ライフサイエンスコーパス: replicative senescence

1 feration after a finite number of divisions (replicative senescence).

2 lowing successive rounds of DNA replication (replicative senescence).

3 uced premature senescence (SIPS) and chronic replicative senescence.

4 beta-galactosidase activity, and accelerated replicative senescence.

5 g the transcriptional program of induced and replicative senescence.

6 nse at telomeres, resulting in p53-dependent replicative senescence.

7 ptional cascade also plays a central role in replicative senescence.

8 o an irreversible cell cycle arrest known as replicative senescence.

9 presents a key event in the establishment of replicative senescence.

10 th is not the molecular signal that triggers replicative senescence.

11 2 expression directly modulated the onset of replicative senescence.

12 positive regulatory role during p53-mediated replicative senescence.

13 lines as well as in primary cells undergoing replicative senescence.

14 e that ING2 is also involved in p53-mediated replicative senescence.

15 ation of multiple CDK inhibitors involved in replicative senescence.

16 tion doublings (PDs) showed no indication of replicative senescence.

17 because naive T cells collectively approach replicative senescence.

18 elomeres is responsible for the induction of replicative senescence.

19 of CD8(+) T cell dysfunction associated with replicative senescence.

20 e genes whose enhanced expression can bypass replicative senescence.

21 vitro, with karyotypic normalcy and without replicative senescence.

22 to contact inhibition, serum starvation, or replicative senescence.

23 s of Cdk2 and Cdc2, and ultimately increased replicative senescence.

24 cle until critically short telomeres trigger replicative senescence.

25 d results in a growth-arrested state, called replicative senescence.

26 an accumulation of lymphocytes that achieved replicative senescence.

27 normal human cells, and eventually leads to replicative senescence.

28 e CD28- cells, believed to be close to or at replicative senescence.

29 phenotypes that overlap with telomere-based replicative senescence.

30 ine production) is a specific consequence of replicative senescence.

31 ngth alone is unlikely to trigger entry into replicative senescence.

32 on of normal human cells by a process termed replicative senescence.

33 progressive shortening of telomeric DNA and replicative senescence.

34 of population doublings, a phenomenon termed replicative senescence.

35 eins that were differentially expressed upon replicative senescence.

36 netic screens to identify genes required for replicative senescence.

37 re to proliferate has been misinterpreted as replicative senescence.

38 endant genomic instability may contribute to replicative senescence.

39 r telomere structure, rather than length, in replicative senescence.

40 ormation is the ability of cells to overcome replicative senescence.

41 ng and enter a state of growth arrest called replicative senescence.

42 eviously been recognized to be involved with replicative senescence.

43 rmal human fibroblasts allows them to escape replicative senescence.

44 damage enter a state that closely resembles replicative senescence.

45 itotic counting mechanism that culminates in replicative senescence.

46 se in collagenase expression observed during replicative senescence.

47 (Cdk) inhibitor critical for cells to enter replicative senescence.

48 d SH-F expresses markers of cells undergoing replicative senescence.

49 nduce cell migration and division, and delay replicative senescence.

50 on exogenous growth factors and escape from replicative senescence.

51 critical role for HuR during the process of replicative senescence.

52 ng eukaryotic chromosome ends and preventing replicative senescence.

53 c cells enter a growth arrest state known as replicative senescence.

54 of these cells to divide as they enter into replicative senescence.

55 t of an age-related phenotype, and premature replicative senescence.

56 manent state of cell cycle arrest resembling replicative senescence.

57 t progression by overcoming oncogene induced replicative senescence.

58 cytes, but Id-1 did not prevent the onset of replicative senescence.

59 c markers characteristic of cells undergoing replicative senescence.

60 ced by a somatic cell and is associated with replicative senescence.

61 tures of genomic instability and accelerated replicative senescence.

62 H2O2 represents a critical signal mediating replicative senescence.

63 s before entering a nondividing state called replicative senescence.

64 ivide indefinitely due to a process known as replicative senescence.

65 g human aging, clarifying the role played by replicative senescence.

66 vitro being reduced by 80% near the time of replicative senescence.

67 ounteracted the effects on clonogenicity and replicative senescence.

68 ulture and enter a non-dividing state called replicative senescence.

69 vine RPE cultures that were aged in vitro by replicative senescence.

70 ultimately enter a nondividing state called replicative senescence.

71 ryonic tissue, but is lost as cells approach replicative senescence.

72 op an arrest in cell division referred to as replicative senescence.

73 ly accepted criteria, indistinguishable from replicative senescence.

