202 ng is consistent with an important role of K-ras gene mutations in the transformation from normal epi

203 epair capacity, and increased incidence of K-ras gene mutations in women.

204 Genomic DNA was extracted, and K-ras and H-ras gene mutations were determined by a mutant-enriched

205 Furthermore, in tumor cells with Ras gene mutations, inhibition of Shoc2 expression inhib

206 sed p53 and beta-catenin immunoreactivity, K-ras gene mutations, microsatellite instability, and loss

207 Other patients with JMML acquire activating RAS gene mutations.

208 ts independent of the presence of activating ras gene mutations.

209 About 30% of human tumours carry ras gene mutations.

210 contrast, expression of a dominant negative ras gene (N17ras) had no effect.

211 s had mutation in exon 1, codon 12 of the Ki-ras gene; none had mutation in exon 2.

212 mutations in codons 12, 13, and 61 of the K-ras gene occur early in the development of colorectal ca

213 Activating mutations in the c-K-ras gene occur in about 40% of human colorectal carcinom

214 Oncogenic mutations in the K-ras gene occur in approximately 50% of human colorectal

215 ed more than 120-fold higher than are native ras genes of C3H cells.

216 ect sequencing of codons 12 and 13 of the Ki-ras gene on exon 1 from DNA obtained from archival tissu

217 lective effects of the oncogenic cellular Ki-ras gene on integrin beta1-chain glycosylation may accou

218 ncers, irrespective of the status of their K-ras gene, only when tumor cells simultaneously express m

219 and one focal), and no alterations in the K-ras gene or p53 expression were detected.

220 or RAS-driven cancers involving mutations in RAS genes or otherwise activated RAS proteins.

221 many psychiatric disorders, mutations in the RAS genes or their regulators render RAS proteins persis

222 Upon ectopic expression of an activated Ki-ras gene, p53-deficient colon epithelial cells form colo

223 Although RAS1 appears to be the only RAS gene present in the C. albicans genome, strains homo

224 ancreatic and colon adenocarcinomas, mutated ras genes produce mutated proteins that remain locked in

225 ssing a short hairpin RNA that targets the H-Ras gene produces a significant reduction of voluntary c

226 Expression of a dominant negative ras gene product blocks phenylephrine-stimulated NFAT tr

227 ors expressing the G35 to A activated Harvey ras gene product compared with those expressing G35 to A

228 FVB/n mice transgenic for v-Ha-ras gene (R+) were crossed with transgenic C57BL/6 mice

229 The copy number of transfected ras genes ranged from 2-6 in our system.

230 ent expression of a dominant-negative mutant Ras gene (Ras-ala15) in a Drosophila S-2 stable cell lin

231 beta-galactosidase (beta-gal) and activated Ras genes (Ras-gal) was transduced into a small fraction

232 e stable expression of an oncogenic (G12V)Ha-ras gene (Ras9 cells).

233 Using point-mutated human ras genes recombined with different promoters from eithe

234 Tumor cell lines bearing mutant K-ras genes required higher concentrations for inhibition

235 in MM cell lines harboring a mutant N- or K-ras gene requires EZH 2 activity.

236 type) for unknown mutations in the p53 and K-ras genes, respectively, opening prospects as an early d

237 -1beta and have mutations in the K-RAS and N-RAS genes, respectively.

238 Tumors frequently contain mutations in ras genes, resulting in constitutive activation of Ras-a

239 es on 5 kb of 5'-flanking DNA of the human R-ras gene revealed the functional importance of the regio

240 creased levels of RAS-GTP, and sequencing of RAS genes revealed a rare activating mutation in KRAS, r

241 We examined the role of the novel ras gene Rheb2, an activator of the mTOR kinase, in colo

242 ing either the nonspecific sequence or the K-ras gene sequence containing a single dG-N2-TAM at the s

243 ras-retroviral vector used to transduce the ras gene showed an inverse correlation between p18 expre

244 broblasts transformed by different activated ras genes showed two different protease phenotypes, rasu

245 cinomas of the pancreas and that wild-type K-ras gene status and a medullary phenotype characterized

246 GTPase-impairing somatic mutations in RAS genes, such as KRAS(G12D), are among the most common

247 In the ras gene superfamily, codon 12 (-TGGTG-) of the K-ras ge

248 cribed M-Ras or R-Ras3 gene, a member of the Ras gene superfamily.

