ライフサイエンスコーパス: telomere shortening

1 non was independent of culture conditions or telomere shortening.

2 e resection of the 5' end, which could cause telomere shortening.

3 ocytes and hepatocytes showed no age-related telomere shortening.

4 T expression, suppressed TA, and accelerated telomere shortening.

5 ts telomere synthesis from TER1 and leads to telomere shortening.

6 ing cellular senescence that does not entail telomere shortening.

7 lomere dysfunction can result from excessive telomere shortening.

8 mal mononuclear cell cytokine secretion, and telomere shortening.

9 th after a period of slowing due to critical telomere shortening.

10 h a corresponding increase in DNA damage and telomere shortening.

11 types only after several generations, due to telomere shortening.

12 ere chromatin modulates senescence caused by telomere shortening.

13 by the loss of CD27 and CD28 expression and telomere shortening.

14 erexpressing Tel1 TAN mutants did not rescue telomere shortening.

15 nactive forms of TER1 and causes progressive telomere shortening.

16 elomerase enzyme deficiency, and progressive telomere shortening.

17 iption beyond the template region and caused telomere shortening.

18 independent of forced disruption of Tp53 and telomere shortening.

19 wth defects in proliferative tissues through telomere shortening.

20 DNA may inhibit telomerase access, promoting telomere shortening.

21 are independent of telomerase inhibition or telomere shortening.

22 her NTPase protein (NAT10 and GNL3L) induced telomere shortening.

23 idopsis, without increasing the rate of bulk telomere shortening.

24 somal dominant dyskeratosis congenita due to telomere shortening.

25 c cycles of injury, inflammation, repair and telomere shortening.

26 damage, inhibition of telomerase and marked telomere shortening.

27 own to slow cell growth but only after prior telomere shortening.

28 nt dyskeratosis congenita, anticipation, and telomere shortening.

29 y of p53 or telomere length and without bulk telomere shortening.

30 in telomere metabolism and/or known to cause telomere shortening.

31 ita, an inherited disease marked by abnormal telomere shortening.

32 lex pleiotropic of Wrn deficiency relates to telomere shortening.

33 Crisis is thought to be mediated by telomere shortening.

34 and that this is associated with progressive telomere shortening.

35 ng human telomerase RNA (TERC), resulting in telomere shortening.

36 mosome ends may be exposed through extensive telomere shortening.

37 mplicate reduced TEL patch dosage in causing telomere shortening.

38 cellular reverse transcriptase that prevents telomere shortening.

39 6/E7-expressing clones, and is the result of telomere shortening.

40 inX1 inhibits telomerase activity and causes telomere shortening.

41 xonuclease action can directly contribute to telomere shortening.

42 n or temperature sensitivity, accompanied by telomere shortening.

43 rs after several weeks and is accompanied by telomere shortening.

44 of the inflammatory potential of the diet on telomere shortening.

45 sister chromatid pairing and for preventing telomere shortening.

46 sion yeast, the Rpa1-D223Y mutation provokes telomere shortening.

47 environmental mechanisms that contribute to telomere shortening.

48 ory diet on aging and health by slowing down telomere shortening.

49 of existing G-quadruplexes which can lead to telomere shortening.

50 RX triggers a suppression of the pathway and telomere shortening.

51 nds the 3' ends of chromosomes to counteract telomere shortening.

52 I) could significantly slow down the rate of telomere shortening.

53 and suggest a potential link between p53 and telomere shortening.

54 found that acrolein accelerated p53-mediated telomere shortening.

55 development of dysplasia in UC than general telomere shortening.

56 ated aging processes, such as senescence and telomere shortening.

57 and (2) replicative senescence triggered by telomere shortening.

58 e immortalized endothelial cells resulted in telomere shortening.

