ライフサイエンスコーパス: hTERT

1 hTERT binds to Sp1 in vitro and in vivo and stimulates a

2 hTERT promoter is regulated by multiple transcription fa

3 hTERT, the human telomerase reverse transcriptase, is hi

4 hTERT-P785L-expressing cells did not show growth defects

5 hTERT-W930F and hTERT-V791Y reconstitute reduced levels

6 Ad5/3-hTERT-E1A-hCD40L significantly inhibited tumor growth in

7 oncolytic and apoptotic effects, and (Ad5/3-hTERT-E1A-hCD40L)-mediated oncolysis resulted in enhance

8 structed a novel oncolytic adenovirus, Ad5/3-hTERT-E1A-hCD40L, which features a chimeric Ad5/3 capsid

9 uman small airway epithelial cells and cdk-4/hTERT-immortalized human bronchial epithelial cells (HBE

10 approximately 1150 hTR and approximately 500 hTERT molecules per HeLa cell), suggesting the existence

11 In PC-3 or RC-92a/hTERT prostate cancer cells, P-CYP preferentially kills

12 teracts with endogenous proteins to activate hTERT, the catalytic subunit of telomerase, thus avoidin

13 n of endogenous c-Myc/Max proteins activated hTERT promoter.

14 ta-catenin pathway is involved in activating hTERT transcription and inducing telomerase activity (TA

15 HPV16 E6 affects hTERT expression posttranscriptionally through NFX1-123,

16 cancer cells was also highly increased after hTERT overexpression.

17 xposure results in reduced bimodality of all hTERT splice variants and significant upregulation of al

18 a (KLG; also known as KLPH and LCTL) allowed hTERT to immortalize HCECs.

19 Furthermore, altering hTERT levels in four different breast cancer cell lines

20 Although hTERT's role in Wnt signaling was addressed only indirec

21 rimary cilium of a nonphotoreceptor cell (an hTERT-RPE1 epithelial cell), suggesting that it can co-o

22 ey cell cycle regulators and is linked to an hTERT-catalyzed decrease in the levels of the RNA compon

23 phase) breast cancer (MCF7, MDA-MB-231, and hTERT-HME1), normal breast (human mammary epithelial and

24 tradiol (E2) induced telomerase activity and hTERT mRNA expression in the estrogen receptor (ER)-alph

25 MEK1/MEK2, inhibited telomerase activity and hTERT mRNA expression induced by E2.

26 cling CCIC express markers, such as BMI1 and hTERT, are independent of MYC.

27 derived from its catalytic subunit hTERT and hTERT-promoter driven gene therapy have made significant

28 us, there are subpopulations of both hTR and hTERT not assembled into telomerase but capable of being

29 Ki-67 in human hTERT-RPE1, WI-38, IMR90, and hTERT-BJ cell lines and primary fibroblast cells slowed

30 The prosurvival genes Bcl-X(L) and hTERT were downregulated 5-fold by combination drug trea

31 the relationship between telomere length and hTERT splice variant expression patterns in benign and w

32 g expression significantly inhibited NE- and hTERT-induced ovarian cancer cell EMT and invasion.

33 compare DNA damage and repair in the p53 and hTERT gene regions of bladder cancer cell-lines RT4 and

34 me-point, the number and location of p53 and hTERT hybridisation spots was recorded in addition to st

35 We report that hTERT-P721R- and hTERT-R811C-expressing cells exhibited growth defects li

36 Additionally, overexpression of PABPC4 and hTERT led to greater growth of cultured HPV16 E6-express

37 hTERT-W930F and hTERT-V791Y reconstitute reduced levels of DNA synthesis

38 Both hTERT-W930F- and hTERT-V791Y-expressing cells harbor short telomeres, mea

39 TR) and protein component (hTERT) as well as hTERT splicing.

40 We assessed hTERT variants with mutations in motifs implicated in pr

41 f the previously reported disease-associated hTERT alleles give near-normal telomerase enzyme activit

42 work, we compare multiple disease-associated hTERT variants reconstituted with the RNA subunit hTR in

43 Because hTERT expression is regulated in part by DNA methylation

44 yses revealed an inverse correlation between hTERT mRNA and miR-498 in response to 1,25(OH)2D3 in est

45 letion caused telomere shortening in both BJ-hTERT and in HeLa cells.

