ライフサイエンスコーパス: transformed cell

1 rameters, and the initial state of the first transformed cell.

2 er such regulatory loops operate also in non-transformed cells.

3 mitochondrion-STAT3-dependent pathway in Ras-transformed cells.

4 in the localization of activated Ras in CrkI-transformed cells.

5 h ROS levels and As(3+)-induced apoptosis in transformed cells.

6 single isoleucine at a particular position, transformed cells.

7 significantly increased deformability of the transformed cells.

8 ARPi resistance to AML1-ETO and PML-RARalpha transformed cells.

9 mmune recognition of virally and malignantly transformed cells.

10 inhibitors impacts the metabolic program of transformed cells.

11 Gln may also contribute to redox balance in transformed cells.

12 y regulated erythropoietin expression in the transformed cells.

13 ch p53 prevents the malignant progression of transformed cells.

14 presses apical extrusion of the neighbouring transformed cells.

15 ants, and PTMs in primary, immortalized, and transformed cells.

16 ramatically increased in the cadmium-exposed transformed cells.

17 ys a positive role in the elimination of the transformed cells.

18 olarization and migration in both normal and transformed cells.

19 tes increased nucleotide biosynthesis in Myc-transformed cells.

20 tivity in breast cancer cells but not in non-transformed cells.

21 AtABCG14 localizes to the plasma membrane of transformed cells.

22 ability to recognize and kill neoplastically transformed cells.

23 /2) activity via MKP3 in both cancer and non-transformed cells.

24 occurs preferentially in embryonic cells and transformed cells.

25 ng to measure changes between normal and iAs-transformed cells.

26 e of inhibiting the drug resistance of v-Src-transformed cells.

27 ls, an indication of autophagy deficiency of transformed cells.

28 fically at the interface with Src- or RasV12-transformed cells.

29 lex-forming sequence Pu-27 selectively kills transformed cells.

30 une response against infected or malignantly transformed cells.

31 c-mediated tyrosine phosphorylation in virus-transformed cells.

32 , Nrf2 and p62 are highly expressed in these transformed cells.

33 t viral infections and in the elimination of transformed cells.

34 1 alters levels of these proteins in virally transformed cells.

35 6 oncoprotein, and preferentially killed HPV-transformed cells.

36 promoting optimal cell cycle progression in transformed cells.

37 as NKp30 are involved in the recognition of transformed cells.

38 dose-dependently increased levels of ATF4 in transformed cells.

39 d prevents repression of Wnt target genes in transformed cells.

40 transcription of the IRF4 target BIC in EBV-transformed cells.

41 ability increased by WT IGF1 in vitro in non-transformed cells.

42 expressed on a large panel of the tumor and transformed cells.

43 s constitutively expressed and active in EBV-transformed cells.

44 owth, and cell migration and invasion in HPV-transformed cells.

45 g them ideal candidates for misregulation in transformed cells.

46 rget genes, and cell cycle arrest of MLL-AF6-transformed cells.

47 ed through a c-Src-mediated pathway in virus-transformed cells.

48 first line of defense against pathogens and transformed cells.

49 rly provoked a loss of Tax protein in HTLV-1-transformed cells.

50 n, also recognized latently infected, growth-transformed cells.

51 on sites on IRF4 in Epstein-Barr virus (EBV)-transformed cells.

52 ded considerable proliferative advantages to transformed cells.

53 rophic signal required for this expansion of transformed cells.

54 y contribute to immune surveillance of H-Ras transformed cells.

55 levels-a mechanism that may be exploited by transformed cells.

56 fied in the TbetaRI coprecipitates from HER2-transformed cells.

57 roducts ligand-induced cellular migration in transformed cells.

58 ure and a number of metabolic changes in the transformed cells.

59 reduced the anchorage-independent growth of transformed cells.

60 l role in early host defense to infected and transformed cells.

61 tility, invasive properties, and survival of transformed cells.

62 tumors, according to the stage and origin of transformed cells.

63 vels of RNF31 and LMP1 are correlated in EBV-transformed cells.

