ライフサイエンスコーパス: senescence

1 iferation, in part, through induction of ISC senescence.

2 s to identify genes required for replicative senescence.

3 ning, larger litters, and early reproductive senescence.

4 ponse, and consequently attenuating cellular senescence.

5 ignalling, and distinct stem-cell markers in senescence.

6 whereas in old females it leads to cellular senescence.

7 following their transition into replicative senescence.

8 P1 (FOXP1) in transcriptional control of MSC senescence.

9 0E)-induced ERK hyperactivation and cellular senescence.

10 ffect associated with both growth arrest and senescence.

11 TGF-beta, cigarette smoke (CS), and cellular senescence.

12 mechanism of tumor escape from apoptosis and senescence.

13 nt mechanism driving escape from Ras-induced senescence.

14 er ionizing radiation, and prevents cellular senescence.

15 They then explore telomere biology and cell senescence.

16 lpha is essential for HRas-induced premature senescence.

17 at the CDKN2A promoter following LPS-induced senescence.

18 KA, Cyrillic3, a positive regulator of leaf senescence.

19 associated with increased osteoblastic cell senescence.

20 of ZDHHC3 depletion on oxidative stress and senescence.

21 -kinase prevented the MP-induced endothelial senescence.

22 enzyme ATRX is required for therapy-induced senescence.

23 ry diseases by driving premature endothelial senescence.

24 eased their sensitivity to radiation-induced senescence.

25 locks cell cycle progression and accelerates senescence.

26 s found to be uncoupled from drought-induced senescence.

27 re attrition, altered proteostasis, and cell senescence.

28 tion, faster mycorrhization and reduced leaf senescence.

29 broblast proliferation and delaying cellular senescence.

30 red EGFR signaling and the onset of cellular senescence.

31 expression of chloroplast genes during leaf senescence.

32 c fat accumulation and markers of hepatocyte senescence.

33 ty and upregulated p16, indicating premature senescence.

34 ty and telomere length, a marker of cellular senescence.

35 ed CDKN2A/B spatial organization to suppress senescence.

36 amage and thereby reinforce oncogene-induced senescence.

37 nts compared with natural aging and cellular senescence.

38 the p53-CXCR2 axis in mediating RSV-induced senescence.

39 oplankton growth, especially following bloom senescence.

40 tion of LSD1 triggers G1 arrest and cellular senescence.

41 DNA repair responses, and elevated cellular senescence.

42 bition failed to induce cell-cycle arrest or senescence.

43 One such mechanism is senescence.

44 found that such treatment induced premature senescence.

45 P1), and p15(INK4b), preventing OSKM-induced senescence.

46 factor C/EBPbeta in primary MEFs undergoing senescence.

47 nhibition phenotypically results in cellular senescence.

48 s from ACS patients reduced the induction of senescence.

49 r phenotypes from the seedling stage through senescence.

50 reventing repression blocks progression into senescence.

51 raging proliferation and inhibiting cellular senescence.

52 and permanent cell cycle arrest or cellular senescence.

53 CDKN2A expression and reduced cholangiocyte senescence.

54 ght (0.64), and for beech bud break and leaf senescence (0.52 and 0.46).

55 Cellular senescence, a form of stable cell cycle arrest that is t

56 f from intact nuclei of primary cells during senescence, a form of terminal cell-cycle arrest associa

57 ells triggers DNA damage signaling-dependent senescence, a hallmark of RS.

58 Many cellular stresses activate senescence, a persistent hyporeplicative state character

59 METHODS AND Senescence-accelerated mice (SAM, n=18) and control mice

60 vimentin were detected in the plasma of aged senescence-accelerated mouse prone 8 mice, which are kno

61 ction of proteins informally associated with senescence accompanies the use of senescence-associated

62 ing, including telomere shortening, cellular senescence, activation of PI3 kinase-mTOR signaling, imp

63 dissolved PhIP but clearly induced premature senescence activities that may be caused by a limited re

64 n of p16(INK4a), a tumor suppressor gene and senescence/aging biomarker.