59 est quartile experienced the slowest rate of telomere shortening (0.05 T/S units over 5 years; 95% CI

60 e of DHA+EPA experienced the fastest rate of telomere shortening (0.13 telomere-to-single-copy gene r

61 of invasive carcinoma demonstrated moderate telomere shortening (17.5%) or normal telomere lengths (

62 Telomere shortening, a marker of cellular ageing, is lin

63 Unexpectedly, telomere shortening accelerated in plants lacking CST an

64 Progressive telomere shortening activates replicative senescence, wh

65 sociated with a 32% reduction in the odds of telomere shortening (adjusted odds ratio, 0.68; 95% CI,

66 Interestingly, Ala carriers showed lower telomere shortening after 5 years compared with the Pro/

67 investigated the hypothesis that accelerated telomere shortening after aHCT could contribute to the d

68 ciency of cellular efflux pumps, DNA damage, telomere shortening, alteration of cytokine regulation,

69 MeDiet pattern strengthens the prevention of telomere shortening among Ala carriers.

70 analyses and once per 23 weeks according to telomere-shortening analyses.

71 ndrome (HHS) is characterized by accelerated telomere shortening and a broad range of pathologies, in

72 in HMGA2 in HepG2 cells leads to progressive telomere shortening and a concurrent decrease of steady-

73 earch links psychosocial stress to premature telomere shortening and accelerated human aging; however

74 Telomere shortening and alterations of mitochondrial bio

75 However, a causal link between telomere shortening and diabetes risk has not been estab

76 ect resolution of T-loops is a mechanism for telomere shortening and disease causation in humans.

77 s from TRF2 null tumors demonstrated extreme telomere shortening and dramatically increased numbers o

78 ed DNA damage, epigenetic modifications, and telomere shortening and dysfunction.

79 re of DKC1-mutant iPSCs leads to progressive telomere shortening and eventual loss of self-renewal, i

80 erately reduced levels result in accelerated telomere shortening and eventual marrow failure.

81 lomerase haploinsufficiency results in rapid telomere shortening and fatal BM failure in mice, elicit

82 on of BM stem cells is associated with rapid telomere shortening and further increase in senescent ce

83 telomeres did not prevent such catastrophic telomere shortening and fusion events.

84 ctopic expression of WT RTEL1 suppressed the telomere shortening and growth defect, confirming the ca

85 nsults and genetic modifiers that accelerate telomere shortening and increase cell turnover may exagg

86 The loss of Ccq1 results in progressive telomere shortening and persistent ATR-dependent activat

87 Mutations in telomerase components lead to telomere shortening and progressive bone marrow failure

88 mature senescence in vitro, with accelerated telomere shortening and reduced telomerase activity.

89 cted homozygous individuals have significant telomere shortening and reduced TERC levels.

90 Insofar as telomere shortening and replicative senescence prevent g

91 Inactivation of telomerase causes telomere shortening and results in the loss of the telom

92 of Est3p with telomerase in vivo, and cause telomere shortening and senescence.

93 tinuous pattern of changed expression during telomere shortening and some of the changes are senescen

94 We also discuss the relative roles played by telomere shortening and telomere uncapping in the induct

95 mutations cause slow growth independently of telomere shortening and that this slow growth is the res

96 lomere recruitment of telomerase, leading to telomere shortening and the associated pathogenesis.

97 ision history has been studied by monitoring telomere shortening and the dilution of T cell receptor

98 clear phospho-Akt and telomerase resulted in telomere shortening and uncapping in WT myocytes.

99 of the telomere repeat- binding factor TRF2, telomere shortening, and activation of the DNA damage ch

100 leads to the formation of telomeric circles, telomere shortening, and cell senescence.

101 s cause low telomerase activity, accelerated telomere shortening, and diminished proliferative capaci

102 to POT1 abrogated this effect, inducing mild telomere shortening, and generated looped DNA structures

103 n, invasion and metastasis suppressor genes, telomere shortening, and genetic instability).

104 e defects such as sensitivity to DNA damage, telomere shortening, and increased gross chromosomal rea

105 hibition of telomerase activity, progressive telomere shortening, and increased p14(ARF) expression.

