ライフサイエンスコーパス: premature senescence

1 the loss of H-ras-induced cell cycle arrest (premature senescence).

2 cells and found that such treatment induced premature senescence.

3 nificantly inhibits oxidative stress-induced premature senescence.

4 ion of ROS in a manner that is essential for premature senescence.

5 to mitotic failure, genomic instability, and premature senescence.

6 (MTH1), sufficed to induce a DDR as well as premature senescence.

7 se persistent accumulation of ROS and induce premature senescence.

8 ht inhibits plant growth and can also induce premature senescence.

9 us allowing SnoN to stabilize p53 and induce premature senescence.

10 r bodies where it stabilizes p53, leading to premature senescence.

11 dative stress and increases oncogene-induced premature senescence.

12 e activation of p38alpha and p38gamma caused premature senescence.

13 and aneuploidy accompanied by high levels of premature senescence.

14 p21(Waf1/Cip1) protein expression and induce premature senescence.

15 dh1 in primary human fibroblasts resulted in premature senescence.

16 replicative capacity in culture, leading to premature senescence.

17 proliferative defects but did not result in premature senescence.

18 s involves the induction of IGF-1R-dependent premature senescence.

19 f the effectors downstream of p53 to promote premature senescence.

20 of the p53 family and mediates p53-dependent premature senescence.

21 ly shown to be up-regulated in K-ras-induced premature senescence.

22 normal human diploid fibroblasts results in premature senescence.

23 or participates in RAS- and p38 MAPK-induced premature senescence.

24 liferation rate, impaired S phase entry, and premature senescence.

25 es may define the mechanism of activation of premature senescence.

26 olin-1 protein expression and development of premature senescence.

27 and G(2)/M phases, increased apoptosis, and premature senescence.

28 le progression and cell migration and elicit premature senescence.

29 MAPK signaling engage HBP1 and RB to trigger premature senescence.

30 Ectopic expression of MKP2 results in premature senescence.

31 betaG expression, reduced proliferation, and premature senescence.

32 bfertility and, in a transgenic mouse model, premature senescence.

33 ak4 inhibits cell proliferation and promotes premature senescence.

34 --> p21 transcription and the development of premature senescence.

35 ras induces a stable growth arrest known as premature senescence.

36 somerase with short interfering RNA triggers premature senescence.

37 li or oncogenes often causes them to undergo premature senescence.

38 tive mutants of E1A, respectively, to rescue premature senescence.

39 cells, which were resistant to Raf-mediated premature senescence.

40 ing to irreversible proliferation arrest and premature senescence.

41 d differentiation, increased polyploidy, and premature senescence.

42 , including accelerated telomere erosion and premature senescence.

43 early-passage KCs undergo confluency-induced premature senescence.

44 being able to form nodules but with signs of premature senescence.

45 d to acquire genetic alterations that bypass premature senescence.

46 tosis, whereas BU does so mainly by inducing premature senescence.

47 dominant negative activity, inducing p16 and premature senescence.

48 tection of chromosome ends induced immediate premature senescence.

49 ced PML expression was sufficient to promote premature senescence.

50 e similarly to wild-type MEFs and exhibit no premature senescence.

51 ty to ionizing radiation, growth defects and premature senescence.

52 d lymphocytes (PBLs), which may be linked to premature senescence.

53 xygen species-induced acetylation of p53 and premature senescence.

54 cy in mice activates cell death programs and premature senescence.

55 ing to features and diseases associated with premature senescence.

56 fork stalling, reduction of fork speed, and premature senescence.

57 SiR plays an important role in prevention of premature senescence.

58 n by IRE1alpha is essential for HRas-induced premature senescence.

59 ary for proper control of the cell cycle and premature senescence.

60 s leads to induction of these inhibitors and premature senescence.

61 oblasts resulted in proliferative arrest and premature senescence.

62 ts Ataxin-1 and Snurportin-1, and preventing premature senescence.

63 ycle arrest and mediating DNA damage-induced premature senescence.

64 related to a severe deficiency in UV-induced premature senescence.

65 ase activity and upregulated p16, indicating premature senescence.

66 s-induced activation of p53 and induction of premature senescence.

