ライフサイエンスコーパス: immortal

1 ration, the germ line is often thought of as immortal.

2 g lineages within the same population remain immortal.

3 ulture as do wild-type MEFs, but instead are immortal.

4 ughter ensures that the yeast strain remains immortal.

5 for growth and reproduction, and potentially immortal.

6 blasts telomerase-positive and replicatively immortal.

7 The germ lineage is considered to be immortal.

8 ic stem cells age while the germline appears immortal.

9 re restored to those observed in primary and immortal (10)10 MEF cells.

10 exposure of the early passage conditionally immortal 184A1 HMEC line to the viral oncogenes human pa

11 ll capable of rapidly converting conditional immortal 184A1.

12 In IL-3-dependent immortal 32D.3 myeloid cells the ARF/p53 apoptotic pathw

13 quamous cell carcinomas (SCCs), however, are immortal, a phenotype that is associated with p53 and IN

14 Expression of oncogenic H-Ras in the immortal ALT cell line GM847 did not result in their tra

15 rved in normal cells and telomerase-negative immortal ALT cell lines, with up to 300-fold higher acti

16 Furthermore, knockdown of NPM in immortal and cancer cells led to significant down-regula

17 The preneoplastic outgrowth lines were immortal and exhibited activated telomerase activity.

18 Despite being immortal and having a telomere maintenance mechanism, AL

19 Immortal and immeasurable time bias was addressed by ana

20 ative stem cell state and become potentially immortal and invasive.

21 ally and karyotypically stable, are innately immortal and isogenic, and can be derived in an array of

22 ct of AP-1 blockade on the growth of normal, immortal and malignant breast cells.

23 omatic cells and tissues but is activated in immortal and malignant cells.

24 uptake of PNAs and PNA-peptide conjugates by immortal and primary human cells and compare peptide-med

25 t neoplastic stages: a 10W+8 clone, which is immortal and retains the ability to suppress the tumorig

26 in and the transcription factor Gata4 become immortal and therapeutically potent.

27 The immortal and totipotent properties of the germ line depe

28 models of stem cell turnover: the symmetric (immortal) and asymmetric models.

29 e expression may escape this barrier, become immortal, and develop further malignant properties.

30 istocompatibility promoter are conditionally immortal at permissive temperatures and produce monoclon

31 Immortal baby mouse kidney epithelial cells selected in

32 red directly from the plasma membranes of an immortal beta-cell line.

33 e AP-1 inhibitor reduced colony formation of immortal breast cells by over 50% (by 58% in 184B5 cells

34 hRNA-mediated SOX7 silencing, nontumorigenic immortal breast cells display increased proliferation, m

35 extremely sensitive to AP-1 blockade, while immortal breast cells were moderately sensitive.

36 an mammary epithelial cells, intermediate in immortal breast cells, and relatively low in breast canc

37 cyte-derived MCP-1-induced transformation of immortal breast epithelial cells is triggered by transie

38 e-specific markers, and furthermore were not immortal but died after a few months.

39 not only resistant to senescence and became immortal but displayed enhanced S-phase entry and prolif

40 teinase, which is not expressed in normal or immortal but non-tumorigenic epithelial cell lines, was

41 On the other hand, immortal but nonmalignant cell lines that contained epis

42 the effect of the D239Y variant expressed in immortal but nontransformed human and mouse mammary epit

43 ant potential modifier c-Src in two distinct immortal but nontumorigenic human MECs.

44 on of p53 mRNA was observed in the nuclei of immortal, but not primary, CEF cells.

45 For decades, immortal cancer cell lines have constituted an accessibl

46 , in isolated primary cardiomyocytes, and in immortal cardiomyocyte cell lines.

47 chromosome integrity were maintained in all immortal CEF cell lines without detectable telomerase ac

48 ate levels of p53 mRNA markedly increased in immortal CEF cell lines, similar to levels found in prim

49 stive that the downregulation of p53 mRNA in immortal CEF cells occurs through a post-transcriptional

50 All immortal CEF cells tested showed common genetic alterati

51 most of the cyclin genes was up-regulated in immortal CEF cells, which may be associated with the rap

52 nscriptional regulation seem to be unique in immortal CEF cells.