106 suppressed telomerase activity, accelerated telomere shortening, and inhibited tumor cell growth by

107 served residues of the TAN motif resulted in telomere shortening, and its deletion caused the same sh

108 ncreased recombination at telomeres, delayed telomere shortening, and postponed senescence onset.

109 eplicative senescence, which is triggered by telomere shortening, and premature cellular senescence i

110 that a preneoplastic field of inflammation, telomere shortening, and senescence underlies tumor prog

111 Childhood adversity is associated with telomere shortening, and several investigations have sho

112 essors that occurred over the year predicted telomere shortening, and whether engaging in healthy beh

113 ers, if and how LTL is related to brain cell telomere shortening, and whether telomere shortening pla

114 Telomere length and telomere shortening are associated with age-related heal

115 gs support the idea that pathways leading to telomere shortening are involved in the pathogenesis of

116 Because the consequences of telomere shortening are progressive and unsynchronized,

117 Notably, the rates of telomere shortening are similar in the four tissues.

118 arch strengthens the case for stress-induced telomere shortening as a pancultural biomarker of compro

119 To prevent progressive telomere shortening as a result of conventional DNA repl

120 Cellular senescence can be triggered by telomere shortening as well as a variety of stresses and

121 n that plays an essential role in preventing telomere shortening, as expression of TRF2(DeltaB), whic

122 Levels of DHA+EPA were associated with less telomere shortening before (unadjusted beta coefficient

123 n an initial phase, TPMs do not prevent bulk telomere shortening but extend cellular life span by hea

124 ntal studies, they have been shown to induce telomere shortening, but no epidemiologic study to date

125 ative life span of human cells is limited by telomere shortening, but the specific telomeres responsi

126 ccumulate genomic alterations in response to telomere shortening, but the transmission of these aberr

127 Because telomerase is known to counteract telomere shortening by synthesizing telomeric DNA repeat

128 ve limits and cellular senescence induced by telomere shortening can influence the emergence and evol

129 Telomere shortening can lead to chromosome instability,

130 ows all of the hallmarks of aging, including telomere shortening, cellular senescence, activation of

131 mutants that fail to interact with Ccq1 show telomere shortening, checkpoint activation, and loss of

132 logically normal epithelium, suggesting that telomere shortening contributes to the initiation of TII

133 Furthermore, progressive telomere shortening correlated with severity of disease,

134 suggest a potential novel mechanism for how telomere shortening could contribute to aging and diseas

135 ear distribution of telomeres and results in telomere shortening, defects in telomeric heterochromati

136 ribe a mutation of Tpz1 that causes critical telomere shortening despite telomeric accumulation of th

137 ield of chronic inflammation, which leads to telomere shortening, DNA damage, and senescence.

138 to induce the senescent phenotype including telomere shortening, DNA damage, oxidative stress, and o

139 erase-mediated telomere addition counteracts telomere shortening due to incomplete DNA replication.

140 that haploinsufficiency was the mechanism of telomere shortening due to TERT mutations.

141 the HSC is to partially counter the rate of telomere shortening during division of HSCs, thereby pre

142 a indicate that Fancc deficiency accelerates telomere shortening during high turnover of hematopoieti

143 These principles include the absence of telomere shortening during plant development and the cor

144 Both oxidative stress and telomere shortening/dysfunction cause aging-related dege

145 n dysfunctional telomeres, telomere loss and telomere shortening, elevation of telomere sister-chroma

146 iescence, replication-associated DNA damage, telomere shortening, epigenetic alterations, and metabol

147 type Ku70 in these mutants leads to discrete telomere-shortening events consistent with telomere rapi

148 Progressive telomere shortening eventually results in chromosome fus

149 population as a function of the influence of telomere shortening, fluctuations, and cell division.

150 epletion of functional Hsp90 caused dramatic telomere shortening followed by apoptosis.