67 eactive oxygen species (ROS) is critical for premature senescence, a process significant in tumor sup

68 DHX9 in primary human fibroblasts results in premature senescence, a state of irreversible growth arr

69 ents are characterized by slow growth rates, premature senescence, accelerated telomere shortening ra

70 with the dissolved PhIP but clearly induced premature senescence activities that may be caused by a

71 activation of the MAPK cascade implies that premature senescence acts as a fail-safe mechanism to li

72 The rosettes of GGT1 knockouts showed premature senescence after flowering.

73 he oncogenic H-RAS-induced DDR and attendant premature senescence, although it does not affect the ob

74 NIH3T3 fibroblasts resulted in induction of premature senescence, an enlarged and flattened cellular

75 rom Bub3/Rae1 haploinsufficient mice undergo premature senescence and accumulate high levels of p19,

76 specifically required for the development of premature senescence and apoptosis induced by Brca1 defi

77 FoxM1 to control oxidative stress to escape premature senescence and apoptosis.

78 file of the des1-1 mutant corresponds to its premature senescence and autophagy-induction phenotypes,

79 53 mRNA polyadenylation/translation, induces premature senescence and enhances the stability of CPEB

80 iopsies were analyzed for characteristics of premature senescence and fibrosis.

81 KL deficiency leads to premature senescence and impaired Ca2+/Pi homeostasis, w

82 TRIM32-deficient primary myoblasts underwent premature senescence and impaired myogenesis due to accu

83 o be reversible, because HES1 prevented both premature senescence and inappropriate differentiation i

84 expression of cathepsin K in pre-OCs induced premature senescence and increased expression of p19, p5

85 hat ECFC dysfunction in PT might result from premature senescence and investigated the underlying mec

86 c treatment is critical for MM cell entry in premature senescence and is required for the preferentia

87 Confluency and interferon-gamma induced premature senescence and p16 expression was linked to in

88 emonstrating depressed heme synthesis showed premature senescence and reduced expression of NMDAzeta1

89 This cellular phenotype was linked to premature senescence and reduced proliferation.

90 ed by hydrogen peroxide application promotes premature senescence and stimulates the activity of a (-

91 odification of p53 and pRB may play roles in premature senescence and stress response.

92 ithin the ras signaling cascade that lead to premature senescence and, thus, have provided new insigh

93 e maintenance including genomic instability, premature senescence, and accelerated telomere erosion.

94 rease in the accumulation of Pi in siliques, premature senescence, and an increase in transcript leve

95 s, including mediation of cell cycle arrest, premature senescence, and apoptosis.p53 also can associa

96 ssion of let-7b down-regulates EZH2, induces premature senescence, and counteracts immortalization of

97 bnormalities, including telomere shortening, premature senescence, and defects in the activation of S

98 ner associated with decreased proliferation, premature senescence, and error-prone recovery from seru

99 vation of Nrf2-dependent signaling, promotes premature senescence, and inhibits their transformed phe

100 p53/p21(Waf1/Cip1) pathway and induction of premature senescence are compromised in caveolin-1 null

101 syndrome, including genomic instability and premature senescence, are consistent with telomere dysfu

102 These results argue against premature senescence as a converging mechanism of respon

103 Recent studies have identified premature senescence as a regulatory mechanism of tissue

104 r, early-passage Foxm1(-)(/)(-) MEFs display premature senescence as evidenced by high expression of

105 h(-/-)decidual cells progressively underwent premature senescence as marked by increased senescence-a

106 This appears to trigger premature senescence, as shown by an increased expressio

107 e ionizing radiation sensitive and displayed premature senescence associated with the accumulation of

108 ivity to sucrose and nitrogen starvation and premature senescence, both during natural senescence of

109 k shows that RAS and p38 MAPK participate in premature senescence, but transcriptional effectors have

110 light growth advantage and were resistant to premature senescence by a mechanism that involved suppre

111 novel regulator of oxidative stress-induced premature senescence by acting as a link between free ra

112 Moreover, the induction of premature senescence by chronic inflammatory conditions

113 equired for the suppression of DSB-inducible premature senescence by EGFR.

114 l and doxorubicin, triggered p53-independent premature senescence by invoking oxidative stress-mediat

115 dicate that HBP1 is a necessary component of premature senescence by RAS and p38 MAPK.

116 Therefore, oncogenic ras provokes premature senescence by sequentially activating the MEK-

117 ression of CCN1 (CYR61), a potent inducer of premature senescence, by adeno-associated virus serotype

118 -70%, increases heme synthesis, and reverses premature senescence caused by H2O2 or cadmium.