46 pathway (U2OS) or telomerase expression (BJ-hTERT), or in normal human fibroblasts (IMR90).

47 Both hTERT-W930F- and hTERT-V791Y-expressing cells harbor sho

48 lation of MYC target genes, including CCND2, hTERT, and GCLC Analysis of microarray data sets further

49 miR-200a in cultured human myometrial cells (hTERT-HM) suppressed STAT5b and increased 20alpha-HSD mR

50 s, telomerase-immortalized hTERT-RPE1 cells (hTERT-RPE1), or both, were measured after stimulation wi

51 When expressed in ciliated hTERT-RPE1 human cell line, P/rd is localized to cilia.

52 e RNA component (hTR) and protein component (hTERT) as well as hTERT splicing.

53 the reverse transcriptase protein component, hTERT.

54 tions in the essential telomerase components hTERT and hTR cause dyskeratosis congenita, a bone marro

55 upport the idea of a biologically consistent hTERT interaction with the Wnt pathway in human breast c

56 In contrast, hTERT knockdown did not induce apoptosis.

57 tween TFs and chromatin environment controls hTERT transcription.

58 ificial chromosome (BAC) reporters, covering hTERT and mTERT genes and their neighboring loci, via re

59 in gene-specific shRNA effectively decreased hTERT expression, suppressed TA, and accelerated telomer

60 hout HPV16 E6, knockdown of PABPCs decreased hTERT mRNA and telomerase activity and overexpression of

61 nding by c-Myc/Max, USF1 and USF2, decreased hTERT promoter activity, and prevented its activation by

62 ability to degrade p53, E6 does not degrade hTERT protein in vitro or in vivo.

63 lase (HDAC) inhibitor, causes dose-dependent hTERT reporter activation, mimicking HMGA2 overexpressio

64 es were partially relieved in Ki-67-depleted hTERT-RPE1 cells by codepletion of the Rb checkpoint pro

65 in 24 h after initiation of differentiation, hTERT mRNA expression decreased dramatically, accompanie

66 Together, our study revealed a dynamic hTERT regulation by chromatin environment and promoter-b

67 We previously demonstrated that ectopic hTERT expression in primary human mammary epithelial cel

68 omatic cells, we investigated the endogenous hTERT gene regulation during differentiation of human le

69 set of inactive X (Xi) chromosomes in female hTERT-RPE1 cells displayed several features of compromis

70 hTERT-immortalized normal human fibroblasts (hTERT-1604) with a short hairpin RNA construct targeting

71 ith telomeres while preserving the co-folded hTERT-hTR ribonucleoprotein catalytic core.

72 gival tissue was collected and evaluated for hTERT expression by Western blot and immunohistochemical

73 Human telomerase gene hTERT is important for cancer and aging.

74 human telomerase reverse transcriptase gene (hTERT).

75 X, BRCA1, and the telomere maintenance gene, hTERT.

76 types and species (e.g., HEK-293, HeLa, HFF hTERT, C-12, and Cos-1).

77 immortalized human foreskin fibroblasts (HFF-hTERT).

78 5(+) B cells preferentially exhibited higher hTERT positivity than their CD5(-) counterparts.

79 The AgP tissue showed higher hTERT expression compared with CP (P <0.001).

80 demonstrate that depletion of Ki-67 in human hTERT-RPE1, WI-38, IMR90, and hTERT-BJ cell lines and pr

81 cultured hRPE cells, telomerase-immortalized hTERT-RPE1 cells (hTERT-RPE1), or both, were measured af

82 int kinase 1 (ATR-CHK1)) is not activated in hTERT-NHU cells after treatment with a replication inhib

83 int induction and apoptosis were analysed in hTERT-NHU and bladder cancer cell lines.