64 n of the HPV genome, a common feature of HPV-transformed cells.

65 bility to induce terminal differentiation of transformed cells.

66 ltaneous prediction of effects on normal and transformed cells.

67 after binding stress ligands on infected or transformed cells.

68 fferentiation and pluripotency in normal and transformed cells.

69 n and diminishes IRF4 phosphorylation in EBV-transformed cells.

70 that recognize and lyse virally infected or transformed cells.

71 tic proteins is critical for the survival of transformed cells.

72 nds leads to impaired NK cell recognition of transformed cells.

73 r its cytotoxic activity against malignantly transformed cells.

74 tions, while only C>T/G>A are major types in transformed cells.

75 une responses against virally or malignantly transformed cells.

76 Epstein-Barr virus LMPs) to favor spread of transformed cells.

77 epresents an Achilles' heel in p53-deficient transformed cells.

78 e first line of defense against infected and transformed cells.

79 us oncogenes led to CAS up-regulation in non-transformed cells.

80 ically inhibited growth and proliferation of transformed cells.

81 protein constitutively accumulated in these transformed cells.

82 response to virally infected or malignantly transformed cells.

83 Transformed cells adapt metabolism to support tumor init

84 ranscriptional effector of the ISR, protects transformed cells against anoikis - a specialized form o

85 ls, whereas these increases are not shown in transformed cells, an indication of autophagy deficiency

86 ell invasion and motility phenotypes seen in transformed cells and also highlight an important role f

87 (NK) cells induce apoptosis in infected and transformed cells and are important producers of immunor

88 -124a, is constitutively activated in HTLV-I-transformed cells and ATL cells, and activating STAT3 mu

89 was mediated by Rab11 and Drp1 in viral Src-transformed cells and contributed to the biogenesis of p

90 l known that the immune system can recognize transformed cells and control the initiation and growth

91 cluding natural killer (NK) cells, recognize transformed cells and eliminate them in a process termed

92 effective and efficient system to select for transformed cells and generate transgenic cotton plants.

93 Formin activation impairs novel aspects of transformed cells and informs the development of anti-GB

94 granules to directly kill virus-infected or transformed cells and secrete cytokines to communicate w

95 ly induces apoptosis of SV40 large T-antigen transformed cells and significantly reduces colony forma

96 c reprogramming that are unattainable in non-transformed cells and that cooperate to maximize tumor g

97 ecognize and actively eliminate neighbouring transformed cells and that filamin is a key mediator in

98 ctor-beta-induced cellular senescence in non-transformed cells and that HPV E6/E7 targets Notch1 for

99 th LMP1 and IRF7 in Epstein-Barr virus (EBV)-transformed cells and that LUBAC stimulates linear ubiqu

100 of tumors mediates the interface between the transformed cells and the general microenvironment, incl

101 had limited emphasis on interactions between transformed cells and their neighbors within the epithel

102 In Ras-transformed cells and tumors as well as other cancers, N

103 cancer could be induced by a small number of transformed cells and was not prevented by the presence

104 ome amplification is poorly tolerated by non-transformed cells and, in the absence of selection, extr

105 a significant impact on survival of MLL-AF9-transformed cells, and additional Mll1 loss further redu

106 articles), or within (exosomes) activated or transformed cells, and are involved in intercellular tra

107 targeting virus-infected cells, malignantly transformed cells, and immature dendritic cells.

108 sential for promoting chemoresistance in the transformed cells, and targeting NF-kappaB or VLA-4/VCAM

109 ranslocation of TbetaRI was observed only in transformed cells, and the translocation required import

110 entous networks in the cytoplasm, whereas in transformed cells, apoptin is present in the nucleus and

111 re we demonstrate that ATL-derived or HTLV-1-transformed cells are dependent on continuous Tax expres

112 In the first phase, Elimination, transformed cells are destroyed by a competent immune sy

113 ent studies have shown that certain types of transformed cells are extruded from an epithelial monola

114 bly, we find that although genes specific to transformed cells are highly translated, their translati