74 ls progressed normally from early passage to replicative senescence.

75 ation and enter a growth-arrest state termed replicative senescence.

76 ntering a growth arrest state that is termed replicative senescence.

77 expression, they may have reached a state of replicative senescence.

78 pectroscopy, following their transition into replicative senescence.

79 ith Delta133p53alpha and is downregulated at replicative senescence.

80 a133p53alpha is degraded by autophagy during replicative senescence.

81 MCs both derived from plaques and undergoing replicative senescence.

82 shortens with age and predicts the onset of replicative senescence.

83 hanges in HR efficiency as cells progress to replicative senescence.

84 efore entering a proliferative arrest termed replicative senescence.

85 empty vector and serially subcultured until replicative senescence.

86 omatic cell replication, ultimately leads to replicative senescence.

87 adenosine deaminase (ADA), on the process of replicative senescence.

88 ven proliferation, reaching the end stage of replicative senescence.

89 seen in several cancer cell lines and during replicative senescence.

90 iferation, indicating that they are close to replicative senescence.

91 1, a marker for terminal differentiation and replicative senescence.

92 portant role in the regulation of HuR during replicative senescence.

93 hways very similar to those activated during replicative senescence.

94 olve with fibrosis in response to hepatocyte replicative senescence.

95 function, resulting in distinct kinetics of replicative senescence.

96 3 demethylase Ndy1/KDM2B protects cells from replicative senescence.

97 dergo an irreversible growth arrest known as replicative senescence [1].

98 However, p19(Arf) is required for replicative senescence, a condition associated with an a

99 PLA2R1 has been described as regulating the replicative senescence, a telomerase-dependent prolifera

100 trition in primary human fibroblasts induces replicative senescence accompanied by activation of the

101 Replicative senescence accounts for the characteristic B

102 lls exhibited normal karyotype and underwent replicative senescence after 65-70 population doublings;

103 Normal human cells in culture enter replicative senescence after a finite number of populati

104 microvascular endothelial cells also bypass replicative senescence after introduction of hTERT.

105 ive DNA damage, DNA double-strand breaks and replicative senescence, all of which are partially abrog

106 at CD8(+) cells expressing CD57, a marker of replicative senescence, also expressed KLRG1; however, a

107 HIV consists of cells that show features of replicative senescence, an end stage characterized by ir

108 nction of p21Waf1/Cip1/Sdi1 as an inducer of replicative senescence and a major mediator of this phen

109 Telomerase loss results in replicative senescence and a switch to recombination-dep

110 This mouse model also showed accelerated replicative senescence and accumulation of DNA-damage fo

111 corneal epithelial stem/progenitor cells to replicative senescence and apoptosis.

112 The mechanism of replicative senescence and cell immortality is still unc

113 mature senescence was indistinguishable from replicative senescence and could be mediated by either t

114 most primary cells in culture is limited by replicative senescence and crisis, p53-dependent events.

115 Tumour formation is blocked by two barriers: replicative senescence and crisis.

116 (TERT) expression enables cells to overcome replicative senescence and escape apoptosis, which are f

117 Egr1-null mouse embryo fibroblasts bypass replicative senescence and exhibit a loss of DNA damage

118 om irreversibly failing livers show signs of replicative senescence and express genes that simultaneo

119 We describe a method to reversibly bypass replicative senescence and generate mass cultures that h

120 provide an explanation for the induction of replicative senescence and genome instability by shorten

121 EC replicative senescence and IL-1 have been associated wit

122 Selenium levels regulate the entry into replicative senescence and modify the cellular markers c

123 n serially passaged NHP cells, which precede replicative senescence and occur in a cell-autonomous ma

124 orm at lamin B1-associated domains (LADs) in replicative senescence and oncogene-induced senescence a

125 Comparison between replicative senescence and SIPS indicates that replicati

126 protein levels increased in cells undergoing replicative senescence and stress-induced senescence.

127 r a role of ADA in modulating the process of replicative senescence and suggest that strategies to en

128 families are up-regulated during induced and replicative senescence and that up-regulation requires a

129 k repair in influencing both the kinetics of replicative senescence and the rate of chromosome loss i

130 tions implicate Nek4 as a novel regulator of replicative senescence and the response to double-strand

131 and p14ARF, both of which are implicated in replicative senescence and tumor suppression in differen

132 Immortal HMEC that have both overcome replicative senescence and undergone the recently descri

133 roperties may underlie its ability to thwart replicative senescence and, not surprisingly, have been

134 gation causing stem cells to enter premature replicative senescence and/or apoptosis as telomeres bec

135 ortening can lead to chromosome instability, replicative senescence, and apoptosis in both somatic an

136 lified ovarian cancer cells without inducing replicative senescence, and did not inhibit the prolifer

137 played decreased doubling times, escape from replicative senescence, and escape sensitivity to contac

138 r-induced ERK activation, H-Ras(V12)-induced replicative senescence, and H-Ras(V12)-induced transform

139 rucial role in cell differentiation, unequal replicative senescence, and stem cell maintenance.

