ライフサイエンスコーパス: cellular senescence

1 it enhanced cell proliferation but decreased cellular senescence.

2 INK4AB/ARF locus, are crucial regulators of cellular senescence.

3 d Sin3B expression and subsequent entry into cellular senescence.

4 by encouraging proliferation and inhibiting cellular senescence.

5 cellular environment and ultimately leads to cellular senescence.

6 Oxidative stress can induce premature cellular senescence.

7 ntly, Notch signaling has been implicated in cellular senescence.

8 ined dormant and showed all the hallmarks of cellular senescence.

9 otein 2, an important alternate regulator of cellular senescence.

10 patterns in p53/p21 that lead to significant cellular senescence.

11 ession of Sin3B as an essential regulator of cellular senescence.

12 dentify Wnt7a as a novel upstream inducer of cellular senescence.

13 ase genes and permanent cell cycle arrest or cellular senescence.

14 way and suppresses induction of p53-mediated cellular senescence.

15 r lamina upon oncogenic insults to reinforce cellular senescence.

16 amage response, and consequently attenuating cellular senescence.

17 e proliferation and survival, and antagonize cellular senescence.

18 ll growth and proliferation to inhibition of cellular senescence.

19 mb group (PcG) protein BMI1 and induction of cellular senescence.

20 tically processed forms as key regulators of cellular senescence.

21 th the AUF1-elicited prevention of premature cellular senescence.

22 feration, whereas in old females it leads to cellular senescence.

23 he network stabilised at a new late state of cellular senescence.

24 table arrest in cell growth, which is termed cellular senescence.

25 e new mechanistic insights into HRAS-induced cellular senescence.

26 BRAF(V600E)-induced ERK hyperactivation and cellular senescence.

27 le is known about the effects of acrolein on cellular senescence.

28 ts can be generated without being limited by cellular senescence.

29 ense is specifically affected in response to cellular senescence.

30 C properties of iCSCL-10A cells, by inducing cellular senescence.

31 derpins the transition from proliferation to cellular senescence.

32 we have taken a systems biology approach to cellular senescence.

33 ely correlated with markers of lipolysis and cellular senescence.

34 such as TGF-beta, cigarette smoke (CS), and cellular senescence.

35 sed differentiation potential, and premature cellular senescence.

36 it a DNA damage response (DDR) that leads to cellular senescence.

37 patients with diabetes mellitus (DM) due to cellular senescence.

38 vival after ionizing radiation, and prevents cellular senescence.

39 , inflammation, proteostasis, apoptosis, and cellular senescence.

40 protein kinase as antagonistic effectors of cellular senescence.

41 ring RNA (siRNA) attenuated acrolein-induced cellular senescence.

42 ) cells more sensitive to epirubicin-induced cellular senescence.

43 d (SA) beta-galactosidase, a known marker of cellular senescence.

44 y displayed elevated cell doubling and lower cellular senescence.

45 wth, impairing colony formation and inducing cellular senescence.

46 dily measurable cell marker for p53-mediated cellular senescence.

47 supports the role of microRNAs in regulating cellular senescence.

48 melanoma and other tumor cells and promotes cellular senescence.

49 ed glycolysis and triggering p53-independent cellular senescence.

50 functions are not well understood, inhibits cellular senescence.

51 , suggesting that SRSF3 acts on p53-mediated cellular senescence.

52 transient, and was followed by p53-dependent cellular senescence.

53 mbrane potential that invariably resulted in cellular senescence.

54 ter telomerase activity and the avoidance of cellular senescence.

55 at helps sustain proliferation by preventing cellular senescence.

56 nomenon: a cellular stress response known as cellular senescence.

57 sive action was achieved by the induction of cellular senescence.

58 s transcription of these genes, and promotes cellular senescence.

59 g skin fibroblast proliferation and delaying cellular senescence.

60 y adversity and telomere length, a marker of cellular senescence.

61 TS) patients compared with natural aging and cellular senescence.

62 al inhibition of LSD1 triggers G1 arrest and cellular senescence.

63 on maintained in the context of p53-mediated cellular senescence.

64 cell viability and was sufficient to trigger cellular senescence.

65 ely impaired EGFR signaling and the onset of cellular senescence.

66 ive DNA damage triggers telomere erosion and cellular senescence.

67 n vitro and in vivo despite the induction of cellular senescence.

68 ion in various cellular processes, including cellular senescence.

69 at their loss leads to cell-cycle arrest and cellular senescence.

70 , reduced DNA repair responses, and elevated cellular senescence.

71 we show the critical role of mitochondria in cellular senescence.