115 Interestingly, transformed cells are more prone to adopt this fast migr

116 Transformed cells are naturally susceptible to polioviru

117 We further found that HTLV-I- and Tax-transformed cells are not more susceptible to DNA damagi

118 The vGPCR-transformed cells are sensitive to pharmacologic inhibit

119 Furthermore, NUP98-NSD1-transformed cells are sensitive to small-molecule inhibi

120 We previously reported that while non-transformed cells arrest in the latter portion of G1 upo

121 Moreover, both murine MLL-AF6-transformed cells as well as the human MLL-AF6-positive

122 migratory and invasive properties of arsenic-transformed cells (As-transformed cells) have rarely bee

123 activation is characteristic of mutant FLT3-transformed cells, as well as observed residual Akt acti

124 T3 and forced expression of PDCD4 in arsenic transformed cells (AsT) also inhibited cell proliferatio

125 shRNA-mediated knockdown of YAP1 or SOX9 in transformed cells attenuates CSC phenotypes in vitro and

126 transformed 208F cells, suggesting that JSRV-transformed cells became dependent on Zfp111.

127 The transformed cells become immortalized and display morpho

128 HPOB causes growth inhibition of normal and transformed cells but does not induce cell death.

129 HDAC6 inhibitor blocks growth of normal and transformed cells but does not induce death of normal ce

130 tiveness of DNA-damaging anticancer drugs in transformed cells but not normal cells.

131 y responsive to changes in MDM2 level in non-transformed cells, but not in tumor cells.

132 to those seen when pRB is depleted from non-transformed cells, but that the presence of wild-type p5

133 the nuclear genome occurs in neoplastically transformed cells, but we do not exclude the possibility

134 xploit specific metabolic vulnerabilities of transformed cells by acting on them directly, or may act

135 lular surface for recognition of infected or transformed cells by CD8(+) cytotoxic T lymphocytes.

136 They transformed cells by forming a stable complex with the p

137 or suppressor that prevents the emergence of transformed cells by inducing apoptosis or senescence, a

138 Cytotoxic lymphocytes clear infected and transformed cells by releasing the content of lytic gran

139 ny growth is significantly attenuated in the transformed cells by siRNA transfection specific for Nrf

140 Ras-transformed cells can grow in amino acid-poor environmen

141 different human tissue types, including non-transformed cells (cardiomyocytes and lung fibroblasts)

142 anticancer agents since they readily infect transformed cells compared to normal cells, the former a

143 against FLT3 in proliferation assays of FLT3-transformed cells compared with KIT-transformed cells, s

144 phosphotyrosine in cellular proteins in RSV-transformed cells confirmed that v-Src is a tyrosine kin

145 ls, we found that MVs isolated from onco-Dbl-transformed cells contain a unique signaling protein, th

146 broblast and lymphoblast) revealed that only transformed cells contained some unmethylated 12S rRNA t

147 yte differentiation and that loss of TIG3 in transformed cells contributes to the malignant phenotype

148 ll-of-origin in respect to the properties of transformed cells derived from them.

149 nomous effects, abrogating NF-kappaB in PI3K-transformed cells did not decrease proliferation or indu

150 ancer progression but inhibiting Tet1 in non-transformed cells did not initiate cellular transformati

151 ail-safe mechanism is eventually bypassed by transformed cells, due to ill-defined epistatic interact

152 ficient elimination of surplus, damaged, and transformed cells during metazoan embryonic development

153 In transformed cells, enforced expression of SOCS3 or inter

154 We conclude that transformed cells engage surrounding normal cells as act

155 ncy, whereas depletion of Fzd8 in H-Ras(V12)-transformed cells enhances their tumor initiating capaci

156 air leukemia-initiating activity of PML/RARA-transformed cells ex vivo or in vivo.

157 Many transformed cells exhibit altered glucose metabolism and

158 At all times, the transformed cells exhibited complete dependency on hemat

159 Transformed cells exhibited lower rare mutation frequenc

160 rapy-induced senescence in multiple types of transformed cells exposed to either DNA damaging agents

161 Additionally, although transformed cells express a proneural signature, untrans

162 Transformed cells expressed hallmark vascular endothelia

163 nflammatory cells at cancer initiation, when transformed cells first arise in tissues.

