ライフサイエンスコーパス: telomere

1 es, resulting in the formation of an ectopic telomere.

2 with the related DNA damage response at the telomere.

3 binding does not play a role in ALT at these telomeres.

4 nced ALT-associated phenotypes and elongated telomeres.

5 ode of its association with poxvirus hairpin telomeres.

6 omised in telomerase mutant cells with short telomeres.

7 es spread across the genome and distant from telomeres.

8 he recruitment of gammaH2AX-but not 53BP1-to telomeres.

9 med at collapsed replication forks or eroded telomeres.

10 the localization of CSB and RAD52 to damaged telomeres.

11 POLD3 dependent Break Induced Replication at telomeres.

12 g (alt-NHEJ), which did not generate fragile telomeres.

13 proliferation, resulting in aberrantly long telomeres.

14 umor cells escape the critical shortening of telomeres.

15 els of telomerase activity to maintain short telomeres.

16 gate regulates ribonucleotide insertion into telomeres.

17 le to form in the single-stranded 3' ends of telomeres.

18 ch the shelterin protein POT1 (Protection of Telomeres 1) unfolds human telomeric G-quadruplex struct

19 HNF4alpha, even in cells that retained short telomeres, accrued DNA damage, and exhibited p53 stabili

20 However, it is unclear how de novo telomere addition (dnTA) is regulated at DNA double-stra

21 The healing of broken chromosomes by de novo telomere addition, while a normal developmental process

22 universally fast-evolving subtelomere - the telomere-adjacent, repetitive sequence - is a primary dr

23 and analyzed for alternative lengthening of telomeres (ALT) by Fluorescence In Situ Hybridization.

24 meric DSBs and in alternative lengthening of telomeres (ALT) cells, which have spontaneous telomeric

25 The alternative lengthening of telomeres (ALT) facilitates telomere lengthening by a DN

26 combination-based alternative lengthening of telomeres (ALT) pathway that depends on ALT-associated p

27 sms that underpin alternative lengthening of telomeres (ALT).

28 say [a marker for alternative lengthening of telomeres (ALT)], TERT mRNA expression by RNA-sequencing

29 Therefore, regulation of the telomere and 70 bp repeat R-loop levels is important for

30 iption favors accumulation of R-loops at the telomere and 70 bp repeats, providing an intrinsic mecha

31 (tert) mutant zebrafish have premature short telomeres and anticipate cancer incidence to younger age

32 low/non-ALT tumors, continuous shortening of telomeres and decreasing viability occurred in low TERT-

33 rotein can move in coordination with meiotic telomeres and interact with the nuclear envelope protein

34 1 binding protein 3 (HP1BP3) can localize to telomeres and is particularly enriched on telomeres in A

35 n bind to (TCAGGG)(n) variant repeats within telomeres and it has been proposed that this facilitates

36 nded noncanonical DNA structures enriched at telomeres and oncogenes' promoters.

37 stranded DNA-binding protein that stabilizes telomeres and stalled replication forks.

38 ssociation between single PFAS compounds and telomeres, and the first to link PFAS exposure with surv

39 ization of telomerase and its recruitment to telomeres, and the regulation of telomerase activity.

40 ad shorter peripheral blood mononuclear cell telomeres, and were more likely to carry the MUC5B risk

41 Short telomeres are a principal defining feature of telomere b

42 Telomeres are a significant challenge to DNA replication

43 Human telomeres are bound by the telomere repeat binding prote

44 ase activation in HBECs near senescence when telomeres are critically short.

45 t, underlying role of NAD dysregulation when telomeres are short and underscore its relevance to the

46 ever, in pop mutants, TLC1 is more abundant, telomeres are short, and TLC1 accumulates in the cytopla

47 increases exponentially with age when human telomeres are shorter.

48 ing immune cell development, meiosis, and at telomeres as well as from aborted topoisomerase reaction

49 Creating gapless telomere-to-telomere assemblies of complex genomes is one of the ult

50 s and generate some of the first telomere-to-telomere assemblies of whole chromosomes.