65 activity drives characteristic phenotypes of senescence, although the underlying mechanisms responsib

66 Together, we provide evidence that senescence and a stem cell-associated SASP drive cell tr

67 X is a critical regulator of therapy-induced senescence and acts in multiple ways to drive cells into

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

69 ellular and molecular links between cellular senescence and aging and discuss the novel therapeutic a

70 ) and EBNA3C (which inhibit oncogene-induced senescence and apoptosis).

71 their tumorigenic capacity through cellular senescence and apoptosis.

72 ng angiogenesis and inducing cancer-specific senescence and apoptosis.

73 cation stress and genomic breaks that induce senescence and apoptosis.

74 thelial stem/progenitor cells to replicative senescence and apoptosis.

75 turn, triggers cell-cycle arrest, apoptosis, senescence and autophagy in many cancer cells.

76 pro-inflammatory pathway in the cytoplasm in senescence and cancer.

77 luding stress resistance, adipogenesis, cell senescence and energy production.

78 the loss of Rad51 or Brh2 caused accelerated senescence and failure to generate survivors on semi-sol

79 Senescence and fibrosis were measured by quantitative PC

80 camptothecin enhanced LSD1 inhibitor-induced senescence and growth inhibition of cancer cells in vitr

81 results suggest a role for ubiquitination in senescence and imply a common node downstream from ATM t

82 eful tool to delay the artichoke postharvest senescence and improve the reported health-beneficial pr

83 on levels in aged/diseased hCPCs antagonizes senescence and improves functional responses.

84 population dynamics; provided insights into senescence and individual life histories; and revealed c

85 -salt, high-fat diet accelerates endothelial senescence and instigates endothelial inflammation.

86 ional methods and the mMSCs showed decreased senescence and maintained their multipotency and differe

87 ced G1-like cell cycle arrest and control of senescence and melanomagenesis in vitro and in vivo.

88 f DDR-mediated functional antagonism between senescence and MYOD-activated gene expression and indica

89 anisms involved in LPS-induced cholangiocyte senescence and NRAS-dependent regulation of CDKN2A remai

90 Responses ranging from premature leaf senescence and partial canopy dieback to whole-tree mort

91 ted with higher ethylene evolution and ovary senescence and pedicel abscission in fruits that were no

92 t fruit could represent a way to delay fruit senescence and preserve its characteristics.

93 SIN3B was required for PTEN-induced cellular senescence and prevented progression to invasive prostat

94 omote the transition of quiescent cells into senescence and preventing repression blocks progression

95 with complex karyotypes exhibit features of senescence and produce pro-inflammatory signals that pro

96 mportantly, silencing CircPVT1 promoted cell senescence and reversed the proliferative phenotype obse

97 Finally, we show that mice with reduced senescence and SASP responses exhibit decreased tumour-i

98 re analogous and share a common signature of senescence and SASP.

99 discuss the connections between reproductive senescence and somatic aging and give an overview of the

100 Bcl-xL expression: the latter a biomarker of senescence and target of anti-senescence therapeutics, o

101 virus-triggered autophagy prevents extensive senescence and tissue death of infected plants in a larg

102 that are thought to control the cell cycle, senescence and tumor suppression.

103 e identified novel mediators of OSKM-induced senescence and validated previously implicated genes suc

104 consequences to endothelial cells by causing senescence and, therefore, chronically increased TNFalph

105 ogenous phenotypic response characterized by senescence and/or apoptosis in different models, and als

106 egulation coincides with cell cycle defects, senescence and/or apoptosis.

107 tress, genomic breaks, DNA damage signaling, senescence, and apoptosis in bone marrow.

108 tion factor (MITF) correlates with invasion, senescence, and drug resistance.

109 T cell distribution, equal differentiation, senescence, and exhaustion marker expression and were ne

110 drial reactive oxygen species and suppressed senescence, and indirect effects on BM endothelial cells

111 rmation by preventing endothelial apoptosis, senescence, and inflammation.

