ライフサイエンスコーパス: cell transformation

1 g the p62-NRF2 axis, resulting in epithelial cell transformation.

2 lying additional GR loss as a consequence of cell transformation.

3 (PTC) and is causally involved in malignant cell transformation.

4 in related states of post-germinal centre B-cell transformation.

5 suppressors by regulating the occurrence of cell transformation.

6 ell-to-cell variability) are able to trigger cell transformation.

7 with ST and is required for ST-PP2A-induced cell transformation.

8 SRPK1 in mouse embryonic fibroblasts induces cell transformation.

9 inflammatory signal (Src) needed to promote cell transformation.

10 s of STAT3, which is a crucial activator for cell transformation.

11 on of KRAS and was required for KRAS-induced cell transformation.

12 sitive feedback loop linking inflammation to cell transformation.

13 which leads to an epigenetic switch allowing cell transformation.

14 , E6 and E7, which work together to initiate cell transformation.

15 ar link between the normal GC response and B-cell transformation.

16 -Pbx1 to activate target genes and to induce cell transformation.

17 t have been shown to contribute to oncogenic cell transformation.

18 ical feature of cancer and a driver of tumor cell transformation.

19 into the mechanistic basis of Meq-dependent cell transformation.

20 ral replication but also contributes to host cell transformation.

21 scence (OIS), thereby facilitating oncogenic cell transformation.

22 Fer in PDGF-BB-induced STAT3 activation and cell transformation.

23 in MCV DNA replication as well as sT-induced cell transformation.

24 for understanding crucial events leading to cell transformation.

25 y help elucidate crucial events that lead to cell transformation.

26 Pin1 to induce centrosome amplification and cell transformation.

27 partial loss of PP2A function contributes to cell transformation.

28 it impaired the efficiency of EBV-induced B cell transformation.

29 ta receptor, causing receptor activation and cell transformation.

30 sms for HER2-induced sustained signaling and cell transformation.

31 nvasion in a manner essential for neoplastic cell transformation.

32 n target, and both were reported to regulate cell transformation.

33 IAH2, thus contributing to breast epithelial cell transformation.

34 icted a tumor-suppressor role for RUNX1 in T cell transformation.

35 tor of IKKepsilon-induced mammary epithelial cell transformation.

36 on for the regulation of gene expression and cell transformation.

37 ced AP-1 activity and anchorage- independent cell transformation.

38 c-Fos, which regulates anchorage-independent cell transformation.

39 onsible for maintenance of viral latency and cell transformation.

40 ts contributed to an elevation of IR-induced cell transformation.

41 ngth SHIP significantly reduces Ab-MLV pre-B-cell transformation.

42 Pin1 to induce centrosome amplification and cell transformation.

43 UP98-HOXA9 in transcriptional regulation and cell transformation.

44 otein-1 activity, which is a major driver in cell transformation.

45 d opposes oncogenic tyrosine kinase-mediated cell transformation.

46 ells, ultimately contributing to efficient T cell transformation.

47 g by using mutant H3S28A reduced EGF-induced cell transformation.

48 nscription through Brf1 and TBP and promotes cell transformation.

49 nd pathways perturbed by SV40ST during human cell transformation.

50 s is mediated by Karyopherin proteins during cell transformation.

51 PK) pathway plays a major role in neoplastic cell transformation.

52 an important role in EGF-induced neoplastic cell transformation.

53 in genome instability and is associated with cell transformation.

54 d replaced the expression of SV40ST in human cell transformation.

55 EGFR-mediated tumor migration, survival and cell transformation.

56 motility disorders and intestinal epithelial cell transformation.

57 essed in human cancers and is induced during cell transformation.

58 crucial roles in both virus replication and cell transformation.

59 cted efficiently with FOXK1/K2 and inhibited cell transformation.

60 tical role in proliferation, cell cycle, and cell transformation.

61 ng of how cancer cell exosomes contribute to cell transformation.

62 netic changes that lead to ovarian carcinoma cell transformation.