51 GRCh38(2), along with a gapless, telomere-to-telomere assembly of a human chromosome.

52 6-thio-dG treatment causes telomere-associated DNA damages that are sensed by dendr

53 rong dependency of TRF2-null ES cells on the telomere-associated protein POT1B and on the chromatin r

54 Finally, the interaction between telomere attrition from 4 to 18 months and maternal ACEs

55 Telomere attrition from 4 to 18 months interacted with m

56 Telomere attrition is a major risk factor for end-stage

57 mitigates the effects of repeated burden on telomere attrition over 5 years.

58 Childhood Experience questionnaire, greater telomere attrition predicted higher externalizing proble

59 Whether telomere attrition reducing proliferative reserve in blo

60 ch limits cell division after DNA damage and telomere attrition(11-13); another two (MPL and SH2B3) e

61 congenita (DC), a disorder characterized by telomere attrition.

62 ically interacts with the TRFH domain of the telomere binding protein TRF2.

63 This regulation is mediated through the telomere-binding protein telomeric repeat-binding factor

64 HOAP is a telomere-binding protein that has a conserved role in Dr

65 ing proteins, particularly in transcription, telomere biology and genome instability.

66 e may exert a salubrious effect on offspring telomere biology and highlight the importance of enhanci

67 stem cells, offering a promising therapy for telomere biology diseases.

68 elomeres are a principal defining feature of telomere biology disorders, such as dyskeratosis congeni

69 Similar to germline mutations in telomere biology genes leading to bone-marrow failure, t

70 G-quadruplex forming sequence from the human telomere can adopt six distinct topologies that are inte

71 tively, these findings indicate that fragile telomeres can arise from BIR-mediated repair of telomeri

72 eficient cells and altered repair of damaged telomeres, can be explained from this viewpoint.

73 ample MR is performed to test whether longer telomeres cause changes to hematological traits.

74 remain difficult to characterize, including telomeres, centromeres, and other low-complexity regions

75 DNA double strand breaks specifically in the telomeres, ChIP, telomere immunofluorescence, fluorescen

76 ition of ALT cells, which was accompanied by telomere chromatin decompaction, increased presence of C

77 How the telomere chromatin is regulated and maintained in these

78 , indicating that APB functions in promoting telomere clustering can be uncoupled from enriching DNA

79 Indeed, telomere clustering relies only on liquid properties of

80 DSB repair and that this role involves both telomere cohesion and a DAXX-dependent pathway.

81 nce inadequate tankyrase 1 to resolve sister telomere cohesion.

82 on had almost twice the odds of having short telomeres compared with those with the lowest consumptio

83 Telomeres comprise specialized nucleic acid-protein comp

84 Telomeres consist of TTAGGG repeats bound by protein com

85 Nanopore reads generated by the Telomere-to-Telomere consortium and identify a novel (rare) monomer

86 However, because short telomeres constitute a road block to cell proliferation,

87 le insufficient loading of TRF2 at shortened telomeres contributes to the DNA damage response in sene

88 t DDR signaling in response to dysfunctional telomeres creates a preponderance of chromatin fragments

89 of TREX1, the genome alterations induced by telomere crisis primarily involve breakage-fusion-bridge

90 mproved NAD homeostasis, thereby alleviating telomere damage, defective mitochondrial biosynthesis an

91 The presence of extensive centromere and telomere defects suggests a prominent role for CBX2 in h

92 s require this essential, strictly conserved telomere-dependent genome preservation.

93 er, our results uncover a unique response to telomere deprotection during early development.

94 ES cell telomeres devoid of TRF2 instead activate an attenuated

95 y is a key clinical feature of several human telomere disorder syndromes, but how microcephaly is lin

96 is required for histone H3.3 deposition and telomere DNA synthesis.

97 The telomere downstream of the active VSG is transcribed int

98 e pathophysiology and interventions of human telomere-driven diseases.

99 We show that HIRA is enriched at telomeres during the G2 phase and is required for histon

100 omere length (cross-sectional approach), and telomere dynamics (rate of telomere length change over t

101 Our data show that telomere dysfunction acts as a major regulator of HNF4al

102 Here we discuss how telomere dysfunction can initiate genomic complexity and

103 tory diseases in humans, yet whether and how telomere dysfunction causes inflammation are not known.