164 drive the segregation and elimination of the transformed cell from the tissue.

165 Stat1 also protects Ras-transformed cells from the genotoxic effects of doxorubi

166 ifferent DNA methylome from that observed in transformed cells from these tissue types, such as rhabd

167 2 induced malignant transformation and these transformed cells gained the characteristics of CSCs by

168 Rapidly proliferating and neoplastically transformed cells generate the energy required to suppor

169 TERT expression promotes oncogene-transformed cell growth by reducing the inhibitory effec

170 gether, this study demonstrates that cadmium-transformed cells have acquired autophagy deficiency, le

171 properties of arsenic-transformed cells (As-transformed cells) have rarely been studied.

172 In neuronal and transformed cells HMGB4 regulated the expression of an o

173 In Ras-transformed cells, however, mTORC1 activity and lysosome

174 ecreased the tumorigenic properties of HBEGF-transformed cells; however, only EGFR was able to rescue

175 ole of key defense mechanisms in maintaining transformed cells in a dormant state.

176 rin-IGF1 receptor (IGF1R) cross-talk) in non-transformed cells in anchorage-dependent conditions.

177 ive oxygen species (ROS) is extremely low in transformed cells in correlation with elevated expressio

178 equired for the proliferation of Hoxa9/Meis1-transformed cells in culture and that loss of C/EBPalpha

179 with a reduction in the proliferation of the transformed cells in culture, suggesting that, at least

180 ted mTurquoise2 marker to precisely identify transformed cells in order to distinguish true negatives

181 evealed that gene expression patterns of HOX transformed cells in vitro are determined by the nature

182 y is the selective replication of viruses in transformed cells in which tumor suppressor function may

183 etabolic switch and dampens the viability of transformed cells indicating that the MnSOD/AMPK axis is

184 protegerin enabled early growth of SS18-SSX2-transformed cells, indicating a paracrine link between t

185 Gln depletion in MYC-transformed cells induces apoptosis through ATF4-depende

186 Conversion of antigens from pathogens or transformed cells into MHC-I- and MHC-II-bound peptides

187 y, but how TGF-beta function is altered in a transformed cell is not fully understood.

188 ral progression of epigenetic alterations in transformed cells is largely unclear.

189 TRAP1 function in mitochondria of normal and transformed cells is more complex than previously apprec

190 ent, KIF2A in untransformed and mutant K-Ras-transformed cells is regulated by ERK1/2.

191 privation causes G1 cell cycle arrest in non-transformed cells, its impact on the cancer cell cycle i

192 1 by transfection of miR-21 mimics into LMP1-transformed cells led to phosphorylase-mediated activati

193 nd by antigen presentation using a Theileria-transformed cell line and autologous T cells from Theile

194 the experimental design that includes a non-transformed cell line and three tumorigenic cell lines,

195 y in cells originated from malignant tumors: transformed cell line of non-cancer origin, HEK293, was

196 In 2001, a transformed cell line RGC-5 was developed from the rat r

197 In a K-ras transformed cell line we experimentally assessed glutami

198 ere obtained for both blood (N = 24) and EBV-transformed cell-line (N = 36) DNA samples from men aged

199 d development is that they rely primarily on transformed cell lines and animal models that substantia

200 iruses because HRV growth is limited in most transformed cell lines and animal models.

201 in (E555K) was stable in patient-derived EBV-transformed cell lines and cell lines transfected with e

202 sine triphosphate (GTP) in untransformed and transformed cell lines and determine this phenomenon dep

203 i in seven diverse cell lines, including six transformed cell lines and human induced pluripotent ste

204 (HDACis) on HIV reactivation in established transformed cell lines and primary CD4(+) T cells.

205 ed to determine how HDACis reactivate HIV in transformed cell lines and primary cells.

