ライフサイエンスコーパス: immortalization

1 maintaining telomere integrity and cellular immortalization.

2 perone to promote viral latency and cellular immortalization.

3 he oncogenic steps required for Tax-mediated immortalization.

4 unction is necessary for MLL fusion-mediated immortalization.

5 ration can be an essential step for cellular immortalization.

6 rtance of viral integration site in cellular immortalization.

7 HL2 in telomerase activation during cellular immortalization.

8 d pathways that regulate cellular senescence/immortalization.

9 by cellular adaptation, is required for MEC immortalization.

10 ediated extension of host cell life span and immortalization.

11 ing to progeroid phenotypes to those of cell immortalization.

12 downstream induction of telomerase and cell immortalization.

13 but not sufficient, for spontaneous cellular immortalization.

14 ommon signature characteristic of tumor cell immortalization.

15 1 loss cooperate in pRb inactivation and MEF immortalization.

16 c might be able to substitute for E6 in cell immortalization.

17 nce, and its disruption enhances primary MEF immortalization.

18 molecules, which leads to B-cell growth and immortalization.

19 ymphocyte-specific processes and induce cell immortalization.

20 he p16(INK4a)/Rb pathway is not required for immortalization.

21 is usurped by EBV genes essential for B-cell immortalization.

22 spensable for viral replication and cellular immortalization.

23 lomeres) directly contributes to cancer cell immortalization.

24 pressed in tumor cells and mediates cellular immortalization.

25 feron-alpha/beta receptor (IFNAR) by in vivo immortalization.

26 Rb, INK4a, and ARF) that are associated with immortalization.

27 uestion in the biology of EBV-induced B-cell immortalization.

28 lomerase function, is implicated in cellular immortalization.

29 , suggesting this as a common aspect of cell immortalization.

30 ormal human cells rarely undergo spontaneous immortalization.

31 tinue to proliferate and undergo spontaneous immortalization.

32 iated transition through telomere crisis and immortalization.

33 n and correlates with the timing of cellular immortalization.

34 ction of either gene alone did not result in immortalization.

35 cannot interact with p300 to induce cellular immortalization.

36 gth and is an important determinant for cell immortalization.

37 ting that this regulation is acquired during immortalization.

38 phase, and inactivation of p53 promotes cell immortalization.

39 gulation of hTERT expression during cellular immortalization.

40 tein essential for EBV-mediated human B-cell immortalization.

41 -prone recovery from serum deprivation after immortalization.

42 omere maintenance mechanism (TMM) to support immortalization.

43 ming of pluripotency genes may initiate cell immortalization.

44 lenced p16(INK4a) during telomerase-mediated immortalization.

45 cancers to maintain telomere length for cell immortalization.

46 to cells exposed to oxidative stress during immortalization.

47 is essential for genomic stability and cell immortalization.

48 erived from the human embryo without genetic immortalization.

49 II genes increases reaching a plateau during immortalization.

50 epithelial cells without previous culture or immortalization.

51 understanding of the pathways that attenuate immortalization.

52 lerance and its abrogation leads to cellular immortalization.

53 vation or alternative mechanisms of cellular immortalization; (6) angiogenic activity; and (7) the ab

54 ate of EBV-positive B lymphocytes to undergo immortalization (74% vs 17%).

55 e (LFS) patients during spontaneous cellular immortalization, a necessary step in carcinogenesis.

56 leus as well as the p53 degradation and cell immortalization activities of the protein.

57 Thus, reversible immortalization allows the expansion of human RPTECs, le

58 ucible proteins are associated with cellular immortalization, an important early event in the develop

59 intenance is a requisite feature of cellular immortalization and a hallmark of human cancer.

60 tivation of telomerase occur during cellular immortalization and are maintained in cancer cells.

61 on of several genes previously implicated in immortalization and breast cancer progression.

62 als in somatic cells is critical to cellular immortalization and carcinogenesis.

