ライフサイエンスコーパス: cell senescence

1 ion and eventually signal cell cycle arrest (cell senescence).

2 They then explore telomere biology and cell senescence.

3 e-stabilizing agent that induces accelerated cell senescence.

4 ved GFR, decreased sclerosis, and alleviated cell senescence.

5 MP-1 up-regulation with the establishment of cell senescence.

6 e activation of endogenous wild-type p53 and cell senescence.

7 telomeric circles, telomere shortening, and cell senescence.

8 em cell number and an increase in progenitor cell senescence.

9 imulate p53 acetylation and the induction of cell senescence.

10 functionally dependent on p53 in regulating cell senescence.

11 of Rac1 in regulating genomic stability and cell senescence.

12 ght be associated with its ability to induce cell senescence.

13 ersible growth arrest in the early stages of cell senescence.

14 re resistant to apoptosis, growth arrest and cell senescence.

15 n of flat cells, growth arrest, and finally, cell senescence.

16 ty genes for this disease, confer risk for T cell senescence.

17 sions in culture, a state termed replicative cell senescence.

18 ase in normal fibroblasts appears to prevent cell senescence.

19 at the ends of chromosomes, plays a role in cell senescence.

20 nt role for p27(Kip1) in promoting satellite cell senescence.

21 ation and colony formation but induced tumor cell senescence.

22 chanism without the complementary process of cell senescence.

23 ues, and this process has been implicated in cell senescence.

24 ed to the telomere hypothesis of replicative cell senescence.

25 sponses as cell cycle arrest, apoptosis, and cell senescence.

26 rved between the average telomere length and cell senescence.

27 ion induces p16(INK4A) and p14(ARF)-mediated cell senescence.

28 s was associated with increased osteoblastic cell senescence.

29 growth of MSCs, which developed features of cell senescence.

30 and DNA repair, or can trigger apoptosis or cell senescence.

31 premature chromatin changes and accelerated cell senescence.

32 elomere attrition, altered proteostasis, and cell senescence.

33 ident self-renewing cells by preventing stem cell senescence.

34 , is associated with vascular DNA damage and cell senescence.

35 a critical length is achieved, precipitating cell senescence.

36 xpression of cell cycle inhibitors and tumor cell senescence.

37 beta-galactosidase staining, an indicator of cell senescence.

38 vin, which resulted in growth inhibition and cell senescence.

39 Cell senescence, a putative tumor-suppression mechanism,

40 Ercc1(d/-) mice showed increased vascular cell senescence, accelerated development of vasodilator

41 There were no changes in markers of CD8(+) T-cell senescence after ART and no differential changes in

42 omere protection occurs during physiological cell senescence and ageing, due to attrition of telomeri

43 t that cAMP-elevating agents prevent cumulus cell senescence and allow them to continue to exert bene

44 Telomere attrition induces cell senescence and apoptosis.

45 ession is accompanied by the upregulation of cell senescence and apoptotic markers.

46 ACTH expression, induces corticotroph tumor cell senescence and cell cycle exit by up-regulating p27

47 re, we have demonstrated that P2Y14 modifies cell senescence and cell death in response to tissue str

48 ential feature of cancer is dysregulation of cell senescence and death.

49 , including stress resistance, adipogenesis, cell senescence and energy production.

50 al hip BMD loss, whereas markers of CD4(+) T-cell senescence and exhaustion (CD4(+)CD28(-)CD57(+)PD1(

51 rested cells displayed phenotypic markers of cell senescence and failed to form colonies.

52 ivity mimicking levels in PDAC led to acinar cell senescence and generated inflammation and fibrosis

53 JNK2 prevents Ras-induced cell senescence and growth arrest by reducing the expres

54 ntigen receptor group (DARC), inducing tumor cell senescence and interrupting IL-8-mediated vascular

55 ng G1 phase cell-cycle arrest accompanied by cell senescence and let-7 inducing G2-M phase cell-cycle

56 mere length, which are known determinants of cell senescence and longevity, in peripheral blood monon

57 the pathogenesis of AGA both in relation to cell senescence and migration but also secretion of know

58 of genes associated with various aspects of cell senescence and organism aging.

59 nding renal aging, focusing on mechanisms of cell senescence and possible interventions to modulate a

60 red muscle growth, associated with satellite cell senescence and premature sarcopenia.