119 Premature senescence caused by lower Bub1 levels depends

120 lates p53 mRNA translation and p53-dependent premature senescence, cell proliferation, apoptosis, and

121 (MEF) derived from RAP80(-/-) mice underwent premature senescence compared with wild-type (WT) MEFs,

122 Inhibiting premature senescence could have therapeutic benefit in k

123 imary mammalian cells, oncogenic ras induces premature senescence, depending on an active MEK-extrace

124 This premature senescence depends on p53 induction.

125 ull primary mouse embryo fibroblasts undergo premature senescence despite normal growth profiles at e

126 ) cells are refractory to H-Ras(V12)-induced premature senescence, despite the activation of a cascad

127 ad, it results in impaired proliferation and premature senescence due to compensatory activation of p

128 Here we show that Atm-/- astrocytes exhibit premature senescence, express constitutively high levels

129 Normal human keratinocytes (NHKs) undergo premature senescence following exposure to ionizing radi

130 Oncogene-mediated premature senescence has emerged as a potential tumor-su

131 in which few transcriptional regulators for premature senescence have been shown.

132 , mitochondrial membrane depolarization, and premature senescence in a p38MAPK- and p53-dependent man

133 essors, including PTEN and VHL, also induces premature senescence in a p53- or Rb-dependent manner.

134 ell proliferation but enhances apoptosis and premature senescence in a p53-dependent manner.

135 he level of p53 protein, leading to enhanced premature senescence in a p53-dependent manner.

136 the impact of accelerated cognitive loss and premature senescence in a vulnerable at-risk population

137 Exogenous application of JA caused premature senescence in attached and detached leaves in

138 In addition, induction of premature senescence in BM hematopoietic cells also cont

139 MI1 expression and PRC1 activity, and induce premature senescence in breast cancer cells.

140 DNA-damaging agents can induce premature senescence in cancer cells, which contributes

141 A lack of K-Ras(G12D)-induced premature senescence in caveolin-1-null mice results in

142 Activated Ras also induces premature senescence in Cdk4(-/-)Ink4a/Arf(-/-) cells an

143 ncogene (c-Jun-/- MEF) undergo p53-dependent premature senescence in conventional culture.

144 rs, exhibit cytoskeletal defects and undergo premature senescence in culture.

145 ytotoxic oxidative stress is known to induce premature senescence in diploid fibroblasts.

146 l cells mediates endothelial dysfunction and premature senescence in diverse cardiovascular and renal

147 e results suggest that reoxygenation induces premature senescence in Fancc-/- BM hematopoietic cells

148 man FECD endothelium, and suggest a role for premature senescence in FECD.

149 -1 was required for oxidative stress-induced premature senescence in fibroblasts.

150 p53/p21(Waf1/Cip1) pathway and induction of premature senescence in fibroblasts.

151 PTP1B was necessary and sufficient to induce premature senescence in H-RAS(V12)-expressing IMR90 fibr

152 Overall, our data illustrate that premature senescence in H-RAS(V12)-transformed primary c

153 IF knockdown exacerbated doxorubicin-induced premature senescence in H9C2 myoblasts, the effect was a

154 f knocking down its expression, which causes premature senescence in human fibroblasts and epithelial

155 ntioxidant treatment almost fully suppressed premature senescence in Hus1(neo/Delta1) cultures, sugge

156 and inducible overexpression of MKK9 causes premature senescence in leaves and in whole Arabidopsis

157 hibits oncogenic K-Ras (K-Ras(G12V))-induced premature senescence in mouse embryonic fibroblasts and

158 d malondialdehyde additionally contribute to premature senescence in mutant leaves.

159 This study investigated the role of premature senescence in myocardial fibrosis.

160 cytotoxic level of hydrogen peroxide induces premature senescence in NIH 3T3 cells and increases endo

161 an anti-oncogenic defense mechanism known as premature senescence in normal cells.

162 p38-mediated up-regulation of caveolin-1 and premature senescence in normal human mammary epithelial

163 ression of caveolin-1 induces stress induced premature senescence in p53 wild-type but not p53 knocko

164 ith cancer, but it also produces paradoxical premature senescence in primary cells by inducing reacti

165 Oncogenic RAS (H-RAS(V12)) induces premature senescence in primary cells by triggering prod

166 cogenic Ras causes proliferation followed by premature senescence in primary cells, an initial barrie

167 Oncogenic Ras induces premature senescence in primary cells.

168 Disrupted complex I assembly causes premature senescence in primary cells.

169 We now show that the ability to induce premature senescence in primary murine embryonic fibrobl

170 ting endogenous DEC1 attenuates p53-mediated premature senescence in response to DNA damage.

171 eneral population, suggesting a phenotype of premature senescence in SLE.

172 s the predominant cell population undergoing premature senescence in the heart.

173 n in a high percentage of cells and slightly premature senescence in the population.