72 veal the mechanism by which OGT functions in cellular senescence.

73 p16 expression in tumor cells, and promoted cellular senescence.

74 nhances G1 arrest and a phenotype resembling cellular senescence.

75 t E6/E7 inhibition phenotypically results in cellular senescence.

76 ) cells more sensitive to paclitaxel-induced cellular senescence.

77 s that autophagy promotes the development of cellular senescence.

78 nt biological function in ROS production and cellular senescence.

79 ly, increased ROS production and accelerated cellular senescence.

80 provide basic insights into the dynamics of cellular senescence, a central tumor- suppressive mechan

81 persistent DNA damage response contribute to cellular senescence, a degeneration process critically i

82 Cellular senescence, a form of stable cell cycle arrest

83 in lung cancer, but is also known to induce cellular senescence, a major barrier imposed on tumor ce

84 Here, we show that SRSF3 regulates cellular senescence, a p53-mediated process to suppress

85 Cellular senescence, a process that imposes permanent pr

86 although H4K20me3 abundance increases during cellular senescence, a stable proliferation arrest and t

87 Cellular senescence, a state of cell-cycle arrest accomp

88 Cellular senescence, a state of irreversible cell cycle

89 Cellular senescence, a state of persistent cell cycle ar

90 Cellular senescence, a state of stable cell cycle arrest

91 Cellular senescence, a stress-induced irreversible growt

92 p53 also promotes cellular senescence, a tumor-suppressive program that in

93 s suggest that acrolein induces p53-mediated cellular senescence accompanied by enhanced telomere att

94 rks of aging, including telomere shortening, cellular senescence, activation of PI3 kinase-mTOR signa

95 lls is known to cause genome aberrations and cellular senescence, although the molecular basis for th

96 beta activity contributes to accelerated EPC cellular senescence, an effect reversed by small molecul

97 Cellular senescence, an irreversible growth arrest trigg

98 an alter the tumor microenvironment, causing cellular senescence and activating cancer-promoting infl

99 pression in several aging phenotypes such as cellular senescence and age itself.

100 We define a particular distinction between cellular senescence and ageing and propose that caveolin

101 hondrial dysfunction has been linked to both cellular senescence and ageing.

102 iew the cellular and molecular links between cellular senescence and aging and discuss the novel ther

103 h blocked their tumorigenic capacity through cellular senescence and apoptosis.

104 Cellular senescence and associated tumor suppression dep

105 he tumor suppressor TAp63, thereby promoting cellular senescence and blocking skin tumorigenesis.

106 k loop cascade during DDR and contributes to cellular senescence and chemotherapy resistance in ovari

107 ency in mice causes chromosomal instability, cellular senescence and early onset of age-related pheno

108 satively linked to perpetual DSBs signaling, cellular senescence and fibrosis.

109 monstrate the phenomenon of oncogene-induced cellular senescence and immune-mediated clearance of sen

110 ese pathways include telomere dysfunction in cellular senescence and induction of the senescence-asso

111 ol occurred independently of lymphocytes and cellular senescence and instead ensued as part of the tu

112 p protein Bmi-1 is an essential regulator of cellular senescence and is believed to function largely

113 ecent advances on the contribution of p53 to cellular senescence and its implication for cancer thera

114 Telomerase plays a pivotal role in bypassing cellular senescence and maintaining telomere homeostasis

115 th N-acetylcysteine or metformin ameliorated cellular senescence and metabolic abnormalities.

116 and apoptosis, p53 activation also modulates cellular senescence and organismal aging.

117 ng DNA damage, HOTAIR has a critical role in cellular senescence and platinum sensitivity.

118 SIN3B was required for PTEN-induced cellular senescence and prevented progression to invasiv

119 These results identify a novel form of cellular senescence and provide a potential molecular ba

120 to nuclear accumulation of p21, resulting in cellular senescence and reduced tumorigenic potential.

121 We assessed markers of cellular senescence and senescence-associated secretory

122 These cells possessed characteristics of cellular senescence and showed a strong activation of Sp

123 histone demethylase implicated in bypass of cellular senescence and somatic cell reprogramming, is m

124 nd has adverse effects on H-Ras(V12)-induced cellular senescence and transformation.

125 cuss the link between mosaic NRAS mutations, cellular senescence, and clinical phenotype in these nev

126 ing chronic inflammatory markers, markers of cellular senescence, and imaging to assess muscle mass t

127 mulates in aging tissues, is a biomarker for cellular senescence, and limits stem cell function in vi

128 ncreased lung tumorigenesis owing to reduced cellular senescence, and not reduced apoptosis, or autop

129 uss their implications for lineage fidelity, cellular senescence, and reprogramming.