104 impacted by telomere shortening, progressive telomere dysfunction impaired hepatic endoderm formation

105 Aging-associated inflammation, telomere dysfunction, and adaptive immune system senesce

106 In mice with telomere dysfunction, telomerase reactivation in the int

107 on of gammaH2AX foci and of 53BP1-containing telomere dysfunction-induced foci (TIFs), indicating def

108 any years, increasing evidence suggests that telomere dysfunctions also perturb chromosome segregatio

109 that telomeric origin firing does not cause telomere elongation, and the role of Rif1 in regulating

110 POT1 alterations cause rapid telomere elongation, ATR kinase activation, telomere fra

111 omponent (hTR), a noncoding RNA required for telomere elongation.

112 What do the insights into telomere end protection in pluripotent cells mean for th

113 ends are significantly weaker than those at telomere ends, suggesting that they are located in diffe

114 izing the BLM-TOP3A-RMI (BTR) complex to ALT telomere ends.

115 iency in CD4 T cells accelerates DNA damage, telomere erosion, and cell apoptosis in HIV-infected ind

116 The non-CpG DNA methylation at telomere fits a binomial model and may result from a ran

117 BIR also promoted fragile telomere formation in cells with FokI-induced telomeric

118 tion by helicases, thereby promoting ectopic telomere formation.

119 dysfunction increases DNA damage signaling, telomere fragility and sister chromatid exchanges.

120 telomere elongation, ATR kinase activation, telomere fragility, and accelerated tumor development.

121 tion and are prone to replication stress and telomere fragility.

122 that the persistent cohesion protects short telomeres from inappropriate recombination.

123 review, we describe the impact of ncRNAs on telomere function and discuss their implications in sene

124 e subtelomere perturb subtelomere-dependent, telomere functions.

125 also known as Terf2) ES cells do not exhibit telomere fusions and can be expanded indefinitely.

126 DNA damage response that lacks accompanying telomere fusions, and propagate for multiple generations

127 response at telomeres, resulting in frequent telomere fusions.

128 Most notably, telomeres have a broad impact on pluripotency and differ

129 Short telomeres have been linked to cancer risk, yet other evi

130 atic chromosome ends are recapped by de novo telomere healing.

131 d highly repetitive genomic features such as telomeres, heterochromatic knobs, and centromeres.

132 However, these sequences can form ectopic telomeres if BIR is made less processive.

133 breaks specifically in the telomeres, ChIP, telomere immunofluorescence, fluorescence in situ hybrid

134 to telomeres and is particularly enriched on telomeres in ALT cells.

135 UPF consumption and the risk of having short telomeres in an elderly population of the Seguimiento Un

136 We report that analogous to CFSs, fragile telomeres in BLM-deficient cells involved double-strand

137 These observations suggest a role of telomeres in extra-telomeric functions.

138 s of single chromatin loci, centromeres, and telomeres in live cells and analyzed their dynamics usin

139 n whether physiological aging leads to short telomeres in the lung, thus leading to IPF with aging.

140 to be active in vitro and to maintain yeast telomeres in vivo, whereas the DeltaCEH and 1- and 2-bp

141 cell lines lack (TCAGGG)(n) repeats in some telomeres, indicating that direct NR binding does not pl

142 ; acquisition of MoTeR insertions by 'plain' telomeres; insertion of the MAGGY retrotransposons into

143 rmine the mechanisms by which MoTeRs promote telomere instability.

144 rdependent relationship between H3K27me3 and telomere integrity in stem cell lineage commitment that

145 d it has been proposed that this facilitates telomere interactions in ALT+ cells.

146 mechanism to convert the ITS to a functional telomere is by telomerase-catalyzed addition of telomeri

147 ermination of BIR and creation of an ectopic telomere is promoted by Mph1/FANCM helicase, which has t

148 Extension of telomeres is a critical step in the immortalization of c

149 how microcephaly is linked to dysfunctional telomeres is not known.