140 usal relationships between telomere loss and replicative senescence, and telomerase activation and im

141 erved in normal human fibroblasts undergoing replicative senescence, and was associated with the upre

142 in dividing somatic cells can contribute to replicative senescence, apoptosis, or neoplastic transfo

143 Cell cycle, apoptosis, and replicative senescence are all influenced by the cyclin-

144 ng progressive T-cell differentiation toward replicative senescence are maintained actively by inhibi

145 (SIPS) and how similar this mechanism is to replicative senescence are not well understood.

146 to provide evidence for clonal exhaustion or replicative senescence as a mechanism underlying the dec

147 Moreover, Notch1 appears to mediate replicative senescence as well as transforming growth fa

148 s as well as by cell origins, and argue that replicative senescence at the molecular level is a diver

149 ey role in mammalian cells when they undergo replicative senescence at their Hayflick limit.

150 ers SIPS and telomere DNA damage accelerates replicative senescence, both mediated via p53.

151 However, HMEC that have overcome replicative senescence but have not undergone conversion

152 were remarkably similar to those induced by replicative senescence but occurred in only 13 days vers

153 gulated when WI-38 human fibroblasts undergo replicative senescence, but not quiescence, and extends

154 rescued populations of ku80(-/-) cells from replicative senescence by enabling spontaneous immortali

155 driven to the nonproliferative end stage of replicative senescence by multiple rounds of Ag-driven c

156 erference, we showed its requirement for the replicative senescence caused by hSNF5 but not the growt

157 To compare the replicative senescence caused by hSNF5 in A204 cells to

158 ogenous adenosine accelerates the process of replicative senescence, causing a reduction in overall p

159 Replicative senescence/crisis is thought to act as a tum

160 We show that, in a mouse model of replicative senescence, decline in muscle satellite cell

161 -deficient cells, the absence of NHEJ delays replicative senescence, decreases loss of viability duri

162 dependent differential proteomic analysis of replicative senescence, directly in primary rat embryo f

163 and p14(AFR) expression, but in contrast to replicative senescence, display neither attrition of tel

164 ARF induction by oncogenes or replicative senescence does not alter NPM/B23 protein le

165 Replicative senescence, due to the shortening and dysfun

166 ndicate that p63 proteins may play a role in replicative senescence either by competition for p53 DNA

167 riety of processes, including tumorigenesis, replicative senescence, excision repair and response to

168 s been the basis of their use as a model for replicative senescence for many years.

169 ated telomeres, propagated in culture beyond replicative senescence for more than 300 cell doublings

170 mary human cells inevitably enter a state of replicative senescence for which the specific molecular

171 lasts whose cell-cycle arrest at the time of replicative senescence has been blocked and demonstrate

172 he pathways that link shortened telomeres to replicative senescence has been severely hindered by the

173 ne system, including cell cycle progression, replicative senescence, hemopoietic stem cell quiescence

174 contribute to the molecular understanding of replicative senescence, Hh-mediated oncogenesis, and pot

175 nhancing escape from both RasV12-induced and replicative senescence, however, both primary and immort

176 from the loss of T cells that have attained replicative senescence (i.e., the Hayflick limit).

177 he skin, the influence of cellular aging and replicative senescence (i.e., the inability, after a cri

178 inhibit full-length p53, is downregulated at replicative senescence in a manner independent of mRNA r

179 of CD28 expression, the signature change of replicative senescence in cell culture, was retarded in

180 p53 isoform switching regulates replicative senescence in cultured fibroblasts and is as

181 iously that wild type p53 can rapidly induce replicative senescence in EJ human bladder carcinoma cel

182 gest that the differences in the kinetics of replicative senescence in haploid and diploid telomerase

183 Since replicative senescence in heterogeneous primary fibrobla

184 n-induced genome instability and accelerated replicative senescence in HGPS.

185 r studies define a phenotype associated with replicative senescence in HIV-specific CD8(+) T cells, w

186 ribe BRD7 and BAF180 as unique regulators of replicative senescence in human cells.