112 nt, programmed cell death, organ abscission, senescence, and plant responses to their biotic and abio

113 , is a result of increased osteoblastic cell senescence, and that ST-SPI diet early in life has modes

114 ndividual processes, such as improvement and senescence, and the among-individual effects of selectiv

115 wo recent papers highlight the roles of p53, senescence, and the immune system in preventing the outg

116 e T cells, evidence of T cell exhaustion and senescence, and variable loss of T cell CD28 expression.

117 (SA-beta-Gal) activity, a marker of cellular senescence; and elevated levels of phosphorylated H2AX (

118 ation of the cell to a specific immune cell, senescence, apoptosis, and many more.

119 it the cell cycle, before other hallmarks of senescence appear.

120 get of rapamycin complex 1 (mTORC1) and cell senescence are intimately linked to each other and to or

121 vivo and how MITF-low cells in tumors escape senescence are poorly understood.

122 the SASP causes a subsequent cell-intrinsic senescence arrest to counter the continued regenerative

123 truct, and this prevents cells from engaging senescence arrest.

124 Our data unveiled regulation of senescence as a novel way by which mechanistic target of

125 DNA damage to drive cells into apoptosis or senescence as outcomes of the DNA damage response (DDR).

126 Senescence, as assessed by senescence-associated beta-ga

127 evels in proliferating fibroblasts triggered senescence, as determined by a rise in senescence-associ

128 SMCs were not apoptotic but displayed senescence associated-ss-galactosidase activity and upre

129 modeoxyuridine incorporation; an increase in senescence-associated beta-galactosidase (SA-beta-Gal) a

130 itutive DNA damage response (DDR) signaling, senescence-associated beta-galactosidase (SA-betagal) ac

131 gered senescence, as determined by a rise in senescence-associated beta-galactosidase activity, highe

132 ivergent sub-populations displayed increased senescence-associated beta-galactosidase activity, lower

133 ting MPs from ACS patients induced increased senescence-associated beta-galactosidase activity, oxida

134 Senescence, as assessed by senescence-associated beta-galactosidase activity, was i

135 iated with senescence accompanies the use of senescence-associated beta-galactosidase as a collection

136 osphate-buffered saline for cytotoxicity and senescence-associated beta-galactosidase assays, which w

137 Senescence was evaluated by senescence-associated beta-Galactosidase staining and by

138 and screened for antibodies that recognized senescence-associated cell-surface antigens by FACS anal

139 Among the differentially expressed senescence-associated circRNAs (which we termed 'SAC-RNA

140 ing ATRX in senescent cells destabilizes the senescence-associated heterochromatic foci.

141 Many senescence-associated markers result from altered transc

142 dditionally, P2Y14 R overexpression reversed senescence-associated morphology and reduced levels of m

143 Aspects of the senescence-associated phenotype were also observed in mo

144 45 DEGs including defense-related genes like senescence-associated proteins, resveratrol synthase, 9s

145 Loss of Sav1 induced Stat3 activation and a senescence-associated secretory phenotype (SASP) that co

146 mour progression through the activation of a senescence-associated secretory phenotype (SASP), whethe

147 ariety of proteins collectively known as the senescence-associated secretory phenotype (SASP), which

148 eir secretion of factors contributing to the senescence-associated secretory phenotype (SASP).

149 and the GATA4/NFkB branch that controls the senescence-associated secretory phenotype (SASP).

150 Proliferation arrest and the senescence-associated secretory phenotype collaborate to

151 ic chromatin-cGAS-STING pathway promotes the senescence-associated secretory phenotype in primary hum

152 ed secretion of many bio-active factors (the senescence-associated secretory phenotype, or SASP), and

153 roinflammatory cytokines and chemokines, the senescence-associated secretory phenotype.

154 very, and possibly the many-sided effects of senescence-associated secretory phenotype.

155 man haematological malignancies, reveal that senescence-associated stemness is an unexpected, cell-au

156 expressing oncogenic K-Ras have bypassed the senescence barrier.

