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1 These cells also displayed expression of the senescence associated beta-galactosidase.
2 ent with reacquisition of p16 expression and senescence associated beta-galactosidase.
3 1 delay in the cell cycle, and expression of senescence associated beta-galactosidase.
4 ent, G2/M cell cycle phase cells, GATA4, and senescence-associated beta-galactosidase.
5 cent cells as evidenced by the expression of senescence-associated beta-galactosidase.
6 size, appeared more granular, and expressed senescence-associated beta-galactosidase.
7 ically enlarged cells expressed both p16 and senescence-associated beta-galactosidase.
8 h a senescence-like phenotype, production of senescence-associated beta-galactosidase (a biochemical
9 characteristic senescence markers including senescence-associated beta-galactosidase, accumulation o
10 used an increased expression of p21/WAF1 and senescence -associated -beta-galactosidase activity, but
11 tion and differentiation potentials, reduced senescence associated beta-galactosidase activity and re
12 DC marker genes and attenuated induction of senescence associated beta-galactosidase activity, a mar
13 layed increased senescent markers (increased senescence associated-beta galactosidase activity, p16,
14 ease of cell doubling and a 39% reduction in senescence-associated beta-galactosidase activity (p < 0
15 ple features such as increased expression of senescence-associated beta-galactosidase activity (SA be
16 vivo corneas were identified by staining for senescence-associated beta-galactosidase activity (SA-be
17 tion of gammaH2AX foci, and the induction of senescence-associated beta-galactosidase activity and ce
18 nduction of cellular senescence, verified by senescence-associated beta-galactosidase activity and ce
19 of clonogenic ability, and the induction of senescence-associated beta-galactosidase activity and fl
20 ion of senescence as shown by an increase in senescence-associated beta-galactosidase activity and fo
21 luorescence and p16-high cells showed higher senescence-associated beta-galactosidase activity and in
22 magnesium-deficient conditions had increased senescence-associated beta-galactosidase activity and in
23 growth arrest characterized by induction of senescence-associated beta-galactosidase activity and in
24 assic characteristics of senescence, such as senescence-associated beta-galactosidase activity and li
25 escence, as observed by a marked increase in senescence-associated beta-galactosidase activity and p2
26 rks of senescence, such as the expression of senescence-associated beta-galactosidase activity and se
27 rotracted and associated with an increase in senescence-associated beta-galactosidase activity at pH
28 ized by altered morphology and expression of senescence-associated beta-galactosidase activity in MCF
30 el of endothelial senescence was assessed as senescence-associated beta-galactosidase activity using
31 A higher prevalence of cells positive for senescence-associated beta-galactosidase activity was al
32 a decrease in DNA synthesis, an increase in senescence-associated beta-galactosidase activity, and a
33 crease in the proportion of cells expressing senescence-associated beta-galactosidase activity, apopt
34 gered senescence, as determined by a rise in senescence-associated beta-galactosidase activity, highe
35 ivergent sub-populations displayed increased senescence-associated beta-galactosidase activity, lower
36 ting MPs from ACS patients induced increased senescence-associated beta-galactosidase activity, oxida
37 cell youthfulness associated with decreased senescence-associated beta-galactosidase activity, prese
38 scent-like morphology and displayed elevated senescence-associated beta-galactosidase activity, reduc
39 of acrolein on cell proliferative capacity, senescence-associated beta-galactosidase activity, the k
40 res of senescence, such as loss of lamin B1, senescence-associated beta-galactosidase activity, upreg
42 f BRG1 causes growth arrest and induction of senescence-associated beta-galactosidase activity, which
54 enescence, as evidenced by the expression of senescence-associated beta-galactosidase and 5-bromo-2-d
55 that serves both as a recognition moiety for senescence-associated beta-galactosidase and a caging gr
56 pe, correlating with a reduced expression of senescence-associated beta-galactosidase and fewer numbe
57 cells to express senescence markers, namely senescence-associated beta-galactosidase and increased p
58 inducing cell death, causes the induction of senescence-associated beta-galactosidase and inhibition
59 id not induce growth arrest or expression of senescence-associated beta-galactosidase, and Rb remaine
60 hanges of cellular morphology, activation of senescence-associated beta-galactosidase, and suppressio
61 markers of senescence, including p16, EGFP, senescence-associated beta-galactosidase, and the senesc
62 iated with senescence accompanies the use of senescence-associated beta-galactosidase as a collection
63 th changes in cell morphology, expression of senescence-associated beta-galactosidase, as well as dec
64 tic drugs and combinations, we established a senescence associated beta-galactosidase assay as a scre
66 osphate-buffered saline for cytotoxicity and senescence-associated beta-galactosidase assays, which w
67 s in fibroblasts, such as the acquisition of senescence-associated beta-galactosidase (beta-gal) acti
69 Finally, cell senescence, as assessed by senescence-associated beta-galactosidase, demonstrated s
70 etained persistent p21 expression; expressed senescence-associated beta-galactosidase; displayed an e
71 llular senescence was evaluated by measuring senescence-associated beta-galactosidase expression and
73 on, rejuvenated EPCs, resulting in decreased senescence-associated beta-galactosidase expression, inc
74 and induction of p53, p16Ink4a, p21Cip1, and senescence-associated beta-galactosidase expressions.