151 gesting a mechanism of action independent of telomere shortening for the effects of imetelstat on the

152 ctively, these data suggest a causal role of telomere shortening for the functional deficiencies of H

153 Critical telomere shortening (for example, secondary to partial t

154 rying heterozygous RTEL1 mutations displayed telomere shortening, fragility and fusion, and growth de

155 Telomere shortening has been linked to multiple aging-re

156 Telomere shortening has been linked to rare human disord

157 Telomere shortening has been shown to contribute to a pe

158 he significance of p16(INK4a) in response to telomere shortening have been hampered by the concomitan

159 By contrast, we examine stress and telomere shortening in a non-Western setting among a hig

160 were significantly associated with critical telomere shortening in adjacent, morphologically normal

161 t AF and no evidence of relative atrial cell telomere shortening in AF.

162 However, the significance of telomere shortening in age-associated decline of immune

163 lence of TERC and TERT gene mutations and of telomere shortening in an unselected population of patie

164 we also observed that Ape1 depletion caused telomere shortening in both BJ-hTERT and in HeLa cells.

165 ld reductions in telomerase RNA levels cause telomere shortening in both humans and the yeast Sacchar

166 g-term treatment with BRD4 inhibitors caused telomere shortening in both mouse and human cells, sugge

167 caused inhibition of telomerase activity and telomere shortening in breast and prostate cancer cells.

168 the present study was to investigate whether telomere shortening in CHD is restricted to specific per

169 Little is known about risk factors for telomere shortening in childhood.

170 We report progressive telomere shortening in developing mouse cardiomyocytes a

171 degradation of p53 compensates for continued telomere shortening in E6/E7 cells and demonstrate that

172 Interestingly, telomere shortening in elo3Delta cells was almost comple

173 es not provide direct evidence for leukocyte telomere shortening in famine survivors.

174 n of telomerase is not sufficient to prevent telomere shortening in highly proliferative Treg.

175 results lend support to the hypothesis that telomere shortening in human beings contributes to morta

176 nt inhibition of telomerase induces a severe telomere shortening in human T-cell leukemia virus type-

177 These results suggest that the rapid telomere shortening in infants is largely determined by

178 lies that mass famine may be associated with telomere shortening in male descendants of famine surviv

179 Here, we demonstrate that telomere shortening in NOTCH1-haploinsufficient mice is

180 Telomere shortening in patients with CHD could potential

181 Telomere shortening in populations of human mammary epit

182 of phytoceramide seem to be dispensable for telomere shortening in response to loss of ELO3.

183 Telomere shortening in somatic tissues largely reflects

184 n the inflammatory potential of the diet and telomere shortening in subjects with a high cardiovascul

185 00 after aHCT was followed by an accelerated telomere shortening in t-MDS/AML patients when compared

186 Finally, we demonstrated progressive telomere shortening in tbKU80-deficient mutants.

187 Telomere shortening in telomerase knockout strains cause

188 ive passage through culture, and the rate of telomere shortening in telomerase-deficient (Tert(Delta)

189 oss of telomere function through progressive telomere shortening in the absence of telomerase leads t

190 We found marked telomere shortening in the majority (52.5%) of invasive

191 The latter was unable to detect telomere shortening in the tissues.

192 acetylates histone H4 lysine 16 (H4K16), and telomere shortening in tlc1 mutants was accompanied by a

193 ecreased telomerase activity and progressive telomere shortening in vivo.

194 the "end-replication problem" contribute to telomere shortening in vivo.

195 loss of telomerase processivity in vitro and telomere shortening in vivo.