84 Here, we show that PABPCs are critical in hTERT regulation by HPV16 E6.

85 Overexpression of EMSY in hTERT-immortalized mammary epithelial cells, and in brea

86 3b was constitutively increased 5-20-fold in hTERT/CDK4-immortalized human bronchial epithelial cells

87 ein binding, which results in an increase in hTERT gene expression.

88 onary fibrosis cases also carry mutations in hTERT and hTR.

89 l free ends (SFEs), yet SFEs persist only in hTERT-V791Y cells, which undergo apoptosis, likely as a

90 evidence that PABPCs have a targeted role in hTERT regulation leading to a growth advantage in cells

91 Depletion of RPGR in hTERT-RPE1 cells interferes with ciliary localization of

92 and hypersensitivity to oxidative stress in hTERT-immortalized human foreskin fibroblasts (HFF-hTERT

93 together they posttranscriptionally increase hTERT expression, the catalytic subunit of telomerase.

94 NFX1-123, which were important for increased hTERT expression, were also important in the augmentatio

95 ess hormone norepinephrine (NE) could induce hTERT expression and subsequently ovarian cancer progres

96 eased miR-498 and decreased the diet-induced hTERT expression in tumors.

97 Unexpectedly, NE induced hTERT transcript and protein expression, and subsequentl

98 expression, profoundly attenuated NE-induced hTERT expression.

99 Wnt-3a conditioned medium treatment induced hTERT mRNA expression and elevated TA in different cell

100 f a dominant negative form of TCF4 inhibited hTERT expression in cancer cells.

101 Of interest, hTERT-W930F is more defective in translocation than hTER

102 These results provide novel insights into hTERT function in tumor progression in addition to its r

103 m used by p53 and its family members to keep hTERT expression under tight control.

104 ntly telomere dysfunction in cells that lack hTERT activity.

105 Intermediate levels of full-length hTERT and telomere length were found in follicular varia

106 ly correlated with percentage of full-length hTERT expression rather than with total hTERT expression

107 Full-length hTERT includes conserved domains that encode reverse tra

108 telomeres and high fractions of full-length hTERT transcripts were associated with follicular and pa

109 long telomeres and low levels of full-length hTERT were associated with benign thyroid nodules.

110 to these sites were critical in maintaining hTERT transcription during differentiation.

111 Our results reveal that a major hTERT splice variant can confer a growth advantage to ca

112 The studies suggest that miR-498-mediated hTERT downregulation is a key event mediating the anti-l

113 Our data indicate that mitochondrial hTERT works as a hTR-independent reverse transcriptase,

114 ted that, unlike HBZ, which solely modulates hTERT expression via JunD, both APH-3 and APH-4 acted po

115 ivated Akt, Ras, NF-kappaB, HIF-1alpha, myc, hTERT and IRF4; for biological aggressiveness; and for s

116 vitro analysis of the human uterine myocyte hTERT-HM cell line revealed that tunicamycin (TM)-induce

117 Using immortalized human myometrial (hTERT-HM) cells stably expressing wild-type PR-A or PR-B

118 Nonetheless, hTERT-W930F, but not hTERT-V791Y, immortalizes limited-l

119 passaged cells from a karyotypically normal hTERT immortalised human ovarian surface epithelial line

120 Nonetheless, hTERT-W930F, but not hTERT-V791Y, immortalizes limited-lifespan human cells.

121 We observed hTERT, MYC, and p53 immunoreactivity only in intestinal

122 Finally, we demonstrate that absence of hTERT specifically in mitochondria with maintenance of i

123 cells, accompanied by a strong activation of hTERT promoter.

124 that hypomorphic loss-of-function alleles of hTERT and hTR should cause a similar disease spectrum in

125 ChIP analysis of hTERT-HM cells stably expressing PRWT or PRmDBD revealed

126 to find evidence for physical association of hTERT with BRG1 or beta-catenin; instead, we present evi

127 ry after photobleaching analysis of cilia of hTERT-RPE1 cells showed that the movement of ciliary ops

128 e known to be important for tight control of hTERT in normal tissues, but the molecular mechanisms le

129 e by mechanisms that involve derepression of hTERT expression.