63 antiapoptotic protein, plays a role in cell immortalization and chemoresistance in a number of human

64 ion, which renders MEFs prone to spontaneous immortalization and confers an early growth advantage th

65 vation by K1 is involved in endothelial cell immortalization and contributes to KSHV-associated tumor

66 ing HCECs as knockdown of KLG regarding both immortalization and down-regulation of the tumor suppres

67 tified universal genes regulating senescence/immortalization and found that the key regulator genes r

68 antigen 3C (EBNA 3C) is essential for B-cell immortalization and functions as a regulator of viral an

69 PMs contribute to tumorigenesis by promoting immortalization and genomic instability in two phases.

70 protein is important for EBV-mediated B-cell immortalization and is a potent gene-specific coactivato

71 rotein 1 (LMP1), is essential for EBV B-cell immortalization and is sufficient to transform rodent fi

72 An improved understanding of cell immortalization and its manifestation in clinical tumors

73 coplasma-mediated promotional effect in cell immortalization and its potential clinical implications

74 strate that, in the context of hematopoietic immortalization and leukemogenesis, individual HOX prope

75 atent antigen EBNA3C is implicated in B-cell immortalization and linked to several B-cell malignancie

76 in this repression, allowing for the classic immortalization and loss of cell contact inhibition seen

77 e mouse TERT protein is sufficient to confer immortalization and maintenance of telomere length and f

78 promoter is a bystander effect of oncogenic immortalization and not likely causal in GC pathogenesis

79 of telomerase has been associated with cell immortalization and oncogenesis.

80 ndependent primary hMEC strains led to their immortalization and preneoplastic transformation.

81 ffected by human papillomavirus type 16/E6E7 immortalization and proinflammatory cytokine stimulation

82 We report herein that sequential immortalization and ras-transformation of mouse fibrobla

83 A second step coincides with immortalization and results in hundreds of additional DN

84 In contrast, following spontaneous immortalization and the loss of functional p53 signaling

85 early region 1A (E1A) protein promotes cell immortalization and transformation by mediating the acti

86 The role of HPV oncogenes in cellular immortalization and transformation has been extensively

87 osis plays an important role in the cellular immortalization and transformation induced by E6 and E7

88 from high-risk HPV types contributes to the immortalization and transformation of cells by multiple

89 Ectopic T antigen expression results in the immortalization and transformation of many cell types in

90 embryonic fibroblasts with respect to their immortalization and transformation properties.

91 tion in vitro, and HTLV-1 has a preferential immortalization and transformation tropism of CD4+ T cel

92 anisms are used by T antigens to induce cell immortalization and transformation.

93 ish that TERT promoter mutations can promote immortalization and tumorigenesis of incipient cancer ce

94 d keratinocytes is not required for inducing immortalization and, more importantly, that irradiation

95 kine that regulates cell proliferation, cell immortalization, and cell death, acting as a key homeost

96 ooperate in promoting pRb inactivation, cell immortalization, and H-ras(V12)/c-myc-induced loss of co

97 inases became required following HPV-induced immortalization, and the requirement for two kinases, SG

98 d chemical compound mediating efficient cell immortalization, and this finding could have wide-rangin

99 to alterations in signaling, proliferation, immortalization, and transformation.

100 ed that it might be involved in cell growth, immortalization, and/or senescence.

101 modulate receptor-mediated effects; 9) cause immortalization; and 10) alter cell proliferation, cell

102 ma pathogenesis, including growth, survival, immortalization, angiogenesis and metastasis.

103 luenced by the genetic lesion that triggered immortalization, as alpha3beta1-dependent fibulin-2 expr

104 nd immortalization of keratinocytes with E7, immortalization assays were performed using specific mut

105 r a 9-week period using in vitro cell growth/immortalization assays.

106 t majority of genes dysregulated during cell immortalization belongs to gene families that converge i

107 t HBZ was not required for in vitro cellular immortalization, but enhanced infectivity and persistenc

108 s competent for viral replication and B-cell immortalization, but quantitative assays showed that clo

109 d the foundation for the field of senescence/immortalization, but were labor intensive and the result

110 with lenti-MnSOD(K122-R) inhibited in vitro immortalization by an oncogene (Ras), inhibited IR-induc

111 portant for both binding KIX and bone marrow immortalization by E2A-PBX1.