53 nd serum-independent growth patterns seen in immortal CEF cells.

54 r cells, we established and characterized an immortal cell line (CRBL) isolated from the cerebellum o

55 feline BAC further, we established the first immortal cell line (SPARKY) and transplantable scid mous

56 differentiation of UB/OC-1, a conditionally immortal cell line derived from the mouse cochlea.

57 diated recombination allowed us to derive an immortal cell line from the ventricular myocardium that

58 Using primary neuronal culture and immortal cell line models, we show that expression of no

59 rimary cell isolation to establishment of an immortal cell line, may take up to 2 months.

60 ouble-strand break engineered to occur in an immortal cell line.

61 The animal germline is an immortal cell lineage that gives rise to eggs and/or spe

62 The germ line is an immortal cell lineage that is passed indefinitely from o

63 of experimental behavior and fits data from immortal cell lines (HeLa S3 and 293T) and somatic cells

64 tissue culture, leading to the formation of immortal cell lines (SV40-transformed human mesothelial

65 However, a number of immortal cell lines and tumors can achieve telomere main

66 In most immortal cell lines and tumors, telomere maintenance is

67 (MORF4) to induce replicative senescence in immortal cell lines assigned to complementation group B.

68 Examination of immortal cell lines demonstrated p16(INK4a) promoter met

69 further transferred by microcell fusion into immortal cell lines derived from human and rat mammary t

70 These immortal cell lines frequently had sustained deletions o

71 of Abelson murine leukemia virus (A-MuLV) in immortal cell lines has been well studied, while the eff

72 Some telomerase-negative tumors and immortal cell lines maintain long heterogeneous telomere

73 Most human tumors and immortal cell lines maintain their telomeric DNA via the

74 es can provide an alternative to traditional immortal cell lines or primary cells as a quantitative c

75 Reintroduction of p16(INK4a) into immortal cell lines resulted in rapid growth arrest.

76 Importantly, treatment of immortal cell lines with 5-aza-2'-deoxycytidine, an inhi

77 23-qter restored cellular senescence in four immortal cell lines, derived from human and rat mammary

78 ndent cell cycle entry in a variety of tumor/immortal cell lines.

79 Tissue culture of immortal cell strains from diseased patients is an inval

80 s been shown to oncogenically transform some immortal cell types, their activity in primary cells rem

81 of active telomere maintenance mechanisms in immortal cells allows the bypass of senescence by mainta

82 Telomeres in most immortal cells are maintained by the enzyme telomerase,

83 mRNA was detected in our telomerase-positive immortal cells but not in pre-crisis cells or telomerase

84 ved in the rapid p53 mRNA destabilization in immortal cells by expression analysis of 5'- and 3'-dele

85 xpression and growth arrest, indicating that immortal cells continuously require inactivation of p53.

86 te length, from which rare, rapidly dividing immortal cells emerged.

87 lls was significantly elevated compared with immortal cells from the same population, suggesting that

88 mRNA were relatively similar in primary and immortal cells grown in the presence or absence of CHX.

89 t telomere length was similar to that of the immortal cells in the culture that was sorted.

90 Yet, all of the immortal cells lines exhibited hyperphosphorylated Rb.

91 ession, with the result that both normal and immortal cells maintain the same average number of CTCF

92 ese cells without using viral protein, these immortal cells represent an authentic in vitro model sys

93 However, Myc overexpression in these immortal cells results in remarkably discordant regulati

94 cell derivation rigorously selects for those immortal cells that have erased the "epigenetic memory"

95 mmortalization by HPV and for progression of immortal cells to papillomas and carcinomas.

96 se negative, TGFbeta sensitive conditionally immortal cells to the fully immortal phenotype.

97 n likely contributes to the vulnerability of immortal cells to transformation by oncogenes that alter

98 ription in bronchial epithelial cell-derived immortal cells was performed.

99 vidence of crisis and, as anticipated, these immortal cells were anchorage- independent for growth.

100 ion of transfected p53 cDNA was inhibited in immortal cells, but restored upon CHX treatment.