63 lation within the nucleus, thereby promoting cell transformation.

64 ole in EGF-stimulated cell proliferation and cell transformation.

65 m to induce c-Myc, which may be critical for cell transformation.

66 the essential latent antigens for primary B-cell transformation.

67 e-limiting for expression of an oncogene and cell transformation.

68 with H-RasV12 or c-Myc to promote fibroblast cell transformation.

69 lymphoproliferative disorders from MF large-cell transformation.

70 d Drak cooperated with EGFR to promote glial cell transformation.

71 sform cells alone or to act as a promoter of cell transformation.

72 ression from earliest pro-B-cell stages in B-cell transformation.

73 ly might affect development or contribute to cell transformation.

74 k essential signalling pathways and foster T cell transformation.

75 fibroblasts and recapitulates early steps of cell transformation.

76 with RUNX3-a protein induced by EBV during B cell transformation.

77 iomarkers of early fallopian tube epithelial cell transformation.

78 n in vitro model of human mammary epithelial cell transformation.

79 how the number of partial EMT states affects cell transformation.

80 in assembly in FA-mediated transcription and cell transformation.

81 process involved in Cryptosporidium-induced cell transformation.

82 cancer, and some of them have been linked to cell transformation.

83 utations, indicating that RUNX1 suppresses T-cell transformation.

84 lls increases cell proliferation and induces cell transformation.

85 n of the Musashi2 variant 2 isoform promoted cell transformation.

86 CYSLTR1 and CYSLTR2) contribute to malignant cell transformation.

87 nts of these GTPases is sufficient to induce cell transformation.

88 g myelomagenic mutations that promote plasma cell transformation.

89 nizes ligands whose expression is induced by cell transformation.

90 and represents an ideal model for study of T-cell transformation.

91 t genetic and epigenetic etiologies for GC B-cell transformation.

92 t, which became silenced during EBV-driven B-cell transformation.

93 ut is not required for MCV sT-induced rodent cell transformation.

94 h inhibits EBV infection and virus-induced B-cell transformation.

95 uppressor role by interfering with malignant cell transformation.

96 ion and thereby regulates macrophage to foam cell transformation.

97 ted tumor-stage MF,with no evidence of large-cell transformation.

98 Tax and the antisense protein APH-3 promote cell transformation.

99 es, we found one squamous cell and two small-cell transformations.

100 e in IFN-gamma-induced inflammation and foam cell transformation, a better understanding of the mecha

101 is stably expressed in Src-Y527F-transformed cells, transformation activities are blocked, indicating

102 could not be phosphorylated antagonized the cell transformation activity of MCV sT.

103 3+, NANOG+ and OCT3/4+ liver progenitor/stem cell transformation, along with inactivation of transfor

104 tance of the NOTCH1-MYC regulatory axis in T cell transformation and as a therapeutic target in T-ALL

105 trigger its nuclear accumulation leading to cell transformation and cancer.

106 anistic link between oncogene E6/E7-mediated cell transformation and circadian (BMAL1) disruption.

107 ferase activity, promotes mammary epithelial cell transformation and cooperates with H-RasV12 or c-My

108 at they cooperate to enhance virus-induced B cell transformation and decrease the antigenic load of v

109 sting that other viral proteins are key to T-cell transformation and development of adult T-cell leuk

110 n epigenetically mediated miRNA control in B cell transformation and DLBCL.

111 anscription factor that promotes oncogenic B-cell transformation and drug resistance in B-ALL.

112 eal an important role for RUNX3/CBF during B cell transformation and EBV latency that was hitherto un

113 of Kras activation and Pten deletion during cell transformation and epithelial-to-mesenchymal transi

114 oduction of let-7 microRNAs was critical for cell transformation and expansion of prostate CSC.

115 sion adapter protein paxillin contributes to cell transformation and extends our knowledge of the div

116 We show that GWL overexpression promotes cell transformation and increases invasive capacities of

117 cell transformation, enhances MycWT-induced cell transformation and increases the size of MycWT-indu

118 gly activated mTOR/p70S6K signaling, induced cell transformation and invasion, and remarkably, caused

119 ne KLF5 loss as a critical event in squamous cell transformation and invasion.