174 0-hydroxycamptothecin (SN-38), an inducer of premature senescence in tumor cells.

175 s lacking the autophagy protein Atg7 undergo premature senescence in vitro and accumulate products of

176 Premature senescence in vitro has been attributed to oxi

177 androgenetic alopecia (AGA) patients undergo premature senescence in vitro in association with the ex

178 Furthermore, oxidants induced premature senescence in vitro, with accelerated telomere

179 of LB1 slows cell proliferation and induces premature senescence in WI-38 cells.

180 arette smoke extracts promote stress-induced premature senescence in wild type but not caveolin-1 nul

181 stimulation promotes acetylation of p53 and premature senescence in wild-type but not caveolin-1 nul

182 omere effects are the predominant trigger of premature senescence in WRN cells.

183 peractivation of PI3K/AKT signaling leads to premature senescence; in the presence of BRAF(V600E), MC

184 C(-/-) embryos exhibit reduced growth rates, premature senescence, increased apoptosis and delayed ce

185 DDB2-deficient cells fail to undergo premature senescence induced by culture shock, exogenous

186 f or p53 locus could rescue fibroblasts from premature senescence induced by Dicer ablation.

187 Interestingly, premature senescence induced by hydrogen peroxide is gre

188 Premature senescence induced by oncogenic Ras also decre

189 rding to the "free radical theory" of aging, premature senescence induced by oxidative stress contrib

190 f intrinsic senescence but are vulnerable to premature senescence induction by chronic proinflammator

191 he mechanism of chronic inflammation-induced premature senescence involves an abrogation of tmTNF/TNF

192 s initially mitogenic but eventually induces premature senescence involving the p53 and p16(INK4a) tu

193 primary murine cells causes growth defects, premature senescence, IR sensitivity, and inability to s

194 Ras-induced premature senescence is considered as a tumor-suppressin

195 This premature senescence is phenotypically similar to replic

196 Importantly, induction of premature senescence is recovered when caveolin-1 levels

197 Thus, reoxygenation-induced premature senescence may be a novel mechanism underlying

198 escence and they suggest the hypothesis that premature senescence may represent a tumor suppressor fu

199 embryos displayed severe defects, including premature senescence, mitotic aberrations, sensitivity t

200 y independent short hairpin RNAs resulted in premature senescence of a variety of melanoma cell lines

201 We also show that premature senescence of adult NSCs into non-neurogenic a

202 Premature senescence of balding DPC in vitro in associat

203 of enforced telomerase expression to rescue premature senescence of cultured cells from individuals

204 turn leads to spontaneous immortalization or premature senescence of Dnmt3b-deficient MEFs via a p53-

205 port to the idea of the pathogenetic role of premature senescence of endothelial cells in diabetic ma

206 In conclusion, premature senescence of endothelial cells is progressive

207 We investigated premature senescence of fetal membranes in women with pP

208 gate the molecular mechanisms underlying the premature senescence of HIV-1-specific T cells, we focus

209 Premature senescence of human ARPE-19 cells was induced

210 Development of premature senescence of HUVECs on GC could be prevented

211 evels of senescence marker genes, leading to premature senescence of KO siliques, whereas RCS and sen

212 torin treatment suggest that victorin causes premature senescence of leaves.

213 ely a consequence of replicative failure and premature senescence of lymphocytes, supporting a role o

214 These results imply that premature senescence of muscle satellite cells is an und

215 Premature senescence of myoblasts was also observed in v

216 Our data establish premature senescence of myofibroblasts as an essential a

217 Bmi-1 thus prevents the premature senescence of neural stem cells by repressing

218 Analysis of these data indicates that premature senescence of oral mucosal cells and subsequen

219 ent for elevated cdki expression, leading to premature senescence of primary cells.

220 C/EBPbeta is required for premature senescence of primary mouse fibroblasts induce

221 DNA damage response that ultimately leads to premature senescence of susceptible cells.

222 mblance of pPROM and term membranes suggests premature senescence of the membranes is a mechanistic f

223 a concentration of abscisic acid that causes premature senescence of the petals.