101 In immortal cells, forskolin induced expression of Per1 aft

102 In immortal cells, the existence of a mechanism for the mai

103 Similar to immortal cells, the majority of breast cancer cell lines

104 rns were markedly different in normal versus immortal cells, with the latter showing widespread disru

105 t in pre-crisis cells or telomerase-negative immortal cells.

106 relatively long 23 h compared to only 3 h in immortal cells.

107 eraction between FOXM1 and NPM in cancer and immortal cells.

108 evels of p53 mRNA were dramatically lower in immortal chicken embryo fibroblast (CEF) cell lines comp

109 ow that stable expression of AEG-1 in normal immortal cloned rat embryo fibroblast (CREF) cells induc

110 increased telomerase activity, as do variant immortal clones that bypass replicative crisis.

111 The platform provides an immortal collection of diverse germplasm, a high-density

112 lture, ie., 11 of 11 Type I EL clones became immortal compared with 1 of 10 Type II EL clones.

113 izinc catalysts also perform very well under immortal conditions, showing improved control, and are a

114 expressing either LT (nonimmortal) or E6/E7 (immortal), converted the cells to anchorage independence

115 In these immortal cultures RB/E2F targets were deregulated in a c

116 d only in the original tumors from which the immortal cultures were derived.

117 dysregulate centrosome dynamics in HeLa and immortal diploid RPE-1 cells.

118 hCSCs with immortal DNA form a pool of nonsenescent cells with long

119 These analyses reveal that immortal DNA strand cosegregation is also regulated by I

120 d confirm the original implicit precept that immortal DNA strand cosegregation is specific to cells u

121 ic self-renewal that limits their number and immortal DNA strand cosegregation that limits their accu

122 lls that exhibit asymmetric self-renewal and immortal DNA strand cosegregation.

123 egulators of ASC asymmetric self-renewal and immortal DNA strand cosegregation.

124 Based on the premise of the immortal DNA strand hypothesis, we propose that stem cel

125 kinetics, we confirmed both the existence of immortal DNA strands and the cosegregation of chromosome

126 findings also lead us to propose a role for immortal DNA strands in tissue aging as well as cancer.

127 Immortal DNA strands inherited through asymmetric chroma

128 hat contain old template DNA strands (i.e., "immortal DNA strands").

129 sorting to retain preferentially the oldest 'immortal' DNA strand.

130 ring self-renewing divisions so that older ('immortal') DNA strands are retained in daughter stem cel

131 Immortal EGF-R null cells grew more slowly, achieved a l

132 human pediatric B-ALL cell line, SEM, and an immortal erythroid precursor cell line, HUDEP-2, to allo

133 n therapeutically inert mammalian cells into immortal exosome factories for cell-free therapies.

134 ines may represent a common strategy towards immortal fate in plants and animals.

135 function of myosin VI at the Golgi complex, immortal fibroblastic cell lines of Snell's waltzer mice

136 p53 is not the mediator of v-Abl toxicity in immortal fibroblasts and does not determine the suscepti

137 so known as Cdkn2a locus) protein levels and immortal fibroblasts deficient in components of the Arf-

138 and does not determine the susceptibility of immortal fibroblasts to v-Abl transformation.

139 mesticated origin and access to standardized immortal fish lines would be of great benefit.

140 SV40 large T antigen, and activated Ras were immortal, formed colonies in soft agar, and expressed DN

141 TSEC culture and techniques for establishing immortal FTSEC lines.

142 Once established, immortal FTSECs can typically be maintained for at least

143 We have tested this hypothesis by treating immortal, genetically stable human cells with representa

144 maize (26 diverse founders and 5000 distinct immortal genotypes) to dissect the genetic basis of comp

145 the notion that metazoans have a potentially immortal germ line separated from a mortal soma, and evo

146 es can continue indefinitely, because of its immortal germ-cell lineage.

147 cells that divide in syncytial tissues, and immortal germline cells.

148 g complete bypass of senescence and apparent immortal growth consistent with loss of a suppressor gen

149 transferred BAC results in reversion to the immortal growth phenotype of the parental cancer cell li

150 loss of DNA damage response and an apparent immortal growth, suggesting loss of p53 functions.

151 ng an abnormal IkappaBalpha mechanism in the immortal HaCaT versus normal keratinocyte.

