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-P785L-expressing cells did not show growth defects

4 hTERT-W930F and hTERT-V791Y reconstitute reduced levels

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

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

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

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

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

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

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

12 cancer cells was also highly increased after hTERT overexpression.

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

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

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

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

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

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

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

20 e c-MYC, KRAS, c-KIT, HIF-1alpha, PDGF-A and hTERT.

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

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

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

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

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

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

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

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

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

30 1 (NDRG1) in MCPyV gene-expressing NIKs and hTERT-MCPyV gene-expressing human keratinocytes (HK) com

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

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

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

34 somes from karyotypically normal primary and hTERT-immortalized human cell lines to catalog NORs in t

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

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

37 ysis of CRISPR/Cas9-engineered zebrafish and hTERT-RPE1 cells, we demonstrated that dysfunction of AR

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

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

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

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

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

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

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

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

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

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

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

49 s immortalized normal pancreatic duct cells, hTERT-HPNE.

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

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

52 the reverse transcriptase protein component, hTERT.

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

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

55 In contrast, hTERT knockdown did not induce apoptosis.

56 tween TFs and chromatin environment controls hTERT transcription.

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

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

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

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

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

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

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

64 By employing hTERT as a model gene, we show the coordination of the s

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

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

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

68 actor, NOVA1, that acts as an enhancer of FL hTERT splicing, increases telomerase activity, and promo

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

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

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

72 The human telomerase gene (hTERT) is repressed in most somatic cells.

73 n, introns 2 and 6 of human telomerase gene (hTERT) were critical for regulating its promoter in soma

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 (3D) tissue constructs engineered with iMyoD-hTERT-NHDFs, normal human dermal fibroblasts transduced

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

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

85 ver, a decrease in wound healing capacity in hTERT-MCPyV gene-expressing HK was observed.

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

87 3b was constitutively increased 5-20-fold in hTERT/CDK4-immortalized human bronchial epithelial cells

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

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

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

91 In addition, NDRG1 overexpression in hTERT-MCPyV gene-expressing HK or MCC cells resulted in

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 diates epidermal growth factor (EGF)-induced hTERT expression in MCF10A cells.

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

99 expression, profoundly attenuated NE-induced hTERT expression.

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

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

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

103 ration, providing a mechanistic insight into hTERT activation during tumorigenesis.

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

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

106 ntly telomere dysfunction in cells that lack hTERT activity.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 he microcephalin 1/BRCT-repeats inhibitor of hTERT (MCPH1/BRIT1) protein, mutated in primary microcep

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

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

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

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

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

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

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

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

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

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

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

163 s, are also participating in the splicing of hTERT to FL in cancer.

164 ation of telomerase involves the splicing of hTERT transcripts to produce full-length (FL) TERT.

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

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

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

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

169 We exposed preneoplastic, hTERT-immortalized Barrett's cell, CP-C and CP-A, to the

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 in cancer cells indicate that PTBP1 reduces hTERT FL splicing and telomerase activity.

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 sitive cells, but it activated the repressed hTERT promoter and altered histone modifications only in

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

182 s interaction in HCT116, 293T, HeLa, and RPE-hTERT cells; demonstrated that the interaction occurs sp

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

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

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

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

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

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

189 transfect the telomerase catalytic subunit (hTERT) and the simian virus 40 large-tumour antigen (SV4

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

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

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

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

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

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

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

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

198 930F is more defective in translocation than hTERT-V791Y.

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

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

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

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

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

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

205 nts of hTR in Cajal bodies (CBs) reveal that hTERT controls the exit of hTR from CBs.

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

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

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

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

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

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

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

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

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

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

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

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

218 The hTERT promoter contains two estrogen response elements (

219 The hTERT promoter was more active than its mouse counterpar

220 How transcription factors activate the hTERT promoter in its repressive chromatin environment i

221 factor X (MAX) synergistically activate the hTERT promoter via two identical, but inverted, composit

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

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

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

225 for maintaining repressive chromatin at the hTERT promoter.

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

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

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

229 nconsistent with the structure formed by the hTERT wild-type sequence.

230 eins to the Ets/E-box motifs derepresses the hTERT promoter by inducing an active promoter configurat

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

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

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

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

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

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

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

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

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

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

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

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

243 ) and depended on the chromatin state of the hTERT promoter.

244 CF4 showed more effective stimulation on the hTERT promoter.

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

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

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

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

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 ETV5 bound to the hTERT promoter in both telomerase-negative and -positive

252 -Myc facilitated each other's binding to the hTERT promoter.

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

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

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

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

257 th G-quadruplex forming potential within the hTERT promoter is disputed.

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

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

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

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

262 plex that contains the reverse transcriptase hTERT and RNA template TERC/hTR.

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

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

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

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

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

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

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

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

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

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

286 and human telomerase reverse transcriptase (hTERT).

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

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

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

290 om mouse fibroblasts containing a transgenic hTERT reporter.

291 I cleavage assay we found that the wild type hTERT core promoter folds into a stacked, three-parallel

292 We found with certainty that the wild-type hTERT promoter sequence does not form a hairpin structur

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

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

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

296 istic ETV5/c-Myc activation disappeared when hTERT promoter repression became relieved because of the

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

298 to date have been described to interact with hTERT and promote the production of FL TERT.

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

300 experiments reveal that PTBP1 interacts with hTERT pre-mRNA in a NOVA1 dependent fashion.

301 lly preventing the association of NOVA1 with hTERT pre-mRNA.