130 ve mitophagy leads to CS stress-induced lung cellular senescence, and restoring mitophagy delays cell

131 tion exhibited enhanced ER stress, decreased cellular senescence, and/or enhanced tumorigenicity.

132 tosidase (SA-beta-Gal) activity, a marker of cellular senescence; and elevated levels of phosphorylat

133 wever, the signaling mechanisms that trigger cellular senescence are incompletely understood, particu

134 salivary function was closely accompanied by cellular senescence, as evidenced by a persistent DNA da

135 ease in p16INK4a expression, with subsequent cellular senescence, as evidenced in a mouse model of el

136 me for treatments aiming to delay or reverse cellular senescence at late time points.

137 impaired antiprotease defenses, DNA damage, cellular senescence, autoantibody generation, and cortic

138 Cellular senescence both protects multicellular organism

139 The lead compound induces cellular senescence but does not inhibit telomerase acti

140 Pin1 deletion increases cellular senescence but not differentiation or cell deat

141 confirmed that DLX3 mutation (Q178R) delayed cellular senescence, but also prevented aging-mediated b

142 dergo G0/G1 cell-cycle arrest, apoptosis and cellular senescence, but without the induction of lytic

143 We found that acrolein induced cellular senescence by increasing both p53 and p21.

144 ces ovarian cancer growth while antagonizing cellular senescence by repressing the expression of cycl

145 TBK1/IKKepsilon inhibition promoted cellular senescence by suppressing p65-NF-kappaB and ind

146 In aggregate, cellular senescence checkpoint functions may influence d

147 Yet, it remains unclear as to how cellular senescence checkpoint functions may interact wi

148 pports aRMS initiation by enabling bypass of cellular senescence checkpoints.

149 ific aspects of the aging process, including cellular senescence, chronic inflammation, and the age-d

150 by UVB diminished G1 arrest, DNA repair, and cellular senescence coincident with enhanced cell death

151 Cellular senescence contributes to age-related tissue dy

152 Cellular senescence contributes to aging and decline in

153 Because cellular senescence contributes to renal aging and promo

154 layed oncogene-like characteristics inducing cellular senescence corroborated by the induction of G0/

155 in early pubertal mice results in premature cellular senescence, depleted MSPCs pool, and impaired o

156 ) results in a number of cellular responses (cellular senescence, deregulated nutrient sensing and de

157 Additionally, enhanced cellular senescence, determined by senescence-associated

158 Our study demonstrates that cellular senescence drives hepatic steatosis and elimina

159 n Cell have uncovered an unexpected role for cellular senescence during development, as a process tha

160 isingly, there is a significant induction of cellular senescence during salamander limb regeneration,

161 This investigation of heat stress-induced cellular senescence elucidates the mechanisms underlying

162 Ectopic NR2E1 expression inhibits cellular senescence, extending cellular lifespan in fibr

163 The process of cellular senescence generates a repressive chromatin env

164 Studying the phenomenon of cellular senescence has been hindered by the lack of sen

165 Cellular senescence has been recently linked to the prom

166 Cellular senescence has historically been viewed as an i

167 alterations, mitochondrial dysfunction, and cellular senescence) have been proposed as essential mec

168 t mPR promotes immortalization by preventing cellular senescence, impeding up-regulation of both the

169 RSV induced S-phase arrest and cellular senescence in a dose-dependent manner in U2OS a

170 CCN1 acts by triggering cellular senescence in activated hepatic stellate cells

171 r is tempered by the activation of premature cellular senescence in an NF1-deficient background.

172 ingly, overexpression of caveolin-1 restores cellular senescence in both A549 and H460 lung cancer ce

173 tion of damaged mitochondria associated with cellular senescence in both human lung fibroblasts and s

174 eration contributes to aging associated with cellular senescence in c-kit+ cardiac progenitor cells (

175 lication and oxidative stresses in mediating cellular senescence in cancer cells treated with RSV.

176 We examined whether acrolein induces cellular senescence in cultured normal human lung fibrob

177 accelerated aging to investigate the role of cellular senescence in HFpEF development.

178 end joining and of gamma irradiation-induced cellular senescence in human cells that are not apoptosi

179 (killer cell Ig-like receptor 2DL4) induces cellular senescence in human NK cells in response to sol

180 ce of short dysfunctional telomeres triggers cellular senescence in human somatic tissues, thus contr

181 l as transforming growth factor-beta-induced cellular senescence in non-transformed cells and that HP

182 gs also resulted in telomere dysfunction and cellular senescence in normal human cells, demonstrating

183 mitochondrial mass accumulation, and delayed cellular senescence in Parkin-overexpressing cells.