224 Premature senescence of the vascular endothelium is hypo

225 itus in vivo and GC exposure in vitro elicit premature senescence of the vascular endothelium, a proc

226 y shRNA (short hairpin RNA) synthesis led to premature senescence of untransformed human fibroblasts,

227 d that activation of the IGF-1R promotes the premature senescence of UVB-irradiated keratinocytes thr

228 In addition, prevention of premature senescence of vascular endothelium through con

229 iated with a loss in proliferative capacity (premature senescence) of corneal endothelial cells (CECs

230 3) Inactivation of Dnmt3b resulted in either premature senescence or spontaneous immortalization of M

231 amage triggered through oncogene activation (premature senescence) or the loss of telomeres following

232 cited as being responsible for induction of premature senescence, our findings indicate that a broad

233 , HBP1, and RB as important components for a premature-senescence pathway with possible clinical rele

234 Cells overexpressing SUMO-2/3GG showed a premature senescence phenotype as revealed by cellular m

235 The premature senescence phenotype is suppressed when MKK9 i

236 nsitivity of the uvh3 mutant to H2O2 and the premature senescence phenotype might result from failure

237 inhibited cell proliferation, and induced a premature senescence phenotype that was also observed in

238 , H2O2 and ionizing radiation and displays a premature senescence phenotype.

239 imary A-T patient fibroblasts can rescue the premature senescence phenotype.

240 GPS-iPSCs to SMCs leads to the appearance of premature senescence phenotypes associated with vascular

241 No differences in premature senescence phenotypes between normal and telom

242 interfering RNA significantly alleviated the premature senescence phenotypes in SUMO-2/3GG overexpres

243 Importantly, p400shRNA-induced premature senescence phenotypes were rescued by coexpres

244 at down-regulation of Wip1 expression during premature senescence plays a pivotal role in regulating

245 These findings suggest that W-CIN triggers premature senescence, presumably to prevent the propagat

246 glycosylation end products in development of premature senescence preventable with a peroxynitrite sc

247 Inactivation of the premature senescence program by genetic ablation of p53

248 n of oncogenes such as activated Ras induces premature senescence rather than transformation.

249 ession of oncogenes such as Ras(V12) induces premature senescence rather than transformation.

250 Furthermore, IGF-1R-dependent UVB-induced premature senescence required the phosphorylation of p53

251 However, the induction of premature senescence requires both p53 and pRb.

252 Plants further display reduced fertility and premature senescence revealing a crucial function of PSI

253 t dysfunctions, such as increased apoptosis, premature senescence, senescence-like phenotype, or poor

254 the development of both acute stress-induced premature senescence (SIPS) and chronic replicative sene

255 What triggers stress-induced premature senescence (SIPS) and how similar this mechani

256 ave undergone damage-mediated stress-induced premature senescence (SIPS) has not been studied in mous

257 Stress-induced premature senescence (SIPS) of endothelial cells (ECs) h

258 s and molecular mechanisms of stress-induced premature senescence (SIPS) of vascular endothelial cell

259 development: (1) stress- or oncogene-induced premature senescence (SIPS/OIS), mediated via the p16-Rb

260 f-Mdm2-p53-p21 pathway in natural as well as premature senescence states.

261 ncluding telomeric abnormalities and undergo premature senescence, suggesting defects in telomere met

262 that X-linked DC patient cells averted from premature senescence support normal levels of rRNA pseud

263 own of WIP1 (a p38 MAPK phosphatase) induced premature senescence that also required HBP1.

264 creased rate per population doubling and the premature senescence this loss induces can be bypassed b

265 In premature senescence, this novel secretory phenotype was

266 at lung cancer cells escape oncogene-induced premature senescence through down-regulation of caveolin

267 or Xbp1 splicing promotes growth arrest and premature senescence through hyperactivation of the IRE1

268 fully in low oxygen (3% O2), indicating that premature senescence under conventional culture conditio

269 mechanism, which gives sorghum resistance to premature senescence under soil moisture stress during t

270 ces p21 expression and induces p53-dependent premature senescence upon forced PML expression.

271 oked mitochondrial network fragmentation and premature senescence via a mechanism involving superoxid

272 sely, ectopic expression of CXCR2 results in premature senescence via a p53-dependent mechanism.

273 ained intact, the TRF2(DeltaBDeltaM)-induced premature senescence was indistinguishable from replicat

274 found that the extent of DNA damage-induced premature senescence was substantially decreased by over

275 m of senescence, often termed stress-induced premature senescence, was described.

276 s-of-function and gain-of-function models of premature senescence were used to determine its pathophy

277 (AA/AA)/MMTV-c-neu carcinoma cells underwent premature senescence when cultured under conditions used

278 ry effect of RNPC1 on cell proliferation and premature senescence, whereas combined knockdown of TAp7

279 of the heterochromatic marker H3K27me3, and premature senescence, which is prevented by telomerase.

280 eous chromosomal abnormalities and underwent premature senescence, while higher Hus1 expression in Hu