112 rate that degradation of p53 is required for immortalization by E6/E7, while increased telomerase act

113 al role for CD40-CD40L interaction in B-cell immortalization by EBV, indicating that LMP1 does not ad

114 is the EBV oncoprotein essential for B-cell immortalization by EBV.

115 ave indicated that EBNA-LP may contribute to immortalization by enhancing EBNA2-mediated transcriptio

116 Although in vitro immortalization by HTLV-I virus is very efficient, we re

117 ole of Dot1 in hematopoietic progenitor cell immortalization by MLL fusion proteins.

118 ed AF9/ENL interacting site is essential for immortalization by MLL-AF9, indicating that DOT1L intera

119 his suggests that miR-155 contributes to EBV immortalization by modulation of NF-kappaB signaling and

120 of p16 is the primary event associated with immortalization by nickel, a human non-genotoxic carcino

121 Using this model, we show that keratinocyte immortalization by p53-null mutation causes a switch in

122 re potent isoform, we show that mPR promotes immortalization by preventing cellular senescence, imped

123 Forced expression of KDM2B promotes immortalization by silencing these miRNAs through locus-

124 c activity in human primary T cells and that immortalization by Tax is rare.

125 in gene expression, and reversal of cellular immortalization by telomerase.

126 Regardless, cell immortalization by the Myc + E7 genes occurred independe

127 The common factor in cell immortalization by the three gene sets (E6 + E7, Myc + E

128 Immortalization by TPMs requires a gradual up-regulation

129 Some human cancer cells achieve immortalization by using a recombinational mechanism ter

130 s can be overcome, a process commonly called immortalization, by the introduction of the catalytic su

131 In cell cultures, the immortalization capacities of APH-2 mutant viruses were

132 ral gene expression, protein production, and immortalization capacity.

133 Upon spontaneous immortalization, Cebpd-deficient fibroblasts acquire tra

134 showed that the BAC-derived virus was B-cell immortalization competent.

135 with successive rounds of cell division, and immortalization correlates with stabilization of telomer

136 the genes and pathways regulating senescence/immortalization could provide novel molecular targets fo

137 Interestingly, an immortalization-defective E6 mutant localized to the hTE

138 An immortalization-defective HPV-18 E6 mutant genome was al

139 B cell immortalization depends on expression of viral latency g

140 e p16INK4A/pRB checkpoint of epithelial cell immortalization does not necessarily lead to centrosome-

141 Despite the lack of immortalization, E6 was functional in the fibroblasts, m

142 ey events of the viral life cycle, including immortalization, episomal maintenance, late promoter act

143 r essential tumor-specific traits, including immortalization, escape from antimitogenic signaling, ne

144 ponding postnatal cell types, and to require immortalization for clonal isolation and expansion, thes

145 This strategy for immortalization has found special utility in the central

146 antigen 3C (EBNA 3C) is essential for B-cell immortalization, has potent cell cycle deregulation capa

147 t are shared with some cancers, most notably immortalization, hyperproliferation, and dissemination.

148 that transition through telomere crisis and immortalization in breast cancer occurs during progressi

149 a novel mesenchymal stem cell origin for ALT immortalization in cell lines and mesenchymal tissues.

150 ely contribute to HVS-mediated lymphoid cell immortalization in culture and lymphoma induction in pri

151 eplication but is required for lymphoid cell immortalization in culture and lymphoma induction in pri

152 eplication but is required for lymphoid cell immortalization in culture and lymphoma induction in pri

153 ced Tax expression, hyper-proliferation, and immortalization in culture.

154 A prerequisite for cellular immortalization in human cells is the elongation of telo

155 This work explores spontaneous immortalization in keratinocytes, derived from two skin

156 on of these same pathways causes spontaneous immortalization in MEFs, and oncogenic transformation by

157 omere function and is considered critical to immortalization in most human cancer cells.