249 These included mutations in all three Ras genes; ten in HRAS, four in KRAS2 and four in NRAS a

250 nucleotide polymorphism in codon 12 of the K-ras gene that are frequently occurring in early stages o

251 latory element in intron 1 of the mouse c-Ha-ras gene that contains the consensus half-site of a gluc

252 centage (2-7%) of C3H cells transfected with ras genes that are expressed less than 20 times higher t

253 and without ras mutations, (iii) retroviral ras genes that are oncogenic without point mutations, an

254 Mutations in RAS genes that encode constitutively active, GTP-bound,

255 echanism hardwired into the very sequence of RAS genes that underlies how such similar proteins impac

256 are selectively observed in only one of the ras genes, the acquisition of the transformed phenotype

257 Unlike the prototypic ras genes, the disruption of the R-ras gene in mice resu

258 ll line has been transfected with a mutant H-ras gene to mimic carcinogenesis in vitro.

259 e apoptosis, and cooperate with an activated ras gene to oncogenically transform primary rodent cells

260 (ii) stimulatory effect of estrogen on c-Ha-ras gene transcription and suggest that alteration in tr

261 -independent regulatory mechanisms for the R-ras gene transcription.

262 Inducible expression of a mutated K-ras gene under the control of the K5 promoter led to the

263 either three or seven copies of the Kirsten ras gene under the same promoter (HrKr) were produced.

264 fer into primary fibroblasts of an activated ras gene (V12ras) rapidly accelerates development of the

265 Studies examining RAS gene variants and cardiovascular disease have focuse

266 human RAS and test the significance of human RAS gene variants by a combined transgenic and gene targ

267 Oncogenic activation of RAS genes via point mutations occurs in 20%-30% of human

268 spFRET detection of point mutations in the K-ras gene was accomplished in PMMA microfluidic devices u

269 The K-ras gene was amplified by polymerase chain reaction and

270 Mutation of the Ki-ras gene was found in 41% of the cancers and was associa

271 tribution of carcinogen-DNA adducts in the K-ras gene was mapped at the nucleotide sequence level usi

272 The K-ras gene was sequenced at codon 12 and 13 to confirm the

273 th either a constitutively activated N- or K-ras gene was used.

274 ras (WM35 transfected with mutant N-ras or H-ras genes), we demonstrated significant decreases (p < 0

275 Mutations in the Ki-ras gene were detected in 32% of tumors.

276 nd single activating mutations in any of the ras genes were also independent predictors of poor survi

277 Point mutations in the Tp53 and Ki-Ras genes were detected that are also characteristic of

278 These ras genes were expressed more than 120-fold higher than

279 BRAF as well as RAS genes were mutated in a large proportion of cases (4

280 nd the subsequent determination that mutated ras genes were present in a wide variety of human cancer

281 HIV-1 nef and v-ras genes, but not the c-ras gene, were shown to substitute functionally for SIV

282 rearranged c-myc alleles, and also in the N-ras gene which is also amplified in this cell line.

283 Transduction with an activated v-Ha-ras gene, which signals downstream of the EGF-R, induced

284 ssion of heparanase variants with a mutant H-Ras gene, which was sufficient to enable growth of invas

285 ep in the constitutive expression of mutated ras genes, which are present in more than 27% of oral ca

286 re are at least five different Dictyostelium Ras genes, whose functions are not yet known.

287 acquisition of an activating mutation endows RAS genes with functional autonomy, recent studies sugge

288 cells stably transfected with mutated K or N-ras genes with wild-type ras-expressing control cells id

289 Gln to CTA Leu) mutations in the Harvey (H)-ras gene within 12 h after treatment.

290 own that the targeted expression of a mutant ras gene within the interfollicular cell compartment of

291 G to A point mutations in codon 12 of the K-ras gene would occur.

292 of the pancreas typically contain a mutant K-ras gene, yet all three RER+ carcinomas had wild-type K-