157 Here we demonstrate elevated abundance of senescence biomarkers in IPF lung, with p16 expression i

158 e results indicate that FOXP1 attenuates MSC senescence by orchestrating their cell-fate switch while

159 an cancer growth while antagonizing cellular senescence by repressing the expression of cyclin-depend

160 Rapamycin treated cells demonstrated less senescence by X-beta-Gal SA staining and by lower expres

161 s, such as cell cycle arrest, apoptosis, and senescence, by activation or repression of its target ge

162 mplicitly leave open the possibility that if senescence-causing alleles could be identified, or if an

163 ce at late puberty undergo normal programmed senescence, characterized by loss of nestin expression.

164 minished G1 arrest, DNA repair, and cellular senescence coincident with enhanced cell death in human

165 is allows for the prospective design of anti-senescence compounds to address whether homeostasis can

166 and induces neural-like differentiation and senescence, consistent with NF-kappaB pathway inhibition

167 Targeting endothelial senescence could be a new therapeutic avenue in HFpEF.

168 we investigated whether chemotherapy-induced senescence could change stem-cell-related properties of

169 e show that, in a mouse model of replicative senescence, decline in muscle satellite cell-mediated re

170 Aged CPCs have increased senescence, decreased stemness and reduced capacity to p

171 In both contexts, senescence depends on TGFbeta but is independent of ERK/

172 pubertal mice results in premature cellular senescence, depleted MSPCs pool, and impaired osteogenes

173 at the processes underlying pathogen defence senescence differ between males and females.

174 Our study demonstrates that cellular senescence drives hepatic steatosis and elimination of s

175 at hit-and-run epigenetic events can prevent senescence entry, which may facilitate tumour initiation

176 -bound MDA-vimentin, presumably as part of a senescence eradication mechanism that may become impaire

177 udding of daughter cells was associated with senescence escape.

178 We reported that cholangiocyte senescence features prominently in PSC and that neurobla

179 creased biliary mass, biliary proliferation, senescence, fibrosis, and hepatic stellate cell activati

180 We uncover a role in senescence for the potent tumor suppressor and ATM subst

181 c cell cycle were rapidly down-regulated and senescence genes were strongly up-regulated, particularl

182 However, senescence has also been implicated as a major cause of

183 Studying the phenomenon of cellular senescence has been hindered by the lack of senescence-s

184 Cholangiocyte senescence has been linked to primary sclerosing cholang

185 S), the question whether TNFalpha can induce senescence has not been answered conclusively.

186 RSV induced S-phase arrest and cellular senescence in a dose-dependent manner in U2OS and A549 c

187 ), which can reinforce the arrest and induce senescence in a paracrine manner.

188 ovokes bacterial cell death and early nodule senescence in an allele-specific and rhizobial strain-sp

189 ered by the activation of premature cellular senescence in an NF1-deficient background.

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

191 scription factor for prolonging the onset of senescence in cereals.

192 ibitor 2A (CDKN2A/p16(INK4a)) expression and senescence in cultured cholangiocytes in an NRAS-depende

193 the canonical hypothesis of oncogene-induced senescence in growth arrest and tumor suppression in mel

194 ed aging to investigate the role of cellular senescence in HFpEF development.

195 ogenic K-Ras (K-Ras(G12V))-induced premature senescence in mouse embryonic fibroblasts and normal hum

196 ear foci and is required for therapy-induced senescence in multiple types of transformed cells expose

197 s causes proliferation followed by premature senescence in primary cells, an initial barrier to tumor

198 that AAO4 plays a critical role in delaying senescence in siliques by catalyzing aldehyde detoxifica

199 Finally, by inducing senescence in single cells in vivo in the liver, we demo

200 cogenic K-Ras (K-Ras(G12D)) induces cellular senescence in the lung of wildtype but not caveolin-1-nu

201 e CSC depletion effects of C1572 and induced senescence in TNBC cells.