158 serum-containing medium but does not lead to immortalization in the absence of feeder cells.

159 s engineered to express Ndy1 or Ndy2 undergo immortalization in the absence of replicative senescence

160 progenitor cells is relevant to the role of immortalization in the initiation and progression of can

161 myeloid progenitors in vitro, causing their immortalization in the presence of stem cell factor and

162 EBNA-3B has no significant impact on B-cell immortalization in tissue culture, this finding suggeste

163 ient for MLL-AF6 mediated myeloid progenitor immortalization in vitro and short latency leukemogenesi

164 of 707 transcriptional changes accompanying immortalization including reduced p16(INK4A) mRNA.

165 or signaling in primary fibroblasts, whereas immortalization induced by SV40 large T antigen supporte

166 n-Barr virus (EBV) in vitro results in their immortalization into lymphoblastoid cell lines (LCLs); t

167 With ionizing radiation, immortalization is invariably accompanied by efficient b

168 The up-regulation of survivin during immortalization likely contributes to the vulnerability

169 pes of human cancer and associates with cell immortalization, malignant transformation, and chemoresi

170 Agents that inhibit cell immortalization may have utility for novel molecular che

171 genetic changes that occur during senescence/immortalization may help elucidate crucial events that l

172 lly expressed to construct an ACOO-specific 'immortalization network' comprised of 40 genes, one of w

173 the oncogenic agents alone in the absence of immortalization, nor by expression of exogenously introd

174 rather, pRb loss leads to the expansion and immortalization of an immature progenitor pool character

175 nerated by means of ex vivo immunization and immortalization of antigen-specific human B cells for th

176 eping Beauty transposons in NSCs induced the immortalization of astroglial-like cells, which were the

177 BNA2 and is important for Epstein-Barr virus immortalization of B cells.

178 (EBNA2) is a key latency gene essential for immortalization of B lymphocytes and transactivation of

179 signaling pathways and is essential for EBV immortalization of B lymphocytes.

180 ptional regulator essential for EBV-mediated immortalization of B lymphocytes.

181 of both copies of SEN16 is required for the immortalization of breast epithelial cells at an early s

182 T-antigen immortalization of cells allowed cell growth.

183 lomeres, appears to provide a barrier to the immortalization of cells and development of cancer.

184 ular events leading to transformation and/or immortalization of cells have an impact on their relativ

185 of hTERT results in telomere lengthening and immortalization of D17 without loss of functional wild-t

186 Here we apply this strategy during Ras(V12) immortalization of Drosophila embryonic cells, a phenome

187 may be a critical factor facilitating hTERT immortalization of epithelial cells.

188 er in human old versus young fibroblasts and immortalization of fibroblasts with telomerase resulted

189 Our model is based on (i) immortalization of FTSECs isolated from primary samples

190 st that KLB is an important regulator in the immortalization of HCECs by facilitating FGF19 growth fa

191 omerase reverse transcriptase (hTERT) in the immortalization of HCECs.

192 sis can also identify genes that promote the immortalization of hematopoietic cells, which normally h

193 rs in the MLL fusion protein MLL-AF9 blocked immortalization of hematopoietic progenitors.

194 Here we show that immortalization of HFK with HPV-16 or 18 causes down-reg

195 viral genes essential for the infection and immortalization of human B cells by the cancer-associate

196 way induces B cell proliferation in vivo and immortalization of human B cells in vitro.

197 n 3C (EBNA-3C) is essential for EBV-mediated immortalization of human B lymphocytes and regulates bot

198 Immortalization of human epithelial cells involves both

199 The role of this pathway in immortalization of human epithelial cells is not clear.

200 quired for the conditional reprogramming and immortalization of human epithelial cells.

201 are proposed to contribute to the efficient immortalization of human epithelial cells: the degradati

202 r, it cannot substitute the T antigen in the immortalization of human fibroblasts, indicating that it

203 e E7 protein, is essential for the efficient immortalization of human foreskin keratinocytes (HFKs).

204 ng-defective HPV16 E6 mutations that induced immortalization of human mammary epithelial cells.