196 alysis (STELA) we show that the mean rate of telomere shortening in WS bulk cultures ranges between t

197 Telomere shortening, in the course of somatic cell repli

198 Accelerated telomere shortening, increased G overhang and elevated n

199 telomerase activator (TAT2) modestly retards telomere shortening, increases proliferative potential,

200 and sluggish cell cycle progression; marked telomere shortening indicated proliferative stress-induc

201 sed p16(INK4a) expression, in the absence of telomere shortening, indicates that premature PT-ECFC ag

202 ing of heterozygotes resulted in progressive telomere shortening, indicating that limiting telomerase

203 th the increase in cellular death induced by telomere shortening-induced DNA damage signals, includin

204 Telomere shortening induces a nonproliferative senescent

205 Telomere shortening induces chromosomal instability that

206 This study provides evidence that telomere shortening is a common genetic alteration in ES

207 This proliferation-independent telomere shortening is accompanied by an induction of a

208 Abnormal telomere shortening is also described in cases of acquir

209 Our results support the hypothesis that telomere shortening is associated with increased risk of

210 Telomere shortening is associated with senescence and in

211 Telomere shortening is associated with telomeric DNA dam

212 shorten in response to oxidative stress, and telomere shortening is correlated with reduced survival

213 Telomere shortening is counteracted by the cellular enzy

214 required for maintenance of telomeric DNA as telomere shortening is dramatically accelerated in atr t

215 Telomere shortening is implicated in cancer and aging an

216 Telomere shortening is more prominent in EACs bearing lo

217 Telomere shortening is of pathogenic and prognostic impo

218 In other organisms, the rate of telomere shortening is proportional to the length of the

219 Telomere shortening is proposed to be a primary molecula

220 ecular damage that occurs in HSCs induced by telomere shortening is transmitted to the progenitor cel

221 Accelerated telomere shortening is virtually universal in dyskeratos

222 suppression, which does involve progressive telomere shortening, is crisis, the state that cells rea

223 This suggests that telomere shortening largely occurs after diagnosis, and

224 Progressive telomere shortening leading to growth inhibition and cel

225 Telomere shortening limits the proliferative capacity of

226 Telomere shortening limits the proliferative capacity of

227 tions were invariably associated with marked telomere shortening (<< 1st percentile) in peripheral bl

228 In response to telomere shortening, male germ cells mostly undergo apop

229 ly stages of tumorigenesis, when progressive telomere shortening may be limiting cell viability.

230 In KSHV-infected cells, telomere shortening may be one more mechanism by which L

231 These findings suggest that telomere shortening may be the primary driving force beh

232 Drugs that assist in telomere shortening may contribute to tumor regression.

233 The diverse causes of telomere shortening may explain variability in LTL betwe

234 s important in the initiation of DC, whereas telomere shortening may modify and/or exacerbate DC.

235 To counteract replication-dependent telomere shortening most eukaryotic cells rely on the te

236 Telomere shortening necessitates that tumor cells activa

237 ading to telomere elongation rather than the telomere shortening observed in other telomeropathies.

238 chromosome fusions, suggesting that critical telomere shortening occurred before or concomitant with

239 ads to haploinsufficiency of telomerase, and telomere shortening occurs despite the presence of telom

240 In humans, telomere shortening occurs during aging, while inappropr

241 Progressive telomere shortening occurs with division of normal human

242 Deleting TERT resulted in progressive telomere shortening of 3-6 bp per generation.

243 S mutation predisposes to AA by accelerating telomere shortening of leukocytes via a telomerase-indep

244 d recombination, we characterized effects of telomere shortening on spermatogenesis and oogenesis in

245 t telomeres is triggered by either excessive telomere shortening or disruptions in the function of te

246 d apoptosis in the absence of any detectable telomere shortening or DNA damage response.

247 ed Cdc13N dimerization or DNA binding caused telomere shortening or lengthening, respectively.

248 n occurs during tumorigenesis and aging upon telomere shortening or loss of the telomeric shelterin c

249 impaired and cells can no longer respond to telomere shortening or oncogene activation by entering s

250 f marine omega-3 fatty acids and the rate of telomere shortening over 5 years.

251 n telomerase activity is sufficient to cause telomere shortening over many years.

252 us, mutations in TERT or TERC that result in telomere shortening over time confer a dramatic increase

253 2 m (53+/-8.8%; P<0.05)], accelerated aortic telomere shortening (P<0.01), increased DNA damage (79+/

254 brain cell telomere shortening, and whether telomere shortening plays a causal role in or exacerbate

255 telomeric DNA, suggesting that catastrophic telomere shortening preceded fusion.