61 sults establish EGR1 as a major regulator of cell senescence and previously undescribed upstream "gat

62 s responsible for ionizing radiation-induced cell senescence and protection against oncogene-induced

63 uppression that induces targeted responder T-cell senescence and provide new insights relevant for th

64 Importantly, silencing CircPVT1 promoted cell senescence and reversed the proliferative phenotype

65 t the cellular level, JunB induced epidermal cell senescence and slowed cell growth in a cell-autonom

66 Oxidative stress can promote cell senescence and studies have shown a role for oxidat

67 tic activity of telomerase, causing the same cell senescence and telomere shortening phenotypes as a

68 d that BAP1 interaction with ASXL2 regulates cell senescence and that ASXL2 cancer-associated mutatio

69 teract to promote retinal pigment epithelial cell senescence and that bone morphogenetic protein-4 ma

70 We propose that cell senescence and the associated secretory phenotype c

71 family) and p53 regulate cell proliferation, cell senescence, and apoptosis in many cell types.

72 hondrial DNA damage, including inflammation, cell senescence, and apoptosis, are present in vascular

73 ssor responses such as cell differentiation, cell senescence, and apoptosis.

74 ritically short telomeres produce apoptosis, cell senescence, and chromosomal instability in tissue c

75 of p53 in DNA damage-induced growth arrest, cell senescence, and direct CDK regulation.

76 ow release and progression to normal myeloid cell senescence, and not a direct effect of activation o

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

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

79 age, the functional consequences of vascular cell senescence, and the possibility that preventing acc

80 in advanced lesions, whereas VSMC apoptosis, cell senescence, and VSMC-derived macrophage-like cells

81 ssion and instability, in part, by promoting cell senescence, apoptosis, and inflammation, the direct

82 erentiation of the cell to a specific immune cell, senescence, apoptosis, and many more.

83 n target of rapamycin complex 1 (mTORC1) and cell senescence are intimately linked to each other and

84 been proposed that the genes responsible for cell senescence are located near the telomere and are ac

85 microbial pathophysiology and mechanisms of cell senescence as important mechanistic links to cancer

86 nse to stress, viral defense, apoptosis, and cell senescence as well as protein sequestration, modifi

87 Finally, cell senescence, as assessed by senescence-associated be

88 These data provide the first evidence of cell senescence, as represented by CD31+CD28(null) CD8+

89 n of Hsp72 in certain cancer lines triggered cell senescence associated with activation and stabiliza

90 nfkb1(-/-) fibroblasts exhibit aggravated cell senescence because of an enhanced autocrine and par

91 s were normal up to 30 PDs, with significant cell senescence beginning following 35 PDs.

92 IRIF persistence and increased breast cancer cell senescence both in vitro and in vivo, arguing for t

93 erase enables stem and cancer cells to evade cell senescence by adding telomeric sequences to the end

94 nterestingly, the induction of hematopoietic cell senescence by IR, but not by BU, was associated wit

95 r cells of the hematopoietic system inhibits cell senescence by monitoring and responding to the extr

96 tissues, rapamycin prevents epithelial stem cell senescence by reducing oxidative stress through inc

97 Therapeutics that induce cancer cell senescence can block cell proliferation and promote

98 According to the telomere hypothesis of cell senescence, cells eventually reach a critically sho

99 T-cell senescence, characterized by expansion of cells lac

100 at cellular processes such as damage-induced cell senescence contribute to osteoarthritis and a growi

101 in hepatocytes induces massive p53-dependent cell senescence/death.

102 ery of PML bodies and revealed their role in cell senescence, disease pathogenesis, and responsivenes

103 Hallmarks of ageing include evidence of cell senescence, DNA damage (including telomere attritio

104 -mediated induction of cell cycle arrest and cell senescence) does not recapitulate the tumor suscept

105 differential roles of CD4(+) versus CD8(+) T-cell senescence/exhaustion and effects of antiretroviral

106 d an 85 kb BAC clone, 346J21, that carries a cell senescence gene (SEN16), previously mapped to 16q24

107 have identified a 360 kb YAC that carries a cell senescence gene, SEN16.

108 Although the phenotype of T-cell senescence has been extensively investigated, few s

109 intriguing data on the role of caveolin-1 in cell senescence have emerged.

110 evolution of diploid sexual reproduction and cell senescence (i.e., cell aging).

111 Markers of CD4(+) T-cell senescence (ie, the percentage of CD28(-)CD57(+) ce

112 collagen (GC) express hallmarks of premature cell senescence, ie, increase in the proportion of cells

113 tic subunit plays an important role in human cell senescence, immortalization, and carcinogenesis.

114 This suggests that IR induces hematopoietic cell senescence in a p53-p21(Cip1/Waf1)-dependent manner

115 T-cell senescence in cases was independently associated wi

116 ether, our data suggest that prevention of T cell senescence in Fas-Tg mice may be a factor in induct

117 the average length of telomeres and leads to cell senescence in HeLa cells and cell death in HeLa, U2

118 These findings identify a premature T-cell senescence in ICL that might be caused by chronic T

119 These effects were due to massive cell senescence in mammary tissue, which was associated

120 in mammary epithelium induces premature stem cell senescence in mammary transplants and decreases mam

121 ll proliferation and apoptosis and inhibited cell senescence in normal VSMCs.