120 oncogenic transcription factor MYC induces B-cell transformation and is a driver for B-cell non-Hodgk

121 and apoptosis, which must be overcome during cell transformation and kept at bay throughout all stage

122 FTO enhances leukemic oncogene-mediated cell transformation and leukemogenesis, and inhibits all

123 regulatory loop that positively influences B cell transformation and lymphoma progression.

124 clude that PRMT5 is critical to EBV-driven B-cell transformation and maintenance of the malignant phe

125 non-Ig sites in the genome, which initiates cell transformation and malignancies.

126 MP1) is important for EBV contributions to B cell transformation and many EBV-associated malignancies

127 arity are closely associated with epithelial cell transformation and metastatic capacity.

128 nexpected discovery that E1A also suppresses cell transformation and oncogenesis.

129 n-Barr virus, is required for EBV-mediated B cell transformation and plays a significant role in the

130 LK stimulates signaling pathways that induce cell transformation and promote tumor growth.

131 Oncogenic Ras induces cell transformation and promotes an invasive phenotype.

132 operation between JAK1 and JAK3 mutants in T-cell transformation and represent a new mechanism of acq

133 Age at diagnosis, large cell transformation and secondary bacterial infection we

134 rate a novel role for H2B phosphorylation in cell transformation and show that H2BS32 phosphorylation

135 PL2 was found to antagonize oncogene-induced cell transformation and survival through a pathway invol

136 l downstream mediator for Gli-dependent PDAC cell transformation and survival.

137 Suz12 cooperates with mutant JAK3 to drive T-cell transformation and T-ALL development.

138 naling plays an important role in neoplastic cell transformation and that eriodictyol is a novel natu

139 th loss of Pten is enough to promote ovarian cell transformation and that we have developed a model s

140 eals a novel function of CDK2 in EGF-induced cell transformation and the associated signal transducti

141 eveal transcriptional parallels between germ cell transformation and the generation of iPS cells and

142 t normal human cells, can initiate malignant cell transformation and these transformed cells formed t

143 reases Pol III gene transcription to promote cell transformation and tumor formation in vitro and in

144 sly shown that LOX-PP inhibits breast cancer cell transformation and tumor formation, but mechanisms

145 ge and acts in parallel with p53 to suppress cell transformation and tumor formation.

146 ncrease in translational capacity to promote cell transformation and tumor formation.

147 , WRC disruption also promoted FAK-dependent cell transformation and tumor growth in vivo.

148 ar target genes, which are rate limiting for cell transformation and tumor growth.

149 of embryonic signaling pathways might drive cell transformation and tumor progression in adult tissu

150 biological functions of TIP-1, especially in cell transformation and tumor progression, are still con

151 ar response to hypoxia, which contributes to cell transformation and tumor progression, is a prominen

152 rfering with oncogenic signals driving liver cell transformation and tumor progression, thus providin

153 ic signals, thereby attenuating premalignant cell transformation and tumor progression.

154 uppressor p53 is a key protein in preventing cell transformation and tumor progression.

155 molybdenum but not silica, similarly induced cell transformation and tumor promotion, suggesting the

156 Here, we show that HSF1 is required for the cell transformation and tumorigenesis induced by the hum

157 th inhibition of PDCD4, and caused malignant cell transformation and tumorigenesis of BEAS-2B cells.

158 itive HTLV-1-infected cells and Tax-mediated cell transformation and tumorigenesis.

159 ur in many cancer types and are critical for cell transformation and tumorigenesis.

160 death 4 (PDCD4) in arsenic induced malignant cell transformation and tumorigenesis.