184 -mediated knockdown of ILK partially restore cellular senescence in Pparbeta/delta-null cells.

185 on of the HIRA S231A mutant delays premature cellular senescence in primary human fibroblasts, wherea

186 dings reveal a novel role for p16(Ink4a) and cellular senescence in promoting insulin secretion by be

187 ) plays a tumor suppressive role by inducing cellular senescence in response to oncogenic stress.

188 Concomitantly, increased cellular senescence in the adipose tissue from pol eta(-

189 Considerable evidence implicates cellular senescence in the biology of aging and chronic

190 ion of oncogenic K-Ras (K-Ras(G12D)) induces cellular senescence in the lung of wildtype but not cave

191 to be a primary cause of heat stress-induced cellular senescence in these cells.

192 te, leads to persistent oxidative stress and cellular senescence in vitro and in vivo.

193 P attenuates cancer cell growth by promoting cellular senescence in vivo, which correlates with resto

194 Further analysis revealed the induction of cellular senescence in zebrafish embryos overexpressing

195 l marker CD45RA have many characteristics of cellular senescence, including decreased proliferation,

196 es with a concomitant increase in markers of cellular senescence, including p21, H3K9me3, and p16.

197 cells against mitochondrial dysfunction and cellular senescence induced by oxidative stress.

198 nisms, we explore how replicative limits and cellular senescence induced by telomere shortening can i

199 Cellular senescence involves extensive cellular remodeli

200 HK1S345 phosphorylation and thereby prevents cellular senescence, IPF and carcinoma formation.

201 Cellular senescence irreversibly arrests proliferation i

202 Cellular senescence is a crucial tumor suppressor mechan

203 Cellular senescence is a fundamental aging mechanism tha

204 Collectively, these results indicate that cellular senescence is a fundamental mechanism driving r

205 Cellular senescence is a permanent growth arrest in cell

206 Cellular senescence is a process of cellular growth arre

207 Cellular senescence is a stable arrest of proliferation

208 Cellular senescence is a stable cell cycle arrest that l

209 Cellular senescence is a stable cell cycle arrest that o

210 Cellular senescence is a stable cell growth arrest that

211 Cellular senescence is a stable proliferation arrest ass

212 Cellular senescence is a stable proliferation arrest tha

213 Cellular senescence is a stable proliferation arrest, a

214 Cellular senescence is a state of irreversible cell cycl

215 Cellular senescence is a state of irreversible cell cycl

216 Cellular senescence is a state of irreversibly arrested

217 Cellular senescence is a stress response that accompanie

218 Cellular senescence is a stress-responsive cell-cycle ar

219 Cellular senescence is a terminal cell cycle arrested st

220 Cellular senescence is a terminal stress-activated progr

221 Cellular senescence is a widespread stress response and

222 Cellular senescence is accompanied by dramatic changes i

223 Cellular senescence is also a tumor suppressor mechanism

224 Cellular senescence is an antiproliferative response wit

225 The induction of cellular senescence is an important mechanism by which p

226 Cellular senescence is an important tumor suppression me

227 Cellular senescence is an initial barrier for carcinogen

228 Cellular senescence is associated with the production of

229 Cellular senescence is characterized by a permanent cell

230 Cellular senescence is implicated in several pathologica

231 Cigarette smoke (CS)-induced cellular senescence is involved in the pathogenesis of c

232 Osteoarthritis is an age-related disease and cellular senescence is predicted to be a significant com

233 ) and p19(Arf) involved in the activation of cellular senescence is sufficient to convert human fibro

234 Cellular senescence is thought to contribute to age-asso

235 sing a mouse model of liver carcinoma, where cellular senescence is triggered in vivo by inducible p5

236 The molecular mechanism by which CS induces cellular senescence is unknown.

237 Cellular senescence is widely believed to play a key rol

238 trate that heat stress induces p21-dependent cellular senescence-like cell cycle arrest.

239 -to-N-cadherin switch, reduced expression of cellular senescence markers and reduced expression of se

240 Cellular senescence markers are detectable within IPF lu

241 sulted in an up-regulation of cell death and cellular senescence markers compared with scrambled trea

242 to be associated with biological aging, and cellular senescence markers in HIV-infected adults.

243 Cellular senescence may be a key factor in HIV-related p

244 targeting of a basic aging mechanism such as cellular senescence may have a large impact on disease p

245 rate organogenesis and support the view that cellular senescence may have arisen in evolution as a de

246 Cellular senescence occurs by proliferative exhaustion (

247 ritical role by regulating proliferation and cellular senescence of HNSCC cells.