256 that tankyrase1 RNA interference results in telomere shortening proportional to the level of knockdo

257 wth rates, premature senescence, accelerated telomere shortening rates, and genome instability.

258 d a differentiative pathway with progressive telomere shortening reflecting antecedent in vivo prolif

259 ying genetic mutations and the mechanisms of telomere shortening remain unknown for as many as 50% of

260 erited TL shortening or acquired accelerated telomere shortening restricted to the hematopoietic syst

261 Here we show that telomere shortening results in DNA damage accumulation a

262 sue of Blood, Wang et al elegantly show that telomere shortening results in DNA damage that induces a

263 infiltrating leukocytes were associated with telomere shortening, senescence, and reduced p53 express

264 effect on cell growth but caused progressive telomere shortening similar to that observed upon TERT d

265 mutations in human cells led to accelerated telomere shortening, similar to the telomere phenotypes

266 s in telomerase, the enzyme that counteracts telomere shortening, suggesting a telomere-based disease

267 nd its misregulation is linked to cancer and telomere-shortening syndromes.

268 ell analyses show that, well before critical telomere shortening, telomerase is continuously required

269 rigenesis in this setting is associated with telomere shortening that can be observed in the nondyspl

270 odel senescence, we found that with critical telomere shortening, the telomere-binding protein Rap1 (

271 terference stabilizes Pin2/TRF1 and promotes telomere shortening, thereby impairing cell growth.

272 The rate of telomere shortening therefore, agrees with the predicted

273 pid postnatal catch-up growth leads to islet telomere shortening through alterations in antioxidant d

274 Vitamin D may reduce telomere shortening through anti-inflammatory and anti-c

275 telomeres, and oxidative stress accelerates telomere shortening through generation of DNA single-str

276 ession of TRF2 has also been shown to induce telomere shortening, through an unknown mechanism.

277 Telomere shortening ultimately limits the replicative li

278 ce of certain types of survivors of critical telomere shortening via mechanisms dependent on Rad52-de

279 stent with inefficient C-strand maintenance, telomere shortening was accelerated in ku70 tert double

280 Unexpectedly, telomere shortening was accelerated in TIN2(+/DC) mTR(-/

281 7S treatment-induced progressive telomere shortening was associated with growth inhibitio

282 Telomere shortening was closely associated with increasi

283 Furthermore, the rate of telomere shortening was increased approximately 2-fold d

284 Finally, telomere shortening was most prominent in third-generati

285 However, this telomere shortening was not accompanied by changes in to

286 Telomere shortening was not pathognomonic of DC, as appr

287 r normal epithelia studied to date, moderate telomere shortening was observed in benign secretory cel

288 No telomere shortening was observed in Mre11(ATLD1/ATLD1) c

289 c liver cirrhosis with IPF suggests that the telomere shortening we identify has consequences and can

290 has effects other than those associated with telomere shortening, we characterized both mTERT(+)/(-)

291 09 reduces telomerase activity, resulting in telomere shortening, whereas 2'-O methylation at A804 or

292 oduces telomerase inhibition and accelerated telomere shortening, whereas facilitation of the formati

293 cence: Firstly, it has been established that telomere shortening, which is the major contributor to t

294 ufficient and that their deficiency leads to telomere shortening, which limits tissue renewal.

295 d the telomerase TERT leads to rapid, severe telomere shortening, which occurs much more rapidly than

296 results in less telomeric damage and slower telomere shortening, while telomere-dependent growth arr

297 C) mouse embryonic fibroblasts (MEFs) showed telomere shortening with proliferation.

298 Aging was associated with telomere shortening within both subsets, raising the pos

299 vercome the proliferative barrier imposed by telomere shortening without additional tumor-selected mu

300 Genetic depletion of p75 induced telomere shortening without affecting the accumulation o