130 f guanine-rich sequence in the first exon of hTERT and located within the CTCF-binding region can for

131 gether, our data indicate that expression of hTERT does not alter type 1 IFN signaling and/or the gro

132 ed senescence, whereas ectopic expression of hTERT facilitated OIS escape.

133 f the cells with NE or ectopic expression of hTERT induced expression of Slug, ovarian cancer cell ep

134 High expression of hTERT might be associated with periodontal disease progr

135 The protein expression of hTERT shows significant but moderate correlation with GI

136 ression of HMGA2 modulates the expression of hTERT, resulting in cells with enhanced telomerase activ

137 ly, HMGA2 partially replaces the function of hTERT during the tumorigenic transformation of normal hu

138 proliferation is an independent function of hTERT that could provide a new target for the developmen

139 also find that the proliferative function of hTERT, which requires hTERT catalytic activity, is not c

140 henomenon that appeared to be independent of hTERT transcriptional activity.

141 ancer cells, and any detectable influence of hTERT depended on cell type and experimental system.

142 plain the previously reported interaction of hTERT with beta-catenin.

143 CpG island, which occurred with the loss of hTERT expression.

144 Together, our results support a mechanism of hTERT epigenetic control involving a G-quadruplex promot

145 estigate the possible molecular mechanism of hTERT in the promotion of gastric cancer (GC) metastasis

146 However, the precise mechanisms of hTERT's uptake, processing, and presentation on MHC-II m

147 protein-RNA interactions, overexpression of hTERT or TCAB1 had limited if any influence on hTR assem

148 Strikingly, overexpression of hTERT protein caused apoptosis that was rescued by overe

149 In addition, we use a panel of hTERT mutants to demonstrate that this enhanced cell pro

150 Expression patterns of hTERT splice variants were evaluated by quantitative and

151 We showed that activity and processivity of hTERT-T726M failed to be stimulated by TPP1-POT1 overexp

152 a consequence of a defect in recruitment of hTERT-V791Y to telomeres.

153 ed for the posttranscriptional regulation of hTERT by HPV16 E6 and NFX1-123.

154 We found that the up-regulation of hTERT in gastric cancer cells could inhibit the expressi

155 his review, we focus on the co-regulation of hTERT via transcriptional regulation, the presence or ab

156 d essential information on the regulation of hTERT, there has been ambiguity of the role of methylati

157 t with differential cell cycle regulation of hTERT-hTR and TCAB1-hTR protein-RNA interactions, overex

158 G dinucleotide methylation as a regulator of hTERT expression but also provide a possible mechanistic

159 results demonstrated that the repression of hTERT gene was dictated by distal elements and its chrom

160 NME2-mediated transcriptional repression of hTERT in these cells.

161 with increased activity of the repressor of hTERT transcription E2 transcription factor and decrease

162 We thus demonstrate a novel role of hTERT in stress hormone-induced ovarian cancer aggressiv

163 Silencing of hTERT expression abrogated NE-induced ovarian cancer cel

164 to establish the stable repressive status of hTERT gene in human somatic cells.

165 FN-alpha did not affect the translocation of hTERT from the cytoplasm to the nucleus.

166 own of PABPCs in C33A cells had no effect on hTERT mRNA or telomerase activity.

167 s sites at the promoter had little effect on hTERT transcription in ESCs.

168 the KLB ligand FGF19 had a similar effect on hTERT-expressing HCECs as knockdown of KLG regarding bot

169 e effects of G-quadruplex-binding ligands on hTERT expression and observed that several of these liga

170 lation at the hTERT promoter did not prevent hTERT repression or nucleosomal deposition, indicating t

171 e (hTERT) promoter has been shown to promote hTERT gene expression selectively in tumor cells but not

172 reased activation of NF-kappaB that promotes hTERT transcription.