202 osomes than do most tumor cells-they undergo senescence in vascular sprouts and vessels, which sugges

203 N3B has been implicated in the initiation of senescence in vitro Here we show that in a mouse model o

204 s induces irreversible growth inhibition and senescence in vitro, and diminishes growth of cell line

205 ys documented increased oxidative stress and senescence in ZDHHC3-ablated cells.

206 analysis revealed the induction of cellular senescence in zebrafish embryos overexpressing mutant, b

207 ts were characterized by signatures of early senescence, including decreased chlorophyll content and

208 as a potential contributor to age-dependent senescence, increased risk of disease, and even mortalit

209 Ezh2 maintains the repression of key cell senescence inducer genes through H3K27me3, and deletion

210 n mice bearing tumor xenografts treated with senescence-inducing chemotherapy.

211 l three genes were shown to be responsive to senescence-inducing stimuli and posttranscriptionally re

212 dynamic, changing at varying intervals after senescence induction.

213 One way to delay senescence initiation is by regulating key transcription

214 hosphorylation and thereby prevents cellular senescence, IPF and carcinoma formation.

215 Senescence is a form of cell cycle arrest induced by str

216 Cellular senescence is a process of cellular growth arrest linked

217 Cellular senescence is a state of irreversibly arrested prolifera

218 Senescence is a state of stable cell cycle exit with imp

219 Cellular senescence is a terminal cell cycle arrested state, assu

220 Senescence is a terminal differentiation program that ha

221 obust evidence that the manipulation of leaf senescence is an effective strategy for yield improvemen

222 This study shows that although early senescence is an inherent property of a subset of activa

223 Here, we show that cell senescence is an intrinsic part of the developmental pro

224 Cellular senescence is characterized by a permanent cell-cycle ar

225 ritis is an age-related disease and cellular senescence is predicted to be a significant component of

226 Senescence is the process that marks the end of a leaf's

227 In vivo detection of senescence is validated in mice bearing tumor xenografts

228 arkers of T cell maturation, exhaustion, and senescence known to influence immune function.

229 ulmonary expression of H-Ras(G12V) created a senescence-like state caused by excessive MAPK signaling

230 lung epithelial progenitor cells adopting a senescence-like state with permanent cell cycle arrest i

231 lastid transcriptional machinery during leaf senescence Loss-of-function mutants of Arabidopsis thali

232 Key signalling components of the senescence machinery, such as p16(INK4a), p21(CIP1) and

233 Thus, senescence manipulation is a strategy to improve plant y

234 Exclusively, the senescence marker CD57 was significantly up-regulated in

235 dogenous RCS and higher expression levels of senescence marker genes, leading to premature senescence

236 e senescence of KO siliques, whereas RCS and senescence marker levels in wild-type siliques were hard

237 h age in an inverse manner with those of the senescence marker p16INK4A.

238 Cellular senescence markers are detectable within IPF lung tissue

239 creased cell proliferation and expression of senescence markers, but independent of DNA damage and ap

240 asting functional changes and how microglial senescence may contribute to age-related neurodegenerati

241 for the DDR-resistant MYOD mutant to reverse senescence-mediated inhibition of the myogenic program.

242 Using our in vitro senescence model, we found that LPS-induced CDKN2A expre

243 ice (SAM, n=18) and control mice with normal senescence (n=15) were fed normal chow or a high-fat, hi

244 Senescence occurred following cisplatin- or Taxol-treatm

245 one that promotes the ripening of fruits and senescence of flowers thereby reducing their shelf lives

246 letion increased proliferation and decreased senescence of hepatocytes and mouse embryonic fibroblast

247 enescence marker genes, leading to premature senescence of KO siliques, whereas RCS and senescence ma

248 The senescence of mammalian cells is characterized by a prol

249 ymbiosome membranes, indicating either early senescence of these cells or defects in the formation of

250 We show that delayed senescence of transgenic plants and the corresponding lo

251 Oncogene-induced senescence (OIS) is considered a powerful tumor suppress

252 , delayed telomere shortening, and postponed senescence onset.