206 Here, using both transformed cell lines and primary neurons, we investiga

207 5(-/-)/VpreB1(-/-)/VpreB2(-/-) Abelson virus-transformed cell lines and reconstituted these cells wit

208 EBV(+) lymphomas and transformed cell lines exhibited abundant expression of

209 s, worms, mammalian embryonic stem cells and transformed cell lines have found well-positioned nucleo

210 ssion is downregulated in breast cancers and transformed cell lines making it an attractive marker fo

211 nd effects of TFIIB knockdown in primary and transformed cell lines on cellular functionality and glo

212 ncogenic Ras up-regulates autophagy, and Ras-transformed cell lines require autophagy for mitochondri

213 Several earlier studies in transformed cell lines suggested that normoxic stabiliza

214 o move away from the often nonphysiological, transformed cell lines that have been used for decades i

215 In T cells and transformed cell lines used as model systems, HIV-1 asse

216 Finally, treatment of HTLV-1-transformed cell lines with 17-DMAG suppressed HTLV-1 re

217 HRVs, as they generally replicate poorly in transformed cell lines, and host range restriction preve

218 Compared with other transformed cell lines, cultured iCSCL-10A cells exhibit

219 In these cells and transformed cell lines, depletion of Hili increased leve

220 e why EBV infected blasts go on to establish transformed cell lines, we performed global transcriptom

221 ems with the facile in vitro manipulation of transformed cell lines.

222 ments to localize to virological synapses in transformed cell lines.

223 lity to CD3/28 costimulated T cells and some transformed cell lines.

224 alpha and reduces hypoxic gene expression in transformed cell lines.

225 They are also expressed in many transformed cell lines.

226 ociated with telomere length in DNA from EBV-transformed cell-lines.

227 ls (cardiomyocytes and lung fibroblasts) and transformed cells (LNCaP and MCF-7 cancer cells), as wel

228 mary, the JAK3, Fes and PLD2 interactions in transformed cells maintain PLD2 at an enhanced level tha

229 Because transformed cells may override anoikis and survive after

230 also observed after loss of PKCvarepsilon in transformed cell models.

231 ds expressed by stressed, virus-infected, or transformed cells, most inhibitory receptors engage MHC

232 Infected or transformed cells must present peptides derived from end

233 also found in discrete subpopulations of non-transformed cells neighbouring these pre-neoplastic lesi

234 ector cytokines and kill virally infected or transformed cells, NK cells also exhibit adaptive charac

235 In these transformed cells, no synergy is observed between JAK2 a

236 PRMT5 expression was limited to EBV-transformed cells, not resting or activated B lymphocyte

237 istinct open chromatin loci that reflect the transformed cell of origin and suggest that open chromat

238 istones and their differential expression in transformed cells of the nervous system altered the post

239 Accordingly, the dependence of Ras-transformed cells on free extracellular glutamine for gr

240 llowing introduction of mutant IDH1 into Ras-transformed cells or established glioma cells.

241 gs), or host-derived pAgs that accumulate in transformed cells or in cells exposed to aminobisphospho

242 In prostatic cancer cells, but not in non-transformed cells or in prostate stem cells, we found th

243 ress aberrant cellular growth of potentially transformed cells or is simply a result of IR-induced lo

244 Consequently, Ras-transformed cells override a131-induced growth arrest an

245 In arsenic-induced transformed cells, polycomb group (PcG) proteins, includ

246 the heterogeneity and the plasticity of the transformed cell population are enhanced by exposure to

247 nancies that share in common the presence of transformed cells producing osteoid matrix, even if thes

248 erent 2A(pro) were measured comparatively in transformed cells programed with fluorescent reporter sy

249 The transformed cells proliferate at an increased rate compa

250 cells, also competing processes of partially transformed cell proliferation and differentiation/apopt

251 Knockdown of E1A in virus-transformed cells reduced both beta-TrCP and ubiquitinat

252 e of the hypoxic response in both normal and transformed cells, regulating several key aspects of car

253 RD4 and the effects of BET inhibitors in non-transformed cells remain mostly unclear.

254 For example, the transformed cells remodel their metabolic processes to s

255 ying agents that inhibit the growth of FOXC2-transformed cells represents an attractive approach to i