173 al function of the human telomerase protein (hTERT) is to synthesize telomeric DNA, but it has other

174 eered to express SV40 early region proteins, hTERT, and H-RasV12.

175 but poorly with PRmDBD P4 treatment of PRWT hTERT-HM cells caused enhanced recruitment of endogenous

176 From the 12 runs of guanines, 9 putative hTERT G-quadruplex-forming sequences were selected to as

177 rt that loss of NME2 results in up-regulated hTERT expression.

178 n cells with long telomeres have a repressed hTERT epigenetic status (chromatin and DNA methylation),

179 rved that several of these ligands repressed hTERT expression.

180 liferative function of hTERT, which requires hTERT catalytic activity, is not caused by increased Wnt

181 and 68.42% of patients with AgP were showing hTERT mRNA expression, but it was not detected in the co

182 ndividual cells predominantly express single hTERT splice variants, with the alpha+/beta- variant exh

183 cancer-related genes, MAE was gene specific; hTERT was most significantly affected, with a higher fre

184 ng and a concurrent decrease of steady-state hTERT mRNA levels, attenuating their ability to form col

185 ne H3-K9 acetylation and thereby stimulating hTERT expression and telomerase activity.

186 The stringent hTERT repression depended on the native chromatin enviro

187 peptides derived from its catalytic subunit hTERT and hTERT-promoter driven gene therapy have made s

188 ase reverse transcriptase catalytic subunit (hTERT) have previously been identified and shown to be a

189 Using an human telomerase catalytic subunit (hTERT) promoter construct, our results also highlighted

190 In humans, the enzyme telomerase (hTERT) is responsible for the synthesis of new repeat se

191 g catalytic protein component of telomerase (hTERT) that is determined by the length of telomeres.

192 Human TERT (hTERT) can repetitively reverse transcribe its RNA templ

193 current study, we introduced the human TERT (hTERT) gene into a primary human embryonic lung (HEL-299

194 , we investigated the effects of human TERT (hTERT) on Wnt signaling in human breast cancer lines and

195 ts that aid in the regulation of human TERT (hTERT), including numerous transcription factors; furthe

196 930F is more defective in translocation than hTERT-V791Y.

197 Together, our results demonstrate that hTERT facilitates tumor angiogenesis by up-regulating VE

198 We demonstrated that hTERT, MYC, and TP53 are deregulated in intestinal metap

199 Finally, we provide evidence that hTERT links Src to Slug expression in NE-induced ovarian

200 tin immunoprecipitation assay, we found that hTERT is a direct target of beta-catenin.TCF4-mediated t

201 In this study, we report that hTERT is a novel target of the Wnt/beta-catenin pathway.

202 We report that hTERT-P721R- and hTERT-R811C-expressing cells exhibited

203 om whole cell and in organello, we show that hTERT binds various mitochondrial RNAs, suggesting that

204 In addition, we show that hTERT expression levels are positively correlated with t

205 P-specific CD4 T cell clones, we showed that hTERT processing and presentation on MHC-II involve both

206 ing these chromatinized BACs, we showed that hTERT silencing during differentiation to embryoid bodie

207 Here we review work showing that hTERT expression is in part regulated by atypical altern

208 Taken together, our results suggested that hTERT may promote GC metastasis through the hTERT-miR-29

209 nd subunit competition assays suggested that hTERT-hTR interaction is not readily exchangeable.

210 odontal disease progression, suggesting that hTERT could be a potential prognostic marker.

211 ent of telomere maintenance, suggesting that hTERT makes multiple contributions to cancer pathophysio

212 dge, we demonstrated for the first time that hTERT's internalization by dendritic cells requires its

213 The hTERT messenger RNA (mRNA) and protein expression was si

214 The hTERT mRNA expression did not show a correlation with gi

215 The hTERT promoter contains two estrogen response elements (

216 The hTERT promoter was more active than its mouse counterpar

217 ppearance of a nucleosome-free region at the hTERT core promoter.