150 w cells respond to ROS-induced DNA damage at telomeres is still largely unknown.

151 The MLPA telomere kit was used to identify aneuploidy through det

152 nd homology directed repair of dysfunctional telomeres lacking POT1-TPP1.

153 Lagging-strand telomeres lacking TRF1 or BLM form fragile telomeres-str

154 Previously, we showed that eroded telomeres lead to differentiation instability in murine

155 observed that tissue environment with short telomeres leads to increased tumor development.

156 Telomere-led rapid chromosome movements or rapid prophas

157 associations among PFAS congeners, absolute telomere length (cross-sectional approach), and telomere

158 Leukocyte telomere length (LTL) is a heritable biomarker of genomi

159 Leukocyte telomere length (LTL) might be causal in cardiovascular

160 valuated the role of pretransplant leukocyte telomere length (LTL) on survival outcomes in patients w

161 In adults, shorter telomere length (TL) has been reported in association wi

162 Telomere length (TL) is a marker of biological age that

163 nsively studied biological markers of aging, telomere length (TL) provides a valuable tool to underst

164 Leukocyte telomere length (TL) shortens with age and is associated

165 unication is on a potential biomarker, short telomere length (TL), that might serve to identify patie

166 ood sample collection for immunophenotyping, telomere length assessments, and genetic testing.Measure

167 al approach), and telomere dynamics (rate of telomere length change over time, longitudinal approach)

168 s suggesting the mutation causes a defect in telomere length feedback regulation.

169 t genetically influenced common variation in telomere length impacts hematologic traits in the popula

170 recipients compared with their donors, with telomere length in CH vs non-CH CFUs showing varying pat

171 om a genome-wide association (GWA) study for telomere length in individuals of European ancestry (n =

172 PR31 and SERPINB9 genes were associated with telomere length in long-term meditators with a strong st

173 We measured relative telomere length in pretransplant recipient blood samples

174 Among 1267 patients >=40 years old, telomere length in the shortest quartile was associated

175 Short telomere length is a risk factor for age-related disease

176 th high chronic burden do not show decreased telomere length over the 5-year period.

177 of human pluripotent stem cells, while their telomere length set point determines the proliferative c

178 d elongation, but its role in establishing a telomere length set point remains elusive.

179 us locus of human stem cells with an altered telomere length set point.

180 sistently correlate with TERT expression and telomere length suggests an alternative method whereby t

181 ploinsufficient tumor suppressor that limits telomere length to ensure a timely Hayflick limit.

182 al status, copy number, gene expression, and telomere length to provide a comprehensive analysis of t

183 45) was significantly associated with longer telomere length via a recessive model in our cohort (P =

184 Shorter telomere length was significantly associated with older

185 ctivity and activated telomeric origins, yet telomere length was unchanged.

186 or genetic variants strongly associated with telomere length were extracted from a genome-wide associ

187 DS patients and evaluated the association of telomere length with MDS disease characteristics and tra

188 Leukocyte telomere length, a marker of immune system function, is

189 meditation is linked to longevity and longer telomere length, a proposed biomarker of human aging.

190 Short telomere length, mediated by inherited or acquired facto

191 there was a significant 5-year shortening in telomere length, whereas no significant relationships be

192 Recent observations further reveal telomere length-dependent gene regulation and epigenetic

193 e RG7834, rescued TERC 3' end maturation and telomere length.

194 ing is separable from its role in regulating telomere length.

195 evels, telomere sister chromatid exchange or telomere length.

196 on but had no appreciable impact on absolute telomere length.

197 ylation status may play a role in regulating telomere length.

198 ogical age, mortality, mitotic divisions, or telomere length.

199 this through TERT activation or alternative telomere lengthening associated with ATRX or DAXX loss.

200 e lengthening of telomeres (ALT) facilitates telomere lengthening by a DNA strand invasion and copyin

201 sidase activity (p < 0.01) but no changes in telomere lengths and p16(INK4a) levels were observed.

202 mulates copy number variants (CNVs), and its telomere lengths are short but constant.