205 shows that up-regulation of survivin during immortalization of human myofibroblasts is an indirect c

206 Here, we show the immortalization of human prostate epithelial cells (HPrE

207 lear antigen 3C (EBNA3C) is critical for EBV immortalization of infected B lymphocytes and can coacti

208 hat results in successful transformation and immortalization of infected cells.

209 6 are required to allow bypass of crisis and immortalization of keratinocytes with E7, immortalizatio

210 olecule can substitute for E6 in cooperative immortalization of keratinocytes with E7.

211 ) E6 and E7 oncoproteins are critical to the immortalization of keratinocytes.

212 se promoter, potentially contributing to the immortalization of KSHV-infected cells.

213 is by their nature could also be involved in immortalization of leukemic stem cells, and thus represe

214 antly inhibited the frequency of spontaneous immortalization of LFS breast epithelial cells compared

215 eration of primary MECs and results in rapid immortalization of MECs in vitro relative to wild-type c

216 n either premature senescence or spontaneous immortalization of MEF cells.

217 Loss of Rassf5 also resulted in spontaneous immortalization of MEFs at earlier passages than the con

218 nduces premature senescence, and counteracts immortalization of MEFs driven by KDM2B.

219 Resveratrol results in immortalization of mixed progenitor cells with mutant p5

220 Telomerase is essential for immortalization of most human cancer cells.

221 Transduction with mutant Setbp1 led to the immortalization of mouse myeloid progenitors that showed

222 he ARF-p53 tumor suppressor pathway leads to immortalization of murine fibroblasts.

223 reduction by shRNA impairs AML1/ETO-induced immortalization of murine progenitors.

224 As SIPS/OIS bypass is a prerequisite for the immortalization of normal diploid human epithelial cells

225 Interestingly, immortalization of postselection cells using various met

226 EBNA-2 is essential for EBV-mediated immortalization of primary B lymphocytes.

227 o p53 inactivation during transformation and immortalization of primary cells.

228 e been identified as rate-limiting steps for immortalization of primary human epithelial cells.

229 Telomerase activation is critical for the immortalization of primary human keratinocytes by the hi

230 ace expression and to the efficient in vitro immortalization of primary human T cells to interleukin-

231 ation causes constitutive PKA activation and immortalization of primary mouse embryonic fibroblasts (

232 loyed strategy is based on carcinogen-driven immortalization of primary mouse embryonic fibroblasts a

233 in foamy viral vectors caused extremely low immortalization of primary mouse hematopoietic stem/prog

234 Tax-1 PBM in HTLV-induced proliferation and immortalization of primary T cells in vitro and viral su

235 nvestigate the contribution of Rex in HTLV-1 immortalization of primary T cells in vitro and viral su

236 d the contribution of HBZ to HTLV-1-mediated immortalization of primary T lymphocytes in vitro and HT

237 ctional role of APH-2 in the HTLV-2-mediated immortalization of primary T lymphocytes in vitro and in

238 -interacting protein (Tip), required for the immortalization of primary T lymphocytes, targets cellul

239 Similarly, spontaneous immortalization of progerin-expressing cultured keratino

240 frequent event during transformation and/or immortalization of rodent cells.

241 Thus, telomerase expression and consequent immortalization of skin fibroblasts do not alter nucleot

242 Although we focus here on telomerase immortalization of spinal neural progenitors, this is a

243 ctivities, a subset of which likely leads to immortalization of T cells.

244 data with the annotated genome sequence; (3) immortalization of the genome; (4) ability to generate t

245 The immortalization of these cell lines with the expression

246 isolated from a myasthenia gravis patient by immortalization of thymic B cells using Epstein-Barr vir

247 eral miRNAs from early proliferation through immortalization; oncogenic miRNAs were induced, and tumo

248 ints is essential in the process of cellular immortalization, one of the components of the transforma

249 read, which typically does not result in the immortalization or enhanced growth of infected epithelia

250 higher level distribution is not altered by immortalization or long-term culture.