161 Hotspot mutations of Ras drive cell transformation and tumorigenesis.

162 scence and a stem cell-associated SASP drive cell transformation and tumour initiation in vivo in an

163 established model for tumor promoter-induced cell transformation and was used to study the function o

164 ease in our understanding of cell signaling, cell transformation, and cell-cell interactions; gene ex

165 A significantly inhibits MLL-fusion-mediated cell transformation, and coexpressed PBX3 exhibits a sig

166 ion activates the PI3K/AKT pathway, enhances cell transformation, and commonly occurs in human melano

167 rplasia, eosinophil infiltration, less large-cell transformation, and favorable prognosis in MF cases

168 ested, four (stage IV, age > 60 years, large-cell transformation, and increased lactate dehydrogenase

169 nitiate chromosomal instability, DNA damage, cell transformation, and malignancy.

170 1 is sufficient to promote mmp15 expression, cell transformation, and mesenchymal cell migration and

171 the actin cytoskeleton, gene transcription, cell transformation, and other processes that are known

172 YC interaction is necessary for C1/M2-driven cell transformation, and the C1/M2 transcriptional signa

173 nd contact-site mutants share a property for cell transformation, and the domains critical for wild-t

174 COP1 expression promoted cell proliferation, cell transformation, and tumor progression, manifesting

175 red for ERBB2 mutant-induced cell signaling, cell transformation, and tumorigenesis.

176 en implicated in KSHV-associated endothelial cell transformation, angiogenesis, and KS-induced malign

177 e molecular genetic mechanisms that underlie cell transformation are less clear.

178 cell migration but more dramatic effects on cell transformation as assessed by growth in soft agar.

179 of gene expression, cell proliferation, and cell transformation, as well as cancer development.

180 nd inhibition of in vitro characteristics of cell transformation, as well as in vivo tumor growth.

181 on, we utilized the classic two-step NIH/3T3 cell transformation assay and observed that exosomes iso

182 Transcriptome analyses and cell transformation assays further establish a significa

183 id, in vitro pull-down and transient tobacco cell transformation assays.

184 herefore define not only new mechanisms of B-cell transformation but also clinically important subgro

185 IR inactivation in vitro not only prevented cell transformation but also reversed the keratinocyte-t

186 amma-PP2A can inhibit cell proliferation and cell transformation by an unknown mechanism.

187 In vitro and in vivo B-cell transformation by BCR-ABL requires the downregulati

188 trains that confer high cancer risk mediates cell transformation by deregulating host cellular proces

189 s early region 1A (E1A) oncoprotein mediates cell transformation by deregulating host cellular proces

190 2 transcription factor plays a key role in B cell transformation by EBV and defines the two EBV types

191 t subsets of B-cell neoplasms, which promote cell transformation by elevating the global level of H3K

192 e with ROS production in 32D cells inhibited cell transformation by FLT3 ITD in a DEP-1-dependent man

193 1 oxidation as a novel event contributing to cell transformation by FLT3 ITD.

194 ore, could be essential for inducing oxyphil cell transformation by increasing mtDNA/mitochondrial bi

195 ransmitted to other retroviruses and produce cell transformation by itself.

196 wn of endogenous Zfp111 caused a decrease in cell transformation by JSRV Env, while overexpression of

197 oncoprotein, CagA causes gastric epithelial cell transformation by promoting an epithelial-to-mesenc

198 ill lacking to show that Pin1 contributes to cell transformation by Rel/NF-kappaB.

199 y the human c-Rel protein and also increased cell transformation by the potent viral Rel/NF-kappaB on

200 Cell transformation by the v-rel oncogene is mediated by

201 ion is thought to be an important step for T-cell transformation caused by viral infection.

202 2mut) and not wild-type DNMT3A promoted TF-1 cell transformation characterized by cytokine-independen

203 Malignant cell transformation commonly results in the deregulation

204 ful B cell differentiation and prevention of cell transformation depends on balanced and fine-tuned a

205 However, the specific mechanisms of T cell transformation downstream of TLX1 remain to be eluc

206 regulation during embryonic development and cell transformation during oncogenesis share common sign

207 show that Nol5a is necessary for Myc-induced cell transformation, enhances MycWT-induced cell transfo

208 gnaling pathway is necessary, independent of cell transformation, for herpesvirus pathogenesis and th

209 recent studies have demonstrated the direct cell transformation from chondrocytes into bone cells in

210 Epithelial cell transformation has been demonstrated in numerous an

211 a molecular pathway linking inflammation to cell transformation has been discovered.