152 ide-induced Deltapsim depolarization in both immortal hippocampal cells and primary hippocampal neuro

153 Our previous studies of p53(+) immortal HMEC lines indicated that overcoming the string

154 ession in early passage p53(+) conditionally immortal HMEC lines, and that p53(-/-) lines exhibit tel

155 Immortal HMEC that have both overcome replicative senesc

156 s remained comparable in finite lifespan and immortal HMEC.

157 These telomerase(-) 'conditionally immortal' HMEC underwent an additional step, termed conv

158 PPOLs and occurred at high frequency in the immortal HNSCC cell lines.

159 ds (termed "doubled haploids," DHs) produces immortal homozygous lines in only two steps.

160 N2A p14(ARF) and p16(INK4A) is essential for immortal human B-lymphoblastoid cell line (LCL) growth.

161 To overcome this technical barrier, immortal human cell lines are often derived from tumors

162 PNA-peptide conjugates to enter primary and immortal human cells and inhibit gene expression support

163 Immortal human cells maintain telomere length by the exp

164 When tested in early passage normal and immortal human fetal astrocytes, growth inhibition resul

165 1) repressed, features of EMT in transformed immortal human MEC lines.

166 Using a normal immortal human melanocyte cell line and weakly and highl

167 d phenotype and alters metastatic ability in immortal human melanocytes and metastatic melanoma cells

168 of melanoma, but not normal early passage or immortal human melanocytes, is dramatically suppressed a

169 Most existing immortal human ovarian surface epithelial cells were ach

170 lated of human pancreatic beta cells and the immortal human PANC-1 epithelial cell line.

171 hurdle in addressing these issues is lack of immortal human stem/progenitor cells that can be deliber

172 e asexually and form long-lived, potentially immortal hybrids with unique morphologies.

173 3 spontaneously emerge from crisis to become immortal in a 3T3 growth protocol, we do not observe any

174 iffer significantly in the ability to become immortal in continuous culture, ie., 11 of 11 Type I EL

175 Whereas Cdk4(+/+)Ink4a/Arf(-/-) cells are immortal in culture, Cdk4(-/-)Ink4a/Arf(-/-) cells under

176 he absence of senescence and, therefore, are immortal in culture.

177 Many human carcinoma lines are immortal in vitro, suggesting that these cells have a me

178 in apoptosis, and 2) p19(ARF) null cells are immortal in vivo measured by serial transplantion, which

179 urdens, suggesting that while cancers appear immortal, individual cancer cells may suffer diminished

180 way also contributes to the proliferation of immortal Ink4a/Arf null fibroblasts suggesting that, bey

181 a single progression mechanism, resulting in immortal invasive cancers.

182 Bypassing cellular senescence and becoming immortal is a prerequisite step in the tumorigenic trans

183 of gene knockouts via CRISPR/Cas9 using the immortal JK-1 erythroleukemia line.

184 EGF-R-positive immortal keratinocytes formed papillomas in 17% (15 of 9

185 thermore, manipulation of the IFN pathway in immortal LFS fibroblasts through transcription factor IR

186 Treatment of spontaneously immortal Li-Fraumeni fibroblasts with 5-aza-2'-deoxycyti

187 This acquisition of an immortal lifespan usually requires the activation of tel

188 erase in cancer cells necessarily signify an immortal lifespan.

189 ganisms, the germ line traces an essentially immortal lineage.

190 rejuvenation, i.e., the resetting of age in immortal lineages.

191 fferent potencies, isolated as 3 independent immortal lines.

192 p2, in normal human fibroblasts and a set of immortal lines.

193 ll types, including normal primary cells and immortal lines.

194 for resting B-lymphocyte (RBL) conversion to immortal lymphoblast cell lines (LCLs).

195 lines tested as compared with untransformed immortal mammary epithelial cell lines, suggesting that

196 Furthermore, Bmi-1 was overexpressed in immortal MECs and several breast cancer cell lines.

197 We found that these immortal MECs select for reduced p53 protein levels thro

198 n in the high metastatic variants vs. normal immortal melanocytes or weakly metastatic parental clone

199 o modify mda-9/syntenin expression in normal immortal melanocytes, early radial growth phase melanoma

200 Infection of melanoma cells, but not normal immortal melanocytes, with Ad.mda-7 induced a time- and

201 otein 27 in melanoma cells but not in normal immortal melanocytes.