251 odologies to produce hmAbs, including B-cell immortalization or phage display, can be used to isolate

252 tability, which in turn leads to spontaneous immortalization or premature senescence of Dnmt3b-defici

253 However, upon immortalization or tumorigenic transformation of mouse f

254 samples varying for telomerase activity and immortalization parameters.

255 al DNA methylation changes regardless of the immortalization pathway.

256 Ink4a/Arf locus and contributing to the Ndy1 immortalization phenotype.

257 Elevated T-SCE was associated with greater immortalization potential and resultant tumors maintaine

258 iated transcriptional up-regulation and cell immortalization potential in vivo.

259 o MLL-ENL blocks the hematopoietic stem cell immortalization potential of the fusion protein in seria

260 up differences are due to differences in the immortalization procedures used for each group or reflec

261 and TD skin fibroblasts, and (in contrast to immortalization procedures using viral oncogenes) did no

262 f viral and cellular genes important for the immortalization process.

263 ne demonstrated viral replication and B-cell immortalization properties comparable to those of the na

264 ction, the details of its activity on T cell immortalization remain elusive.

265 n-Barr virus (EBV) EBNA-LP protein to B-cell immortalization remains an enigma.

266 plication and drive T-cell proliferation and immortalization remains poorly understood.

267 Self-renewal after immortalization requires continuous Setbp1 expression.

268 wth whereas abrogation of senescence through immortalization results in loss of such tumor promoting

269 Immortalization (senescence bypass) is a critical rate-l

270 A predominant feature of this immortalization signature (ImmSig) was the significant o

271 essential, it is not sufficient for cellular immortalization, suggesting that additional alterations

272 Immortalization, the acquisition of the ability to proli

273 To attempt immortalization, the cells were exposed to retroviral hu

274 se catalytic subunit hTERT leads to cellular immortalization, the endogenous hTERT gene is likely con

275 s and/or epigenetic alterations required for immortalization to occur.

276 an significantly promote, MLL fusion-induced immortalization/transformation of normal mouse bone marr

277 pendently influences the preferential T cell immortalization tropism irrespective of the envelope cou

278 HTLV-1/SU2 shifted the CD4(+) T cell immortalization tropism of wild-type HTLV-1 (wtHTLV-1) t

279 .195) resulted in a shift to a CD8(+) T cell immortalization tropism preference.

280 s involved in determining this CD4(+) T cell immortalization tropism.

281 domains that are involved in determining the immortalization tropism.

282 somal ends, and its crucial role in cellular immortalization, tumorigenesis, and the progression of c

283 in TD cells was significantly improved after immortalization (up to 40% of normal values).

284 egulates PGM, mutation of p53 can facilitate immortalization via effects on PGM levels and glycolysis

285 thelial cell transformation without previous immortalization via genetic influences such as SV40 T-an

286 etween genes that function during astroglial immortalization vs. later stages of tumor development.

287 Immortalization was accompanied by activation of the JAK

288 The transition to cellular immortalization was accompanied by markedly increased ex

289 nhibitor exhibited an extended lifespan, and immortalization was facilitated following transduction t

290 tial role EBNA-LP has in EBV-mediated B-cell immortalization, we asked whether it is a global or gene

291 proposed to be necessary for epithelial cell immortalization, we sought to further characterize the r

292 d/continuous telomerase activity may promote immortalization when differentiation and/or senescent pa

293 l promoters for genes that are necessary for immortalization when it is bound to a cluster of 20 cogn

294 d from tumors or cultured cells selected for immortalization which may have missing or mutated modula

295 n is up-regulated during telomerase-mediated immortalization, which occurs at a relatively early stag

296 s proliferate faster and undergo spontaneous immortalization while retaining both Arf and p53.

297 cking alternative epigenetic routes for cell immortalization will be paramount for understanding cruc

298 e have already observed high-efficiency cell immortalization with the hTERT + E7 or E6 mutant (p53 de

299 iferative capacity and resulted in efficient immortalization without detectable cell crisis.

300 atocytes are amenable to telomerase-mediated immortalization without inducing a transformed phenotype