212 option for type 1 diabetes, pancreatic islet cell transformation has been hindered by immune system r

213 gnaling pathways essential to Myc-mediated B-cell transformation have not been fully elucidated.

214 Kepsilon substrates necessary for regulating cell transformation have not been identified.

215 talizes primary cells and mediates oncogenic cell transformation in cooperation with other viral or c

216 innate immune responses and can also promote cell transformation in culture.

217 voir in vivo and act as cellular targets for cell transformation in humans.

218 ith the inactivation of DLC1 to give rise to cell transformation in MEFs, and the identified genes ar

219 SOD impacts the chain of events that lead to cell transformation in pathologically normal epidermal c

220 ic leukemia for 29 and 7 months before large-cell transformation in the eye.

221 nes represent the molecular basis of oxyphil cell transformation in the parathyroids.

222 pression and EGFR overexpression for Schwann cell transformation in vitro (immortalized human Schwann

223 e, and examined the hallmarks of mesothelial cell transformation in vitro and in vivo.

224 y synergistic effect with HOXA9 in promoting cell transformation in vitro and leukemogenesis in vivo.

225 5 significantly inhibits MLL-fusion-mediated cell transformation in vitro and leukemogenesis in vivo.

226 only EBNA3B is completely dispensable for B cell transformation in vitro.

227 rkedly impaired in their ability to induce B cell transformation in vitro.

228 However, the role of Dnmt3a in T-cell transformation in vivo is poorly understood.

229 alized human cells was sufficient to promote cell transformation in vivo.

230 irus 40 large T antigen (TAg) contributes to cell transformation, in part, by targeting two well-char

231 SCD1 is found upregulated upon renal cell transformation indicating that its activity, while

232 sent study explored a potential mechanism of cell transformation induced by arsenic exposure.

233 the stability of histone H2AX and prevented cell transformation induced by EGF.

234 Our data show that cell transformation induced by endomembrane-restricted o

235 mutant 4E-BP1.S83A partially reverses rodent cell transformation induced by Merkel cell polyomavirus

236 mb proteins, BMI1 and SUZ12 are required for cell transformation induced by organic arsenic exposure.

237 in cells and severely affects chemotaxis and cell transformation induced by PI3Kgamma overexpression.

238 tin assembly represents a novel mechanism of cell transformation induced by the environmental and occ

239 2 plays a critical role in proliferation and cell transformation induced by tumor promoters, such as

240 EBV-mediated B cell transformation involves large changes in gene expre

241 idues serine-17 and tyrosine-416 and mammary cell transformation is driven through a mechanism involv

242 virus-encoded E6 oncoproteins contribute to cell transformation is restricted to human papillomaviru

243 (JSRV) is an oncogene, but its mechanism of cell transformation is still unclear.

244 How this haloacetonitrile promotes malignant cell transformation is unknown.

245 e diversity and potency of TFs as drivers of cell transformation justifies a continued pursuit of TFs

246 ignaling, with PLA2R1-mediated inhibition of cell transformation largely reverted in JAK2-depleted ce

247 Large cell transformation (LCT) in mycosis fungoides (MF) is g

248 dratase-deficient cells, plays a key role in cell transformation, making it a bona fide oncometabolit

249 These results indicate that 4-OH-E2-induced cell transformation may be mediated, in part, through re

250 The mechanisms of malignant cell transformation mediated by the oncogenic anaplastic

251 reases epidermal growth factor (EGF)-induced cell transformation mediated through the downregulation

252 d tested their oncogenic potential in rodent cell transformation models.