76 it increases hallmarks of senescence such as senescence-associated beta-galactosidase, increased p21
77 also revealed a second p21(Cip1)-associated, senescence-associated, beta-galactosidase-independent gr
78 anied by morphological defects, elevation of senescence-associated beta-galactosidase levels, and cha
79 ary murine embryo fibroblasts and stimulates senescence-associated beta-galactosidase levels, consist
80 egulation of cyclin E, and activation of the senescence-associated beta-galactosidase marker in human
81 lat and lengthened in shape, accumulated the senescence-associated beta-galactosidase marker, and inc
83 viving cells expressed an increased level of senescence-associated beta-galactosidase, p16(Ink4a), an
84 cence as evidenced by high expression of the senescence-associated beta-galactosidase, p19(ARF), and
86 ression or treatment increased the number of senescence-associated beta-galactosidase-positive HSCs a
87 pulation doublings followed by p16-positive, senescence-associated beta-galactosidase-positive stasis
88 CD24+ skeletal cells exhibit growth arrest, senescence-associated beta-galactosidase positivity, and
89 RPE cells was assessed by measuring both the senescence associated-beta-galactosidase (SA-beta-Gal) a
91 licative senescence, notably the presence of senescence-associated beta-galactosidase (SA beta-gal) a
92 ator inhibitor (PAI-1) and the appearance of senescence-associated beta-galactosidase (SA-beta-gal) a
93 of molecular markers of senescence, such as senescence-associated beta-galactosidase (SA-beta-Gal) a
94 terations, G1/S cell cycle arrest, increased senescence-associated beta-galactosidase (SA-beta-Gal) a
95 xtent of cellular senescence was assessed by senescence-associated beta-galactosidase (SA-beta-Gal) a
96 modeoxyuridine incorporation; an increase in senescence-associated beta-galactosidase (SA-beta-Gal) a
97 reactive oxygen species (ROS) production and senescence-associated beta-galactosidase (SA-beta-gal) a
99 luding IRAK1, IL6, IL8, and PAI-1, inhibited senescence-associated beta-galactosidase (SA-beta-gal) a
100 senescence, including reduced proliferation, senescence-associated beta-galactosidase (SA-beta-gal) a
101 and spleen atrophy and reduced the number of senescence-associated beta-galactosidase (SA-beta-gal) p
102 premature senescence as marked by increased senescence-associated beta-galactosidase (SA-beta-Gal) s
103 problems, prodrugs, whose design is based on senescence-associated beta-galactosidase (SA-beta-gal),
104 ion tomography (PET) imaging probe targeting senescence-associated beta-galactosidase (SA-beta-Gal),
105 n elevation of cellular senescence marked by senescence-associated beta-galactosidase (SA-beta-gal),
106 OF, underwent senescence: NHOK overexpressed senescence-associated beta-galactosidase (SA-beta-Gal),
107 increase in the number of flat, enlarged and senescence-associated beta-galactosidase (SA-beta-Gal)-p
108 exit, a unique morphology, and expression of senescence-associated beta-galactosidase (SA-beta-Gal).
109 develop a senescence morphology and express senescence-associated beta-galactosidase (SA-beta-gal).
110 itutive DNA damage response (DDR) signaling, senescence-associated beta-galactosidase (SA-betagal) ac
111 sue factor or F3) is robustly induced in the senescence-associated beta-galactosidase (SA-betaGal)-po
112 ibrous caps expressed markers of senescence (senescence-associated beta-galactosidase [SAbetaG] and t
113 elial neoplasia (PanIN), and found that only senescence-associated beta-galactosidase (SAbetagal) act
114 NIR emission, and high "turn-on" ratio upon senescence-associated beta-galactosidase (SABG) activati
115 ncrease in lysosomal content, as measured by senescence-associated beta-galactosidase (Senbeta-Gal) a
116 tem cells were accompanied by an increase in senescence-associated beta-galactosidase staining and a
118 ed with Abeta1-42 oligomers showed increased senescence-associated beta-galactosidase staining and in
119 in situ hybridization in liver tissue and by senescence-associated beta-galactosidase staining in a c
122 enhanced cellular senescence, determined by senescence-associated beta-galactosidase staining, was o
125 sion, caused EPC senescence, as evidenced by senescence-associated beta-galactosidase upregulation, d