253 y tolerant to DNA damage and fail to undergo senescence or regulated cell death upon accumulation of

254 on under hypoxia does not result in cellular senescence, owing to hypoxia-associated impaired mechani

255 y and reduced levels of molecular markers of senescence p16(INK4a) , p53, p21 and mitochondrial react

256 entities generally operate via apoptotic and senescence pathways.

257 atin complex in the ribosomal biogenesis and senescence pathways.

258 associated with significantly greater immune senescence (percentage of CD4+CD28- or CD8+CD28- T cells

259 roliferation and rescued BRAF(V600E)-induced senescence phenotypes in a PARylation-independent manner

260 al, enhanced apoptotic activity and enhanced senescence post IR.

261 sofar as telomere shortening and replicative senescence prevent genomic instability and cancer by lim

262 The senescence program is variably characterized by several

263 Conversely, inducing hepatocyte senescence promotes fat accumulation in vitro and in viv

264 Carcinoma (HNSCC) cell lines and was due to senescence rather than potentiation of cell death.

265 Root cortical senescence (RCS) in Triticeae reduces nutrient uptake, n

266 condition, we found that cells released from senescence re-entered the cell cycle with strongly enhan

267 Cellular senescence refers to a state of irreversible cell-cycle

268 onstrated substantially delayed leaf-out and senescence relative to northern populations.

269 PARP1-mediated senescence rescue was accompanied by transcriptional act

270 hat links the TP53 and GATA4 branches of the senescence response.

271 sly reported to induce regenerative and anti-senescence responses in a variety of experimental models

272 Reprogramming of cellular senescence signaling by SPI-associated isoflavones in os

273 senescence has been hindered by the lack of senescence-specific markers.

274 several proliferative proteins that prevent senescence, such as IGF2BP1, KRAS and HMGA2, encoded by

275 mage and enhanced malondialdehyde levels and senescence symptoms, but not in wild-type siliques.

276 Using genetically switchable models of senescence targeting H3K9me3 or p53 to mimic spontaneous

277 ess vascular remodelling and less markers of senescence than wild-type mice.

278 a biomarker of senescence and target of anti-senescence therapeutics, or senolytics.

279 ncer cells escape oncogene-induced premature senescence through down-regulation of caveolin-1 express

280 plicing promotes growth arrest and premature senescence through hyperactivation of the IRE1alpha RNas

281 drive cells into this state.Therapy induced senescence (TIS) is a growth suppressive program activat

282 ich orchestrates persistent DSB signaling to senescence, tissue-fibrosis and oncogenesis.

283 bnormalities may prime for changing oncogene senescence to addiction for a single key oncogene involv

284 response, also activates AXL and suppresses senescence to impose the MITF-low/AXL-high drug-resistan

285 litterfall rates associated with annual leaf senescence vary by <20%.

286 Senescence was evaluated by senescence-associated beta-G

287 whereas for females systemic immune defence senescence was mainly responsible.

288 Induction of endothelial senescence was prevented by the anti-oxidant N-acetyl cy

289 To identify novel biomarkers of senescence, we immunized BALB/c mice with senescent mous

290 identify modulators of reprogramming-induced senescence, we performed a genome-wide shRNA screen in p

291 lation and Bcl-xL expression were altered in senescence, we subsequently evaluated pano as a senolyti

292 Cardiovascular inflammation and senescence were assessed by immunohistochemical and immu

293 eceptor axis, ductular reaction, and biliary senescence were evaluated in patients with nonalcoholic

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

295 elf life, due to postharvest desiccation and senescence, which limits their global distribution.

296 had an additive effect on constraining cell senescence while promoting cell proliferation and increa

297 n of PGCCs was associated with activation of senescence, while budding of daughter cells was associat

298 Our results showed a delay in plant senescence with an increase in the expression level of p

299 mammals, accumulates in human fibroblasts in senescence with persistent DNA damage.

300 Excess centrosomes induce p53-dependent senescence without DNA damage in endothelial cells.