202 paper addresses both of these issues for the immortal model and demonstrates that approximate Bayesia

203 computation to estimate the parameters in an immortal model of colonic stem cell division.

204 A later modified version of the immortal model that included preferential strand segrega

205 ethylation data were not consistent with the immortal model.

206 This has raised the possibility that an "immortal" mother centriole may help maintain stem cell f

207 hus, the daughter centriole, rather than an "immortal" mother centriole, is ultimately retained in th

208 y young adult mouse colon (YAMC; Apc+/+) and immortal mouse colon epithelium (IMCE; ApcMin/+).

209 Also, there was higher PEA3 in immortal mouse colon epithelium cells (Apc(Min/)(+)) com

210 The immortal mouse lens epithelial cell line alphaTN4-1 was

211 Immortal mouse melanocyte lines (melan-a, melan-b, and m

212 ted caspases and enhanced the sensitivity of immortal MRC-5 cells to oxidative stress.

213 This study, by targeting immortal murine cells for telomerase inhibition, demonst

214 sing this approach, telomerase inhibition in immortal murine fibroblasts resulted in critical telomer

215 rotection of cells against oxidative stress, immortal murine lens epithelial cells (alphaTN4-1) have

216 Similarly, immortal murine NIH-3T3 fibroblasts and myeloid 32D.3 an

217 Analysis of immortal myeloid cells engineered to overexpress c-Myc a

218 , we have exploited the observation that the immortal myogenic C2 C12 cell line forms tumors far more

219 agement for the development of conditionally immortal neuroepithelial stem cell lines for grafting in

220 The production of genetically normal but immortal NHUC lines now provides a valuable platform for

221 erexpression of eIF3h malignantly transforms immortal NIH-3T3 cells.

222 genic capacity of carcinoma cells but not in immortal non-tumoral breast epithelial cells, which prov

223 tion efficiencies of mutant NRAS and KRAS in immortal, non-transformed Ink4a/Arf-deficient melanocyte

224 ts in 184 (finite life span) and HMT3522 S1 (immortal nonmalignant) HMECs on successive days after se

225 breast premalignancy was investigated using immortal, nontumorigenic MCF-10A cells.

226 was observed in human HCC cells compared to immortal normal hepatocytes.

227 e settings, it is sufficient to render cells immortal or induce oncogenic transformation.

228 ublished studies have almost invariably used immortal or tumorigenic cell lines to study Rho GTPase f

229 rst time that there are divergent mortal and immortal pathways for oral SCC development via intermedi

230 ctivated transfected killer (ATAK) cells are immortal phagocytes transfected with a luminescence repo

231 ase action at telomeres is essential for the immortal phenotype of stem cells and the aberrant prolif

232 barrier that inhibits the acquisition of an immortal phenotype, a critical feature in tumorigenesis.

233 ration site in CRL2504 cells, reverted their immortal phenotype.

234 to yield cell populations culminating in the immortal phenotype.

235 ve conditionally immortal cells to the fully immortal phenotype.

236 t cells overcome senescence and switch to an immortal phenotype.

237 elomere length, created telomerase-positive, immortal populations with varying average telomere lengt

238 hypermethylation were present in all of the immortal PPOLs and occurred at high frequency in the imm

239 ifferences in mtDNA among normal stem cells, immortal/preneoplastic cells, and tumorigenic cells.

240 netically related pre-crisis cells and their immortal progeny.

241 Here, we demonstrate that E2a/Pbx1 induces immortal proliferation of stem cell factor (SCF)-depende

242 intact repair capacity is not essential for immortal proliferation.

243 CER is unchanged by Ad.mda-7/IL-24 in normal immortal prostate cells, whereas Ad.mda-7 down-regulates

244 -regulated in many cancers and can transform immortal rodent fibroblasts when slightly overexpressed.

245 LOH of D6S1045 was found in 2/9 immortal SCC lines and was part of a minimally deleted r

246 niques showed that development of mortal and immortal SCCs involves distinct transcriptional changes.