253 r ability to cooperate with oncogenic Ras in cell transformation, NASP expression reduced the transac

254 Oxyphil cell transformation of epithelial cells due to the accum

255 on of Cdk3 resulted in anchorage-independent cell transformation of JB6 Cl41 cells induced by EGF and

256 rease of endothelial cell junctions and foam cell transformation of monocytes, confirming the relevan

257 points to the fundamental role in malignant cell transformation of potent oncogenes expressed in the

258 for epidermal growth factor (EGF)-stimulated cell transformation of the HaCaT immortalized skin cell

259 Large cell transformation often hallmarks cases with a more ag

260 ceptor in cultured mouse cells, resulting in cell transformation or proliferation.

261 egulates a number of critical events such as cell transformation, polarization, development, stress r

262 exhibited suppressed growth and EGF-induced cell transformation, possibly because of decreased activ

263 rget site exhibits an enhanced signaling and cell transformation potential.

264 sphorylate a variety of cellular proteins in cell transformation process including altered cell adhes

265 rotein kinases play crucial roles in several cell transformation processes and are validated drug tar

266 otypic cellular change (inhibit LEF-1-driven cell transformation) provided two lead compounds: lefmyc

267 SUMOylation of p53 is required for efficient cell transformation, provides evidence for the idea that

268 mical carcinogens and identified a subset of cell transformation-related, concordantly modulated m(6)

269 olled by specific PP2A complexes involved in cell transformation remain incompletely understood.

270 hanisms by which HSP70 may support malignant cell transformation remains to be fully elucidated.

271 dren to T-ALL, yet how LMO2 contributes to T cell transformation remains unclear.

272 ing recombinant EBVs, we show that optimal B-cell transformation requires a minimum of 5 W repeats (5

273 These data suggest that efficient cell transformation requires Ras proteins to interact wi

274 (tissue invasion by pathogens and malignant cell transformation, respectively).

275 tress-induced self-molecules associated with cell transformation serves as a mode of cell recognition

276 hese results support a model in which cancer cell transformation shares key genetic components with n

277 the stimulatory effects of NEK6 on STAT3 and cell transformation suggest that this family of serine/t

278 have established epigenetic etiologies for B cell transformation that are being exploited in novel th

279 In combination with whole-cell transformations, the myoglobin-based biocatalyst wa

280 In combination with whole-cell transformations, these biocatalysts enabled the gra

281 EBV orchestrates B cell transformation through its latent membrane proteins

282 an be generated either prior to or following cell transformation through mutations.

283 demonstrated that pseudogenes contribute to cell transformation through several mechanisms.

284 (LSD), which is known to be responsible for cell transformation through targeting of promiscuous E3

285 ated dephosphorylation of MAP4K4 and induces cell transformation through the activation of the Hippo

286 n in vitro model of human mammary epithelial cell transformation to assess how malignancy-associated

287 ved in the progression from HPV infection to cell transformation to cancer.

288 models of Epstein-Barr virus (EBV)-induced B-cell transformation to document the relevance of protein

289 Here, we show that cell transformation triggers a tissue-resident lymphocyt

290 nsic environmental factors promote malignant cell transformation, tumor growth, and metastasis.

291 forme and has been to shown to contribute to cell transformation, tumor initiation, progression, and

292 In cancer, RSKs modulate cell transformation, tumorigenesis, and metastasis.

293 Cell transformation was assessed by soft agar assay.

294 Thus, arsenic-induced cell transformation was blocked by inhibition of PcG fun

295 Indeed, the mutant EGFR-mediated cell transformation was inhibited by Src- as well as EGF

296 To study how ITAM signaling affects mammary cell transformation, we utilized mammary cell lines expr

297 understand how exosomes might contribute to cell transformation, we utilized the classic two-step NI

298 ed by telomerase (HTCE cells) and SV-40 (HCE cells) transformation were suppressed and enhanced by CT

299 Overall, 21 patients (3.8%) developed large-cell transformation, with a significantly higher transfo

300 little evidence exists for human epithelial cell transformation without previous immortalization via