122 ted exacerbation of telomere dysfunction and cell senescence in the absence of any other genetic or e

123 n fibroblasts will better define the role of cell senescence in the aging process and in tumorigenesi

124 We describe a stochastic network model of cell senescence in which a primary role is played by tel

125 omes, including episomes such as ERCs, cause cell senescence in yeast.

126 ll migration and invasion and suppression of cell senescence independent of TAp63 and/or TP53 gene st

127 We hypothesized that cell senescence induced by Nutlin-3a exerted therapeutic

128 Ezh2 maintains the repression of key cell senescence inducer genes through H3K27me3, and dele

129 s originally identified in studies to reveal cell senescence-inducing factors.

130 permanent and irreversible growth arrest of cell senescence is a central paradigm of aging.

131 Cell senescence is a physiological program of terminal g

132 Cell senescence is a process of irreversible arrest of c

133 Cell senescence is an important tumour suppressor mechan

134 Here, we show that cell senescence is an intrinsic part of the developmenta

135 Cell senescence is broadly defined as the physiological

136 two-photon probe (AHGa) for the detection of cell senescence is designed.

137 This satellite cell senescence is due to accumulation of the SUMO ligas

138 Also, cell senescence is found to be useful in the maintenance

139 T cell senescence is thought to contribute to immune funct

140 to be involved in a tissue-specific form of cell senescence, leading to the differentiation of kerat

141 ), whereas EX increased the hepatic stellate cell senescence marker CCN1 (P < 0.01 vs. O-SED).

142 Cell senescence may be an important factor in chronic re

143 tors is important because induction of tumor cell senescence may represent a therapeutic approach for

144 CDKN2A expression (a cell senescence mediator) was measured in peripheral blo

145 Premature T-cell senescence occurs not only in RA, but also has been

146 n that critically short telomeres can induce cell senescence or apoptosis.

147 cytomegalovirus (CMV) are thought to drive T-cell senescence, other microbes may be important for the

148 We evaluated three mechanisms leading to cell senescence: oxidative stress, DNA damage, and repli

149 These cells showed accelerated cell senescence pathway accompanied by increased inflamm

150 SPI-fed rat serum inhibited the osteoblastic cell senescence pathway.

151 veolin-1 expression to suppress osteoblastic cell senescence pathways.

152 mergence of a p21-dependent, p53-independent cell senescence phenotype.

153 amming process via significantly influencing cell senescence, proliferation and chromatin structure.

154 Tumor cell senescence promoted an anti-tumor immune response b

155 progerin production during the induction of cell senescence, providing mechanistic insight into how

156 Although MLN4924-induced cell senescence seems to be dependent on induction of p5

157 entified the role of sirtuin 1 in preventing cell senescence; shed light on the role of polycomb grou

158 tors to late graft loss; features of tubular cell senescence, such as increased p16(INK4a) expression

159 ermore, our data match a simple model of red cell senescence that assumes both an age-dependent destr

160 re likely plays a checkpoint function during cell senescence that underscores its selective role as a

161 gulates diverse signaling pathways involving cell senescence, the cell cycle, and apoptosis.

162 The main conclusion is that, without cell senescence, the evolutionary advantages of sexual r

163 Although p16 may be involved in cell senescence, the physiologic role of p16 is still un

164 s p53 (also known as TRP53)-dependent cancer cell senescence, thereby increasing tumorigenic potentia

165 is the signature marker for age-associated T-cell senescence, these findings provide novel mechanisti

166 that Rac1 activity serves as a regulator of cell senescence through modulation of cellular ROS, geno

167 stress can induce retinal pigment epithelial cell senescence through p53-p21(Cip1/WAF1)-Rb pathway.

168 continuously eliminated, can rapidly induce cell senescence through signaling pathways very similar

169 rovide the first in vivo evidence that links cell senescence to aging due to impaired function of Brc

170 llow repair to occur or trigger apoptosis or cell senescence to prevent propagation of damaged DNA.

171 programming efficiency which may result from cell senescence trigged by up-regulated Ink4a/Arf locus.

172 present studies the possible involvement of cell senescence was investigated.

173 Cervical cancer cell senescence was partially overcome by DEK overexpres

174 eral other changes that have been related to cell senescence were observed: these included markers of

175 to chromatin are thought to be essential to cell senescence, which is key to tumorigenesis and aging

176 elicobacter infection, possibly because of T-cell senescence, which may indirectly protect against th

177 ostate leads to hyperplasia and also induces cell senescence, which may, in turn, function as a barri

178 E6/E7 had an additive effect on constraining cell senescence while promoting cell proliferation and i

179 B2-driven mammary carcinomas triggered tumor cell senescence, without compromising the animals' healt