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1 1 delay in the cell cycle, and expression of senescence associated beta-galactosidase.
2 These cells also displayed expression of the senescence associated beta-galactosidase.
3 ent with reacquisition of p16 expression and senescence associated beta-galactosidase.
4 cent cells as evidenced by the expression of senescence-associated beta-galactosidase.
5 size, appeared more granular, and expressed senescence-associated beta-galactosidase.
6 ically enlarged cells expressed both p16 and senescence-associated beta-galactosidase.
7 h a senescence-like phenotype, production of senescence-associated beta-galactosidase (a biochemical
8 used an increased expression of p21/WAF1 and senescence -associated -beta-galactosidase activity, but
9 layed increased senescent markers (increased senescence associated-beta galactosidase activity, p16,
10 vivo corneas were identified by staining for senescence-associated beta-galactosidase activity (SA-be
11 tion of gammaH2AX foci, and the induction of senescence-associated beta-galactosidase activity and ce
12 of clonogenic ability, and the induction of senescence-associated beta-galactosidase activity and fl
13 ion of senescence as shown by an increase in senescence-associated beta-galactosidase activity and fo
14 magnesium-deficient conditions had increased senescence-associated beta-galactosidase activity and in
15 growth arrest characterized by induction of senescence-associated beta-galactosidase activity and in
16 rks of senescence, such as the expression of senescence-associated beta-galactosidase activity and se
17 rotracted and associated with an increase in senescence-associated beta-galactosidase activity at pH
18 ized by altered morphology and expression of senescence-associated beta-galactosidase activity in MCF
20 el of endothelial senescence was assessed as senescence-associated beta-galactosidase activity using
21 a decrease in DNA synthesis, an increase in senescence-associated beta-galactosidase activity, and a
22 crease in the proportion of cells expressing senescence-associated beta-galactosidase activity, apopt
23 gered senescence, as determined by a rise in senescence-associated beta-galactosidase activity, highe
24 ivergent sub-populations displayed increased senescence-associated beta-galactosidase activity, lower
25 ting MPs from ACS patients induced increased senescence-associated beta-galactosidase activity, oxida
26 cell youthfulness associated with decreased senescence-associated beta-galactosidase activity, prese
27 scent-like morphology and displayed elevated senescence-associated beta-galactosidase activity, reduc
28 of acrolein on cell proliferative capacity, senescence-associated beta-galactosidase activity, the k
30 f BRG1 causes growth arrest and induction of senescence-associated beta-galactosidase activity, which
38 enescence, as evidenced by the expression of senescence-associated beta-galactosidase and 5-bromo-2-d
39 pe, correlating with a reduced expression of senescence-associated beta-galactosidase and fewer numbe
40 cells to express senescence markers, namely senescence-associated beta-galactosidase and increased p
41 inducing cell death, causes the induction of senescence-associated beta-galactosidase and inhibition
42 id not induce growth arrest or expression of senescence-associated beta-galactosidase, and Rb remaine
43 hanges of cellular morphology, activation of senescence-associated beta-galactosidase, and suppressio
44 markers of senescence, including p16, EGFP, senescence-associated beta-galactosidase, and the senesc
45 iated with senescence accompanies the use of senescence-associated beta-galactosidase as a collection
46 th changes in cell morphology, expression of senescence-associated beta-galactosidase, as well as dec
47 tic drugs and combinations, we established a senescence associated beta-galactosidase assay as a scre
48 osphate-buffered saline for cytotoxicity and senescence-associated beta-galactosidase assays, which w
49 s in fibroblasts, such as the acquisition of senescence-associated beta-galactosidase (beta-gal) acti
51 Finally, cell senescence, as assessed by senescence-associated beta-galactosidase, demonstrated s
52 etained persistent p21 expression; expressed senescence-associated beta-galactosidase; displayed an e
54 on, rejuvenated EPCs, resulting in decreased senescence-associated beta-galactosidase expression, inc
55 and induction of p53, p16Ink4a, p21Cip1, and senescence-associated beta-galactosidase expressions.
57 also revealed a second p21(Cip1)-associated, senescence-associated, beta-galactosidase-independent gr
58 anied by morphological defects, elevation of senescence-associated beta-galactosidase levels, and cha
59 ary murine embryo fibroblasts and stimulates senescence-associated beta-galactosidase levels, consist
60 egulation of cyclin E, and activation of the senescence-associated beta-galactosidase marker in human
61 lat and lengthened in shape, accumulated the senescence-associated beta-galactosidase marker, and inc
63 viving cells expressed an increased level of senescence-associated beta-galactosidase, p16(Ink4a), an
64 cence as evidenced by high expression of the senescence-associated beta-galactosidase, p19(ARF), and
66 ression or treatment increased the number of senescence-associated beta-galactosidase-positive HSCs a
67 pulation doublings followed by p16-positive, senescence-associated beta-galactosidase-positive stasis
68 RPE cells was assessed by measuring both the senescence associated-beta-galactosidase (SA-beta-Gal) a
70 licative senescence, notably the presence of senescence-associated beta-galactosidase (SA beta-gal) a
71 reactive oxygen species (ROS) production and senescence-associated beta-galactosidase (SA-beta-gal) a
73 luding IRAK1, IL6, IL8, and PAI-1, inhibited senescence-associated beta-galactosidase (SA-beta-gal) a
74 modeoxyuridine incorporation; an increase in senescence-associated beta-galactosidase (SA-beta-Gal) a
75 ator inhibitor (PAI-1) and the appearance of senescence-associated beta-galactosidase (SA-beta-gal) a
76 premature senescence as marked by increased senescence-associated beta-galactosidase (SA-beta-Gal) s
77 OF, underwent senescence: NHOK overexpressed senescence-associated beta-galactosidase (SA-beta-Gal),
78 increase in the number of flat, enlarged and senescence-associated beta-galactosidase (SA-beta-Gal)-p
79 exit, a unique morphology, and expression of senescence-associated beta-galactosidase (SA-beta-Gal).
80 develop a senescence morphology and express senescence-associated beta-galactosidase (SA-beta-gal).
81 itutive DNA damage response (DDR) signaling, senescence-associated beta-galactosidase (SA-betagal) ac
82 ibrous caps expressed markers of senescence (senescence-associated beta-galactosidase [SAbetaG] and t
83 elial neoplasia (PanIN), and found that only senescence-associated beta-galactosidase (SAbetagal) act
84 tem cells were accompanied by an increase in senescence-associated beta-galactosidase staining and a
86 in situ hybridization in liver tissue and by senescence-associated beta-galactosidase staining in a c
89 enhanced cellular senescence, determined by senescence-associated beta-galactosidase staining, was o
91 sion, caused EPC senescence, as evidenced by senescence-associated beta-galactosidase upregulation, d
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