187 anges in gene transcription occurring during replicative senescence in human fibroblasts and mammary

188 dicate that p53 and p21 are not required for replicative senescence in human fibroblasts.

189 To address the possible role of replicative senescence in human immunodeficiency virus (

190 ession of microRNAs (miRNAs) associated with replicative senescence in human primary keratinocytes.

191 e shortening has been causally implicated in replicative senescence in humans.

192 ity factor on chromosome 4 (MORF4) to induce replicative senescence in immortal cell lines assigned t

193 ity is a widely used biomarker for assessing replicative senescence in mammalian cells.

194 Replicative senescence in MEFs is classically triggered

195 otoxic agents, genomic instability and early replicative senescence in primary fibroblasts.

196 be based on low antigen dose, to decelerate replicative senescence in responding cells and favor lin

197 oliferation and expressed several markers of replicative senescence in response to E2F1.

198 er of population doublings required to reach replicative senescence in several human fibroblast strai

199 elomere length can lead to the prevention of replicative senescence in some human somatic cells grown

200 was observed, Id-1 could delay the onset of replicative senescence in unselected human keratinocyte

201 Normal somatic cells undergo replicative senescence in vitro but the significance of

202 telomeres has been shown to ultimately cause replicative senescence in vitro for a number of differen

203 Additionally, Pin1 overexpression inhibits replicative senescence, increases differentiation, and i

204 Ultimately, the cells underwent replicative senescence, indicating intact cell cycle con

205 Current models of replicative senescence involve protracted procedures to

206 sic studies in cell biology demonstrate that replicative senescence is a common pathway of many cell

207 Replicative senescence is a model for in vivo aging; the

208 Replicative senescence is a natural barrier to cellular

209 Such a scenario would suggest that replicative senescence is a tumor-suppressive mechanism

210 plicative senescence and SIPS indicates that replicative senescence is almost exclusively associated

211 t (i.e., quiescence), supports the view that replicative senescence is associated with alteration of

212 These data show that replicative senescence is caused by a p53-dependent cell

213 Several lines of evidence suggest that replicative senescence is caused by short dysfunctional

214 Replicative senescence is characterized by irreversible

215 in cells with increased T-SCE, the onset of replicative senescence is dramatically accelerated even

216 Thus, replicative senescence is induced by a change in the pro

217 ding on expression of the pRB regulator p16, replicative senescence is not necessarily irreversible.

218 Replicative senescence is the state of irreversible prol

219 Replicative senescence is thought to be a significant ba

220 Replicative senescence is thought to be an intrinsic mec

221 itation of proliferative capacity imposed by replicative senescence is thought to contribute to both

222 Replicative senescence is thought to suppress tumorigene

223 increased during both ras-induced arrest and replicative senescence, leading to a dramatic increase i

224 sociated with proliferation incompetence and replicative senescence, less is known about the function

225 expression of p16(INK4a) by cells undergoing replicative senescence limited the accumulation of DNA d

226 dents suggests that microglia are subject to replicative senescence (loss of mitotic ability after re

227 cle arrest, elevated p16INK4a, and activated replicative senescence markers, such as beta-galactosida

228 rd the functional decrements associated with replicative senescence may lead to novel types of immuno

229 Replicative senescence may result from chronic, low-dose

230 er of cell divisions before growth arrest or replicative senescence, modulated in part by the proinfl

231 dult cardiac muscle exhibits similarities to replicative senescence more generally and constitutes a

232 ion is a consequence of clonal expansion and replicative senescence, multiple CD4(+)CD28(null) T cell

233 studies show that, in addition to inhibiting replicative senescence, Ndy1 inhibits Ras oncogene-induc

234 pe recapitulated several salient features of replicative senescence, notably the presence of senescen

235 ture senescence is phenotypically similar to replicative senescence observed in normal cell strains a

236 tential following PH, and suggest that early replicative senescence of differentiated hepatocytes may

237 Replicative senescence of human diploid fibroblasts (HDF

238 Replicative senescence of human T cells is characterized

239 attrition (by >2-fold) and induced premature replicative senescence of hVSMCs--an effect that was als

240 ly expressed in adult human prostate, in the replicative senescence of NHP cells.

241 oth similarities with, and differences from, replicative senescence of normal cells, was shown to be

242 al, enzymatic, and ploidy changes resembling replicative senescence of normal cells.