247 ion analysis of the introduced chromosome in immortal segregants narrowed the candidate interval to 2

248 Deletion analysis of immortal segregants using polymorphic markers revealed t

249 The immortal SHP-/- fibroblasts displayed characteristics of

250 B-crystallin-/- cells were shown to be truly immortal since they have been passaged for more than 100

251 challenge the concept of the stem cell as an immortal, slow-cycling, asymmetrically dividing cell.

252 ider the zygote to be a human person with an immortal soul.

253 epithelial cells from the nonimmortal to the immortal state as well as from the immortal to the ancho

254 e and more consistent with niche rather than immortal stem cell lineages.

255 expected if crypts were maintained by single immortal stem cells.

256 The immortal strand hypothesis posits that the propensity of

257 not been documented in any tissue, and the 'immortal strand hypothesis' has not been tested in a sys

258 We test the 'immortal strand hypothesis', which predicts that during

259 We aimed to demonstrate immortal strand segregation in CPCs and the enhancement

260 s that the combination, in the stem cell, of immortal strands and the choice of death rather than err

261 of CPCs for asymmetric segregation to retain immortal strands is unknown.

262 But a cell that preserves "immortal strands" will avoid the accumulation of replica

263 nal step, termed conversion, to become fully immortal telomerase(+) lines with uniform good growth.

264 duced into early passages of a conditionally immortal telomerase(-) p53(+) HMEC line led to rapid ind

265 and the single Type II EL clone that became immortal, telomerase activities were invariably activate

266 the nine Type II clones that did not become immortal, the telomerase activities were found to be fur

267 Although hybridomas can be immortal, they may depend on a feeder cell layer and may

268 urvival models, these studies have suggested immortal time bias as responsible for the proposed benef

269 ed on unmeasured predictors of the outcome), immortal time bias can and should be avoided by the corr

270 We conclude that immortal time bias cannot account for the risk reduction

271 COPD discharge with two designs free of any immortal time bias in the General Practice Research Data

272 Immortal time bias is introduced by an "anytime-in-pregn

273 The potential for immortal time bias is pervasive in epidemiologic studies

274 Typically, immortal time bias occurs when: 1) Exposure can be initi

275 of exposure to vaccination within pregnancy (immortal time bias), and confounding from baseline diffe

276 sensitivity analyses accounting for possible immortal time bias, as well as a cohort restricted to ea

277 for guarantee-time bias (GTB), also known as immortal time bias, exists whenever an analysis that is

278 regard to exposure status and hence free of immortal time bias, gave a similar association with expo

279 racteristics that influence the magnitude of immortal time bias, so as to aid readers in gauging its

280 To assess the possibility of immortal time bias, the analysis was performed consideri

281 me-varying variable to control for potential immortal time bias, we evaluated the impact of depressio

282 ased on their propensity scores, to mitigate immortal time bias.

283 metastasis diagnosis and might be subject to immortal time bias.

284 dmarked at 30 days post-operatively to avoid immortal time bias.

285 ment exposure during follow-up may result in immortal time bias.

286 of 5.29 years and a landmark design to avoid immortal time bias.

287 oposed as a simpler approach for controlling immortal time bias.

288 the PTDM approach did not adequately address immortal time bias.

289 g quarterly update in matched pairs to avoid immortal time bias.

290 edical management alone after accounting for immortal time bias.

291 use as a time-varying exposure variable), 3) immortal time cohort (misclassifying the time postoperat

292 In cohort studies, "immortal time" bias refers to a portion of time during w

293 were adjusted for important confounders and immortal time.

294 time-dependent Cox model in the presence of immortal time.

295 Even after adjusting for immortal times and indication bias, combined-modality th

296 al to the immortal state as well as from the immortal to the anchorage-independent state.

297 We describe novel effects of p53 loss on immortal transformation, based upon comparison of immort

298 The mortal and immortal tumors are generated in vivo as judged by p53 m

299 Rare immortal variants exhibiting p53 pathway defects arose f

300 The rare immortal variants that arise from these cultures general

301 is during chase to determine distribution of immortal versus newly synthesized strands.

302 These iBMK cells, engineered to be immortal yet nontumorigenic and retaining normal epithel