218 , inhibition of histone deacetylation at the hTERT promoter did not prevent hTERT repression or nucle

219 iption and that the TCF4 binding site at the hTERT promoter is critical for beta-catenin.TCF4-depende

220 Interestingly, a G-quadruplex motif at the hTERT promoter was essential for occupancy of NME2 and t

221 for maintaining repressive chromatin at the hTERT promoter.

222 n was not observed when compared to both the hTERT gene region and the overall genome, proving the as

223 ressed in the human genomic context, but the hTERT promoter was highly active in the mouse genomic co

224 rgeted chimeric adenovirus controlled by the hTERT promoter and expressing CD40L (CGTG-401) was const

225 Although active in early embryogenesis, the hTERT gene is transcriptionally silenced in almost all s

226 -type gastric cancer, here, we evaluated the hTERT, MYC, and TP53 mRNA and protein expression, as wel

227 identify putative CTCF binding sites in the hTERT proximal exonic region (PER) and determine their f

228 Upon chromosomal integration, the hTERT, but not the mTert, reporter was stringently repre

229 Interestingly, the hTERT locus was located within a nuclease-resistant chro

230 While no genomic alteration of the hTERT (human telomerase catalytic subunit) locus was obs

231 suggested that epigenetic modulation of the hTERT core promoter region may provide an additional lev

232 nding factor (CTCF) to the first exon of the hTERT gene can down-regulate its expression.

233 aining chromatin-dependent repression of the hTERT gene in addition to activating its promoter.

234 m this study indicate that expression of the hTERT gene in HeLa cells is regulated by sequences in th

235 e near the transcriptional start site of the hTERT gene.

236 tion factors and the epigenetic state of the hTERT promoter are known to be important for tight contr

237 ted positively on the transactivation of the hTERT promoter mediated by tested Jun factors.

238 Our study revealed that silencing of the hTERT promoter was a biphasic process.

239 ling correlated with stable silencing of the hTERT promoter.

240 ts of GRHL2 on the methylation status of the hTERT promoter.

241 f NME2 and the REST repressor complex on the hTERT promoter.

242 CF4 showed more effective stimulation on the hTERT promoter.

243 se results indicate that GRHL2 regulates the hTERT expression through an epigenetic mechanism and con

244 x sites at -165 and +44 nt in regulating the hTERT promoter in the native genomic contexts.

245 hat the E-boxes functioned to de-repress the hTERT promoter and allowed its transcription in a repres

246 derately increased during reprogramming, the hTERT promoter was strongly activated in class II cells

247 Here we report that the hTERT promoter is strongly repressed by p53 and the rela

248 a, for the first time, demonstrated that the hTERT promoter was strongly activated in discrete steps,

249 hTERT may promote GC metastasis through the hTERT-miR-29a-ITGB1 regulatory pathway.

250 found to be rapidly repaired relative to the hTERT gene region and the overall genome, a phenomenon t

251 ng, we confirmed the binding of GRHL2 to the hTERT promoter and mapped the minimal binding region at

252 erferes with the recruitment of HDAC2 to the hTERT proximal promoter, enhancing localized histone H3-

253 l panel, we found that beta-deletion was the hTERT transcript that was most highly expressed.

254 D1) co-repressor complex associates with the hTERT promoter in an NME2-dependent way and that this as

255 uppressor non-metastatic 2 (NME2) within the hTERT core promoter in HT1080 fibrosarcoma cells and HCT

256 Consistent with this, hTERT-NHU cells treated with the ATM inhibitor showed in

257 man early neoplastic skin and breast tissue, hTERT expression was detected in cells that displayed fe

258 ues, but the molecular mechanisms leading to hTERT reactivation in cancer are not well-understood.

259 ngth hTERT expression rather than with total hTERT expression levels.