243 DeltaNp73 confers resistance to spontaneous replicative senescence of primary mouse embryo fibroblas

244 The mechanism most likely involves replicative senescence of steatotic mature hepatocytes a

245 Raman and infrared spectroscopy can identify replicative senescence on the single cell level, suggest

246 YCC inhibited cell proliferation and induced replicative senescence only in lines with amplified MYCC

247 uman skin keratinocytes (KCs) that underwent replicative senescence or confluence-induced accelerated

248 cycle arrest; 2) KCs undergoing spontaneous replicative senescence or confluency predominantly expre

249 Upon replicative senescence or STUB1 knockdown, Delta133p53al

250 ber of times in vitro, a phenomenon known as replicative senescence or the Hayflick limit.

251 is initiated by the shortening of telomeres (replicative senescence) or by other endogenous and exoge

252 implicated a possible role for p16 in normal replicative senescence, other studies have suggested tha

253 ding a 55-kd protein that is associated with replicative senescence (p55sen).

254 ta indicate that in HMECs that have overcome replicative senescence, p57 may provide an additional ba

255 echanisms that have been proposed to explain replicative senescence, particular interest has been foc

256 asts derived from PASG mutant embryos show a replicative senescence phenotype.

257 Insofar as telomere shortening and replicative senescence prevent genomic instability and c

258 ith activation of stress-induced rather than replicative senescence programs.

259 anied by continuing apoptotic cell death, or replicative senescence, provides conditions suitable for

260 ion, apoptosis, gene and protein expression, replicative senescence, reactive oxygen species (ROS), r

261 y was to investigate whether the accelerated replicative senescence seen in Werner syndrome (WS) fibr

262 of the T cells, and also imprints them with replicative senescence signatures.

263 rate poorly in culture and undergo premature replicative senescence, somewhat reminiscent of cells de

264 eatedly divide before reaching an anergic or replicative senescence stage; 2) the CD3 zeta-chain-asso

265 ines indicated that overcoming the stringent replicative senescence step associated with critically s

266 arly identical cellular phenotype to that of replicative senescence, suggesting the activation of a c

267 that they have less stringent controls over replicative senescence than human cells.

268 ually lose the capacity to divide because of replicative senescence that results from the inability t

269 Cultured CD8+ blood T lymphocytes underwent replicative senescence that was associated with loss of

270 wn-regulation explains the telomere loss and replicative senescence that we observed in fibroblast cu

271 persistent DNA damage response (DDR) during replicative senescence, the irreversible loss of divisio

272 (ARF), both of which have been implicated in replicative senescence, the state of permanent growth ar

273 -dependent kinase inhibitor is implicated in replicative senescence, the state of permanent growth ar

274 elevated in some fibroblast cell strains at replicative senescence, through this regulation is not a

275 llular response to adriamycin treatment from replicative senescence to delayed apoptosis, demonstrati

276 p53-p21 tumour-suppressive pathways, and (2) replicative senescence triggered by telomere shortening.

277 Replicative senescence triggers mRNA expression patterns

278 SIRT1 also promotes replicative senescence under conditions of chronic stres

279 y2 undergo immortalization in the absence of replicative senescence via a JmjC domain-dependent proce

280 0T cells display a Rad51-dependent bypass of replicative senescence via induction of a highly efficie

281 omere shortening is one postulated basis for replicative senescence, via down-regulation of telomeras

282 Replicative senescence was inactivated in secondary cult

283 However, replicative senescence was induced by progesterone only

284 Moreover, this replicative senescence was not reversed by treating cult

285 Here, using two models of replicative senescence, we describe the influence of the

286 To identify genes essential for entry into replicative senescence, we performed an RNA interference

287 Here, using models of oncogene-induced and replicative senescence, we report novel histone H3 tail

288 Interestingly, cells undergoing replicative senescence were also low in Bub1 expression,

289 Cellular aging and the development of replicative senescence were monitored by the appearance

290 ontrast, cultured KCs undergoing spontaneous replicative senescence were resistant to UV-induced apop

291 tophagy, which have been well established in replicative senescence, were also described in SIPS indu

292 duce permanent growth arrest with markers of replicative senescence when overexpressed in a tetracycl

293 is telomere independent, and (2) accelerated replicative senescence which is associated with accelera

294 xes are coordinately expressed except during replicative senescence, which is characterized by the do

295 hat DNA damage is a common mediator for both replicative senescence, which is triggered by telomere s

296 Progressive telomere shortening activates replicative senescence, which prevents somatic cells fro

297 terations characteristic of cells undergoing replicative senescence with morphological, biochemical a

298 capacity of Bcl2L12 to (1) enable bypass of replicative senescence without concomitant loss of p53 o