203 sly thought, our technique revealed that the telomere lengths of chromosomes harboring the integrated

204 omeric DDR plays a critical role in inducing telomere loss, premature cell aging, and CD4 T-cell apop

205 ncluding DNA damage repair (Fanconi anemia), telomere maintenance (dyskeratosis congenita), and ribos

206 The murine Zscan4 is involved in telomere maintenance and genomic stability of mouse embr

207 SIRT6 regulates telomere maintenance and VSMC lifespan and inhibits athe

208 Germline telomere maintenance defects are associated with an incr

209 gues identified small molecules that restore telomere maintenance in patient-derived stem cells, offe

210 Telomere maintenance is essential for the long-term prol

211 e underlying mechanisms are largely unknown, telomere maintenance may be involved.

212 s) divide for over 200 PD without engaging a telomere maintenance mechanism (almost four times the "H

213 To comprehensively assess the impact of telomere maintenance mechanism (TMM) on clinical outcome

214 ecurrent genomic alterations associated with telomere maintenance mechanisms in cancer.

215 mutations that affect telomerase function or telomere maintenance result in a variety of diseases col

216 Telomere maintenance via telomerase reactivation is a ne

217 ein response, macroautophagy, mitophagy, and telomere maintenance) result in diverse cellular endophe

218 gical functions, such as cell proliferation, telomere maintenance, and DNA recombination.

219 ng multiple pathways including host defense, telomere maintenance, signaling, and cell-cell adhesion.

220 importance of nevogenesis, pigmentation and telomere maintenance, together with identifying potentia

221 totic cell cycle," "DNA recombination," and "telomere maintenance," respectively.

222 es including transcription, replication, and telomere maintenance.

223 effect of season of conception on postnatal telomere maintenance.

224 tures at chromosomal termini participates in telomere maintenance.

225 ss to malignancy, they must overcome a final telomere-mediated proliferative lifespan barrier called

226 c anemia, is characterized by severely short telomeres, often resulting in hematopoietic stem cell fa

227 The adverse impact of shorter telomeres on NRM was independent of recipient comorbidit

228 in the context of the nonlocal influence of telomeres on pluripotency and stemness, we discuss major

229 ly passaged progenitors demonstrated shorter telomeres (P <= 0.05), and reduced rates of cell prolife

230 itive sequence - is a primary driver of the 'telomere paradox'.

231 provide a comprehensive analysis of the TERT/telomere pathway and establish a classification system w

232 We tested whether adult short telomere patients without MDS/AML also had evidence of c

233 model predicts that excessively long somatic telomeres predispose to cancer.

234 Mammalian telomeres protect chromosome ends from aberrant DNA repa

235 Telomeres protect chromosome ends from inappropriately a

236 In contrast, telomere protection and genome stability were maintained

237 by contrast, TRF2 is largely dispensable for telomere protection in mouse pluripotent embryonic stem

238 at the upregulation of ZSCAN4 contributes to telomere protection in the absence of TRF2.

239 Collectively, these data establish that telomere protection is solved by distinct mechanisms in

240 Indeed, these fast-evolving telomere proteins bind, extend, and protect telomeric DN

241 nd flies report pervasive rapid evolution of telomere proteins.

242 At an elevated level, telomere R-loops cause more telomeric and subtelomeric d

243 DSBs proximal to telomeres rarely form COs, likely because of formation o

244 eciated role for mTRF1 in the suppression of telomere recombination, dependent on SMC5 and also POLD3

245 Shortened telomeres recruit insufficient TRF1 and as a consequence

246 ll established that the virus resides in the telomere region, the integration locus is poorly defined

247 omain to the NPC basket protein Nup1 reduces telomere relocalization to nuclear pores early after tel

248 population doublings (PD), a point at which telomeres remain relatively long.

249 rtain loci, such as common fragile sites and telomeres, remain under-replicated during interphase and

250 Human telomeres are bound by the telomere repeat binding proteins TRF1 and TRF2.

251 ection through sequestration of the terminal telomere repeat sequence within a lariat T-loop structur

252 C1 or RTEL1 are more broadly associated with telomere replication defects.

253 n the replication stress response, promoting telomere replication fork progression and restart of sta

254 tion fork progression and restart of stalled telomere replication forks.