260 that human telomerase reverse transcriptase (hTERT) activates vascular epithelial growth factor (VEGF

261 g to human telomerase reverse transcriptase (hTERT) and reconstitution of an active ribonucleoprotein

262 from human telomerase reverse transcriptase (hTERT) and referred as universal cancer peptide (UCP).

263 iral human telomerase reverse transcriptase (hTERT) and/or SV40 large T antigen cDNA vectors, and ant

264 e gene for telomerase reverse transcriptase (hTERT) are associated with diseases including dyskeratos

265 The human telomerase reverse transcriptase (hTERT) gene is repressed in most somatic cells, whereas

266 the human telomerase reverse transcriptase (hTERT) gene promoter.

267 the human telomerase reverse transcriptase (hTERT) gene, which remains repressed in adult somatic ce

268 the human telomerase reverse transcriptase (hTERT) gene.

269 with human telomerase reverse transcriptase (hTERT) in the immortalization of HCECs.

270 n of human telomerase reverse transcriptase (hTERT) induces it.

271 Human telomerase reverse transcriptase (hTERT) is localized to mitochondria, as well as the nucl

272 Human telomerase reverse transcriptase (hTERT) is overexpressed in cancer cells and associated w

273 m of human telomerase reverse transcriptase (hTERT) may be expressed.

274 ased human telomerase reverse transcriptase (hTERT) mRNA expression and cell growth through estrogen

275 Human telomerase reverse transcriptase (hTERT) plays a key role in tumor invasion and metastasis

276 with human telomerase reverse transcriptase (hTERT) plus SV40 large T and small T antigens are transf

277 n, a human telomerase reverse transcriptase (hTERT) promoter for tumor selectivity, and human CD40L f

278 The human telomerase reverse transcriptase (hTERT) promoter has been shown to promote hTERT gene exp

279 n of human telomerase reverse transcriptase (hTERT) that disrupt the interaction of telomerase with T

280 r of human telomerase reverse transcriptase (hTERT) that is targeted by HPV type 16 (HPV16) E6/E6-ass

281 d to human telomerase reverse transcriptase (hTERT) throughout all phases of the cell cycle, and subu

282 The human telomerase reverse transcriptase (hTERT) utilizes a template within the integral RNA subun

283 ase, human telomerase reverse transcriptase (hTERT), is overexpressed in approximately 90% of human c

284 n of human telomerase reverse transcriptase (hTERT), the catalytic component of telomerase, in activa

285 n of human telomerase reverse transcriptase (hTERT), the catalytic subunit of telomerase, which offer

286 and human telomerase reverse transcriptase (hTERT)-immortalized human mammary epithelial cells (hMEC

287 e of human telomerase reverse transcriptase (hTERT)-immortalized normal human urothelial (NHU) and bl

288 and human telomerase reverse transcriptase (hTERT).

289 Human telomerase reverse transcriptase (hTERT; the catalytic protein subunit of telomerase) is s

290 n of human telomerase reverse transcription (hTERT) enzyme in chronic periodontitis (CP) and aggressi

291 environment because transiently transfected hTERT promoters were not repressed in differentiated cel

292 To address these questions, we transfected hTERT-immortalized normal human fibroblasts (hTERT-1604)

293 om mouse fibroblasts containing a transgenic hTERT reporter.

294 GRHL2 and the molecular mechanism underlying hTERT gene regulation by GRHL2.

295 tase activity (hCDC14A(PD)) in untransformed hTERT-RPE1 and colorectal cancer (HCT116) cell lines and

296 s the utility of (a) an in vitro model using hTERT/Cdk4 immortalized human bronchial epithelial cell

297 sure to NE was sufficient to enhance in vivo hTERT expression and metastasis of ovarian cancer cells

298 ment loss (AL) in patients with AgP, whereas hTERT protein expression was strongly correlated with GI

299 Infection with hTERT immortalized these cells, which accumulated neutra

300 NFX1-123 interacts with hTERT mRNA and stabilizes it, leading to greater telomer

301 through NFX1-123, as NFX1-123 interacts with hTERT mRNA and stabilizes it, leading to greater telomer