256 ll death is a hallmark of cancer and renders transformed cells resistant to multiple apoptotic trigge

257 pathway was activated constitutively in KSHV-transformed cells, resulting in chronic induction of IL6

258 extracellular proteins was shown to reduce a transformed cell's dependence on extracellular glutamine

259 Such transformed cells should permit study of the early stage

260 of FLT3-transformed cells compared with KIT-transformed cells, shows no toxicity towards normal huma

261 cy factors resulting from these EBV+, B cell-transformed cell states, we performed parallel genome-wi

262 abolic changes, which may in turn render the transformed cells susceptible to specific assaults in a

263 l death, which is more efficient in oncogene-transformed cells than in normal cells.

264 chromosomal aberrations and the formation of transformed cells that exhibited decreased H4K20me3 and

265 tion and mitochondrial ROS regulation in Ras-transformed cells that is governed by mitochondrial STAT

266 We find that in U2AF35(S34F)-transformed cells the autophagy-related factor 7 (Atg7)

267 cycle arrest response, whereas, in p53-null transformed cells, the absence of arrest enables the los

268 JAK3 and Fes marginally activate PLD2 in non-transformed cells, these kinases greatly enhance (>200%)

269 n treatment suppressed glycolysis in BCR-ABL-transformed cells, these treatments did not induce cell

270 the activity of leukemogenic kinases to kill transformed cells, this approach selectively eliminates

271 is known for its action to selectively kill transformed cells through mechanisms that include increa

272 targeted post-translationally in infected or transformed cells to avoid immune recognition.

273 deficiency, loss of ATM or BRCA1 sensitizes transformed cells to differentiation, suggesting that my

274 pletion of eEF-2K reduced the ability of the transformed cells to proliferate and enhanced the sensit

275 ntercellular communication sets the pace for transformed cells to survive and to thrive.

276 In non-transformed cells, transient activation of the IL6 infla

277 ly, ectopic expression of TRIM37 renders non-transformed cells tumorigenic.

278 TGF-beta1 produced from multiple primary and transformed cell types.

279 to be associated with p53 expression in EBV-transformed cells under physiological and DNA damaging c

280 Here we show that Ras-transformed cells use macropinocytosis to transport extr

281 nate between healthy and virally infected or transformed cells using diverse surface receptors that a

282 This mutation transformed cells via cysteine-mediated intermolecular d

283 ural killer (NK) cells kill virally infected/transformed cells via degranulation of lysosome-related

284 migration of fibroblasts and invasiveness of transformed cells via down-regulation of RhoA activity.

285 resses localized Ras pathway activity in Crk-transformed cells via recruitment and/or activation of R

286 Constitutive activation of this loop in transformed cells was dependent on proteolytic degradati

287 e model, tumor growth of the arsenic-induced transformed cells was dramatically increased.

288 to the final state of differentiation in the transformed cells, we compared the relative tumorigenici

289 y passage Burkitt's lymphoma (BL) tumors and transformed cells, we show that compared with B lymphobl

290 Both HPV-16- and HPV-18-transformed cells were found to be responsive to targete

291 e expression differed between the native and transformed cells were primarily implicated in cell cycl

292 With stably transformed cells which mimic the glyoxylate metabolic p

293 n inhibits the major properties of HER-2/neu-transformed cells, which is inversely modulated by the P

294 n has been demonstrated to specifically kill transformed cells while leaving normal cells unharmed in

295 Our experiments revealed that miR-K10a alone transformed cells with an efficiency similar to that whe

296 we examine the role of mutant IDH1 in fully transformed cells with endogenous IDH1 mutations.

297 Metastatic traits seem to be acquired by transformed cells with progenitor-like cancer-initiating

298 showed that innate immune cells supply early transformed cells with proliferative cues and, by using

299 Treatment of HTLV-1-transformed cells with the HSP90 inhibitor 17-DMAG elici

300 ty and invasive phenotypes characteristic of transformed cells without activation of Src.