ライフサイエンスコーパス: immortal

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

2 ughter ensures that the yeast strain remains immortal.

3 for growth and reproduction, and potentially immortal.

4 blasts telomerase-positive and replicatively immortal.

5 ic stem cells age while the germline appears immortal.

6 The germ lineage is considered to be immortal.

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

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

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

10 Unlike conditional immortal 184A1, the HPV16-E7 and SV40T exposed cells wer

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

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

23 ival factors to induce cell death of several immortal and malignant murine and human hematopoietic ce

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 The immortal and totipotent properties of the germ line depe

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

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

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

30 Immortal baby mouse kidney epithelial cells selected in

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

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

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

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

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

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

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

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

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

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

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

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

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

44 We know that collagen is made relatively immortal by being cross-linked and rather impervious to

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

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

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

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

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

66 which induces a senescent-like phenotype in immortal cell lines assigned to complementation group B

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 ds of chromosomes, has been detected in most immortal cell lines including tumor cells, but is low or

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

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

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

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

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

78 23-qter restored cellular senescence in four immortal cell lines, derived from human and rat mammary

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

80 With continued passage, these conditionally immortal cell populations very gradually converted to a

81 With continued passage, the conditionally immortal cell populations very gradually converted to a

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

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

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

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

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

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

88 vity in the proliferation of human tumor and immortal cells by inhibiting TERT function.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

104 howed that continued growth of conditionally immortal cells with critically short telomeres was repea

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

106 In immortal cells, forskolin induced expression of Per1 aft

107 Ras induces malignant transformation in most immortal cells, it has been shown to cause a senescence-

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

133 Immortal DNA strands inherited through asymmetric chroma

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

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

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

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

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

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

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

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

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

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

144 TSEC culture and techniques for establishing immortal FTSEC lines.

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

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

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

148 has two cell types: mortal somatic cells and immortal germ cells.

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

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

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

152 Reversion to immortal growth could occur due to inactivation of the s

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

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

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

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

157 ns and individual subclones of conditionally immortal HMEC line 184A1 showed that continued growth of

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

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

160 Immortal HMEC that have both overcome replicative senesc

161 s remained comparable in finite lifespan and immortal HMEC.

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

163 The fully immortal HMECs that grew well did not accumulate p57 in

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

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

166 progressive telomere shortening and causing immortal human breast epithelial cells to undergo apopto

167 aromyces are reminiscent of the telomeres in immortal human cell lines and tumors that maintain telom

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

169 nce of cellular senescence over immortality, immortal human cell lines have been assigned to four com

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

171 Immortal human cells maintain telomere length by the exp

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

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

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

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

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

177 Most existing immortal human ovarian surface epithelial cells were ach

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

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

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

181 3 spontaneously emerge from crisis to become immortal in a 3T3 growth protocol, we do not observe any

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

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

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

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

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

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

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

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

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

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

192 MCA-3D mouse immortal keratinocytes growing on fibrillar collagen fai

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

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

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

196 erase in cancer cells necessarily signify an immortal lifespan.

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

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

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

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

201 fferent potencies, isolated as 3 independent immortal lines.

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

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

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

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

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

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

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

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

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

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

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

213 ethylation data were not consistent with the immortal model.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

239 ulations very gradually converted to a fully immortal phenotype of good growth+/-TGFbeta, expression

240 ulations very gradually converted to a fully immortal phenotype of good uniform growth, expression of

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

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

243 to yield cell populations culminating in the immortal phenotype.

244 ve conditionally immortal cells to the fully immortal phenotype.

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

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

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

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

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

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

251 ium to retain the donor chromosome, sporadic immortal revertant clones arose among senescent cells.

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

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

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

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

256 Deletion analysis of immortal segregants using polymorphic markers revealed t

257 The immortal SHP-/- fibroblasts displayed characteristics of

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

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

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

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

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

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

264 The immortal strand hypothesis posits that the propensity of

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

293 nes associated with this transition from the immortal to the malignant phenotype, we employed represe

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

295 vities may greatly accelerate a step in HMEC immortal transformation, conversion, that would be rate-

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

297 Rare immortal variants exhibiting p53 pathway defects arose f

298 The rare immortal variants that arise from these cultures general

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

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