248 et and that Cox4i1 knockdown phenocopies the cellular senescence of TAp73-null cells.

249 ut down of angiogenesis and the induction of cellular senescence of tumor cells [16(**)].

250 intrinsic responses to DNA damage, including cellular senescence or apoptosis, which act to thwart tu

251 perience replication stress that can lead to cellular senescence or apoptosis.

252 to a range of cell fates, such as apoptosis, cellular senescence or cancer, depending on the efficien

253 that drive a permanent proliferative arrest (cellular senescence) or regulated cell death.

254 repression under hypoxia does not result in cellular senescence, owing to hypoxia-associated impaire

255 igenesis through bypass of Pten loss-induced cellular senescence (PICS).

256 ilar to that of Wnt7a, as a novel inducer of cellular senescence, presenting potential future clinica

257 oxidative stress and inflammation, but also cellular senescence processes, may contribute to age-rel

258 in human tumors, as a critical repressor of cellular senescence, providing a novel connection betwee

259 Cellular senescence refers to a state of irreversible ce

260 itically short telomeres, a major trigger of cellular senescence, remains unknown.

261 in wild-type MSCs recapitulates accelerated cellular senescence, resembling WRN-deficient MSCs.

262 uppressor inactivation but is triggered by a cellular senescence response and is mediated by epigenet

263 The cellular senescence response triggered by Tax is caused

264 Reprogramming of cellular senescence signaling by SPI-associated isoflavo

265 tivated protein kinase pathway, induction of cellular senescence signals, and death resulting from lo

266 f DNA damage and activation of p53-dependent cellular senescence similar to the results found in our

267 Cellular senescence suppresses cancer by halting the gro

268 Cellular senescence suppresses cancer by preventing the

269 or-1alpha up-regulation, oncogene-associated cellular senescence, TGF-beta1-associated fibrosis and i

270 SRSF3 represents an endogenous mechanism for cellular senescence that directly regulates the TP53 alt

271 Induction of cellular senescence through activation of the p53 tumor

272 16(INK4A) expression, which in turn triggers cellular senescence through activation of the retinoblas

273 igenesis by overcoming the PTEN loss-induced cellular senescence through inhibition of p21 activation

274 Decreased p-AKT activity in turn promotes cellular senescence through upregulation of p53 and p27

275 Altogether, SelH protects against cellular senescence to oxidative stress through a genome

276 a therapeutic target by exerting effects on cellular senescence to retard HCC progression.

277 ncluding leukocyte recruitment and function, cellular senescence, tumor cell proliferation, survival,

278 ll line HTR8/SVneo induced growth arrest and cellular senescence via activation of p38-mitogen-activa

279 Mechanistically, Wnt7a induced cellular senescence via inactivation of S-phase kinase-a

280 o exhibited impaired mitophagy and increased cellular senescence via suborganellar signaling.

281 Finally, the accelerated cellular senescence was also observed at the organismal

282 Strikingly, Pten-loss-induced cellular senescence was enhanced in vivo when Il1ra knoc

283 Cellular senescence was monitored by beta-galactosidase

284 DUSP3, which regulates cellular senescence, was identified as one of the diseas

285 d oxidative stress are major determinants of cellular senescence, we found that redox-dependent DDR a

286 Signs of cellular senescence were also apparent in irradiated sal

287 of cell proliferation, colony formation, and cellular senescence were evaluated in human HCC cell lin

288 The potential mechanisms for activating cellular senescence were explored using murine subcutane

289 ons (c.533 A>G and c.571_574delGGGG) delayed cellular senescence when they were introduced into pre-o

290 bated fibrosis with a concomitant deficit in cellular senescence, whereas overexpression of hepatic C

291 One such mechanism is cellular senescence, which can cause chronic inflammatio

292 Epidermal Sod2 loss induced cellular senescence, which irreversibly arrested prolife

293 ve oxygen species (ROS) can induce premature cellular senescence, which is believed to contribute to

294 Aging is associated with increased cellular senescence, which is hypothesized to drive the

295 r senescence, and restoring mitophagy delays cellular senescence, which provides a promising therapeu

296 es, in oncogene addiction, and in overcoming cellular senescence, which suggests calcineurin-NFAT sig

297 ge disrupted genomic integrity and triggered cellular senescence, which was accompanied by tumor-prom

298 ant proliferating pineal lesions resulted in cellular senescence, while p53 restoration in invasive p

299 To study cellular senescence within an adult tissue, we developed

300 p16 is a key regulator of cellular senescence, yet the drivers of this stable stat