255 The replication and elongation of telomeres requires the disruption of these G-quadruplex

256 l-molecule PAPD5 inhibitors that demonstrate telomere restoration in vitro, in stem cell models, and

257 restores a canonical DNA damage response at telomeres, resulting in frequent telomere fusions.

258 nked to a defect in ribosomal DNA (rDNA) and telomere segregation, and it ultimately delays cell divi

259 how that when BIR encounters an interstitial telomere sequence (ITS), the machinery frequently termin

260 Surprisingly, this revealed long telomere sequences at the virus-subtelomere junction tha

261 that illustrate how genetic mutations drive telomere shortening and dysfunction in these patients.

262 Collectively, our results suggest that telomere shortening could represent a mechanism that mod

263 ividuals with multiple CH mutations; and (3) telomere shortening determined in granulocytes suggested

264 Progressive telomere shortening during lifespan is associated with r

265 Telomere shortening in human cells leads to a DNA damage

266 Telomere shortening is a hallmark of aging.

267 nstitute a road block to cell proliferation, telomere shortening is currently viewed as a tumor suppr

268 The current study explored whether telomere shortening might have an influence on cognitive

269 In our current study, we report that telomere shortening promotes cancer in a noncell autonom

270 en species production, oxidative damage, and telomere shortening, at the individual and intergenerati

271 found that this phenomenon is caused not by telomere shortening, but by cyclic GMP-AMP synthase (cGA

272 We propose that, upon telomere shortening, early apoptosis leads to cell deple

273 en species (ROS), mitochondrial dysfunction, telomere shortening, genomic instability, epigenetic cha

274 While endoderm derivation is not impacted by telomere shortening, progressive telomere dysfunction im

275 od pattern of acquired, granulocyte-specific telomere shortening.

276 ization (FISH), micronuclei imaging, and the telomere shortest length assay (TeSLA), we show that chr

277 Single-molecule tracking of hTR at telomeres shows that TPP1-mediated recruitment results i

278 They exhibited shortened telomeres similar to nonregressing CLL, indicating prior

279 atin modifications, TERRA expression levels, telomere sister chromatid exchange or telomere length.

280 promyelocytic leukemia (PML) bodies (APBs), telomere sister chromatid exchanges (T-SCEs), and extrac

281 TRF2, a component of the telomere-specific shelterin protein complex, facilitates

282 tions, and then base pairing between hTR and telomere ssDNA promotes long interactions required for s

283 The shelterin protein TPP1 is required for telomere stability and elongation, but its role in estab

284 Our results unveil how telomere stress increases innate sensing and adaptive an

285 d telomeres lacking TRF1 or BLM form fragile telomeres-structures that resemble common fragile sites

286 e truncated TIN2 proteins do not localize to telomeres, suggesting that the mutations create loss-of-

287 target in the treatment of liver disease in telomere-syndrome patients.

288 Our data show that the Mendelian short telomere syndromes are associated with a relatively narr

289 and provide strong rationales for combining telomere-targeting therapy with immunotherapy.

290 t TPP1-mediated recruitment results in short telomere-telomerase scanning interactions, and then base

291 to the low sequence complexity (TTAGGG)n of telomeres that cannot be easily resolved through sequenc

292 lying aging is the progressive shortening of telomeres, the structures that protect the ends of chrom

293 Creating gapless telomere-to-telomere assemblies of complex genomes is on

294 ural variants and generate some of the first telomere-to-telomere assemblies of whole chromosomes.

295 ntinuity of GRCh38(2), along with a gapless, telomere-to-telomere assembly of a human chromosome.

296 prone Oxford Nanopore reads generated by the Telomere-to-Telomere consortium and identify a novel (ra

297 nts initiated through breaks in interstitial telomere tracts that are generated during MoTeR integrat

298 /DAXX(trunc) tumors, which carry an aberrant telomere variant repeat (TVR) distribution as another ge

299 Patient lymphocyte telomeres were unusually long.

300 ML) protein, BRCA1 and the SMC5/6 complex at telomeres, which is associated with increased Homologous