ライフサイエンスコーパス: telomere shortening

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

2 found that acrolein accelerated p53-mediated telomere shortening.

3 development of dysplasia in UC than general telomere shortening.

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

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

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

7 e immortalized endothelial cells resulted in telomere shortening.

8 non was independent of culture conditions or telomere shortening.

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

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

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

12 of ww in females) showed the slowest rate of telomere shortening.

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

14 ing cellular senescence that does not entail telomere shortening.

15 lomere dysfunction can result from excessive telomere shortening.

16 mal mononuclear cell cytokine secretion, and telomere shortening.

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

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

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

20 ere chromatin modulates senescence caused by telomere shortening.

21 tiates premature senescence independently of telomere shortening.

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

23 erexpressing Tel1 TAN mutants did not rescue telomere shortening.

24 as the complete TPP1 KO cell lines, undergo telomere shortening.

25 nactive forms of TER1 and causes progressive telomere shortening.

26 elomerase enzyme deficiency, and progressive telomere shortening.

27 iption beyond the template region and caused telomere shortening.

28 wth defects in proliferative tissues through telomere shortening.

29 DNA may inhibit telomerase access, promoting telomere shortening.

30 are independent of telomerase inhibition or telomere shortening.

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

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

33 somal dominant dyskeratosis congenita due to telomere shortening.

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

35 damage, inhibition of telomerase and marked telomere shortening.

36 he telomere repair complex cause accelerated telomere shortening.

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

38 nt dyskeratosis congenita, anticipation, and telomere shortening.

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

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

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

42 dysfunctional telomeres, without detectable telomere shortening.

43 In addition, the tel2 mutation caused telomere shortening.

44 ss reactive oxygen species (ROS) accelerates telomere shortening.

45 ) in ALT+ cancer cells leads to generational telomere shortening.

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

47 independent of forced disruption of Tp53 and telomere shortening.

48 mplicate reduced TEL patch dosage in causing telomere shortening.

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

50 sister chromatid pairing and for preventing telomere shortening.

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

52 environmental mechanisms that contribute to telomere shortening.

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

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

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

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

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

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

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

60 Unexpectedly, telomere shortening accelerated in plants lacking CST an

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

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

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

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

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

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

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

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

69 ysiological aging in wild-type mice leads to telomere shortening and a reduced proliferative potentia

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

71 Telomere shortening and alterations of mitochondrial bio

72 ciated recombination in G2, concomitant with telomere shortening and damage.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

88 on in malignant cells results in progressive telomere shortening and reduction in cell proliferation.

89 Insofar as telomere shortening and replicative senescence prevent g

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

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

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

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

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

95 ese results support the notion that critical telomere shortening and the consequent onset of telomeri

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

97 form appropriate telomeric structures drives telomere shortening and, in turn, genomic instability.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

126 To determine whether telomere shortening can be a single parameter to predict

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

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

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

130 While the loss of RTEL1 results in rapid telomere shortening, concurrent loss of both RAD51 genes

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

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

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

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

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

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

139 cell cycle in response to stresses including telomere shortening, DNA damage, or oncogenic signaling.

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

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

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

143 Progressive telomere shortening during lifespan is associated with r

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

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

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

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

148 omitant persistent cohesion that occurs with telomere shortening ensures a measured approach to repli

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

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

151 Progressive telomere shortening eventually results in chromosome fus

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

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

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

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

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

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

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

159 Telomere shortening has been associated with multiple ag

160 Telomere shortening has been linked to multiple aging-re

161 Telomere shortening has been linked to rare human disord

162 Telomere shortening has been shown to contribute to a pe

163 ular senescence, a process driven in part by telomere shortening, has been implicated in age-related

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

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

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

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

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

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

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

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

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

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

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

175 We report progressive telomere shortening in developing mouse cardiomyocytes a

176 Interestingly, telomere shortening in elo3Delta cells was almost comple

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

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

179 Telomere shortening in human cells leads to a DNA damage

180 We modelled telomere shortening in human hippocampal progenitor cell

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

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

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

184 Telomere shortening in patients with CHD could potential

185 Telomere shortening in populations of human mammary epit

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

187 y during cell division may be contributed to telomere shortening in SE.

188 Telomere shortening in somatic tissues largely reflects

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

190 00 after aHCT was followed by an accelerated telomere shortening in t-MDS/AML patients when compared

191 Telomere shortening in telomerase knockout strains cause

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

193 nucleoside counterpart of 5-MeCITP leads to telomere shortening in telomerase-positive cancer cells,

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

195 ecreased telomerase activity and progressive telomere shortening in vivo.

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

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

198 Telomere shortening, in the course of somatic cell repli

199 Accelerated telomere shortening, increased G overhang and elevated n

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

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

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

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

204 Telomere shortening induces cellular senescence in proli

205 Telomere shortening induces chromosomal instability that

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

207 Telomere shortening is a hallmark of aging.

208 Telomere shortening is a presumed tumor suppressor pathw

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

210 Abnormal telomere shortening is also described in cases of acquir

211 Telomere shortening is associated with early mortality a

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

213 Telomere shortening is associated with telomeric DNA dam

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

215 Telomere shortening is counteracted by the cellular enzy

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

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

218 Telomere shortening is implicated in cancer and aging an

219 Telomere shortening is more prominent in EACs bearing lo

220 Telomere shortening is of pathogenic and prognostic impo

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

222 Telomere shortening is proposed to be a primary molecula

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

224 Accelerated telomere shortening is virtually universal in dyskeratos

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

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

227 Telomere shortening limits the proliferative capacity of

228 Telomere shortening limits the proliferative capacity of

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

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

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

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

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

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

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

236 Telomere shortening necessitates that tumor cells activa

237 ence, cells undergo alterations that include telomere shortening, nuclear area enlargement, and genom

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

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

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

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

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 development in youths comes from studies of telomere shortening or advanced pubertal development fol

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 Rather, telomere shortening prevents the up-regulation and activ

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

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

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

259 We found that the telomere shortening rate, but not the initial telomere l

260 ious stimuli such as oncogene expression and telomere shortening, referred to as oncogene-induced sen

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

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

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

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

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

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

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

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

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

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

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

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

273 n genetic disorders that result in premature telomere shortening, the concept that inhibiting telomer

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

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

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

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

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

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

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

281 Telomere shortening to a critical length can trigger agi

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

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

284 Telomere shortening was closely associated with increasi

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

286 Telomere shortening was not pathognomonic of DC, as appr

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

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

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

290 09 reduces telomerase activity, resulting in telomere shortening, whereas 2'-O methylation at A804 or

291 Telomere shortening, which is a biomarker of biological

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

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

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

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

296 uting to genome instability, we propose that telomere shortening with age causes systemic chronic inf

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