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1 ntly shown that endothelial immunobiology is anchorage dependent.
2 nded in a fluid and are therefore said to be anchorage dependent.
3                  Normal epithelial cells are anchorage-dependent.
4  reduction of Rad9 renders DU145 cell growth anchorage-dependent.
5        The expression of h2-calponin is cell anchorage-dependent.
6  shRNA-mediated knockdown of KMT1A decreased anchorage dependent and independent cell proliferation a
7                      The immortal cells were anchorage dependent and nontumorigenic, indicating a pre
8                  Rho-immortalized cells were anchorage dependent and were unable to form tumors when
9 oreover, SPARC significantly suppressed both anchorage-dependent and -independent activation of AKT a
10 ficantly increased doubling times, decreased anchorage-dependent and -independent basal growth, and c
11 f AHRR in tumor cells resulted in diminished anchorage-dependent and -independent cell growth and red
12  using siRNA significantly enhanced in vitro anchorage-dependent and -independent cell growth as well
13 cancer cells deleted of 3p21-22 reduced both anchorage-dependent and -independent cell growth in vitr
14  ErbB2 inhibitor, the effect of estradiol on anchorage-dependent and -independent cell growth was inh
15 G3 in HCC cells significantly decreased both anchorage-dependent and -independent cell growth, and in
16                   HI-TOPK-032 also inhibited anchorage-dependent and -independent colon cancer cell g
17 significantly impairs the growth, as well as anchorage-dependent and -independent colony formation of
18  the SRM mutant also attenuated MUC1-induced anchorage-dependent and -independent growth and delayed
19 owed that the role of TGF-beta in regulating anchorage-dependent and -independent growth and migratio
20 s, at least in part, the effects of GGTIs on anchorage-dependent and -independent growth and tumor ap
21                                    Moreover, anchorage-dependent and -independent growth assays, cell
22                                      In both anchorage-dependent and -independent growth assays, IL-4
23                                              Anchorage-dependent and -independent growth in culture a
24 human breast cancer cell lines reduced their anchorage-dependent and -independent growth in vitro and
25 ll proliferation rates in vivo and in vitro, anchorage-dependent and -independent growth in vitro, an
26                          H37 also suppressed anchorage-dependent and -independent growth of A9 mouse
27 -induced recruitment in G1 and inhibition of anchorage-dependent and -independent growth of both cell
28                                 Furthermore, anchorage-dependent and -independent growth of breast ca
29 ein kinase D1 (PKD1) as a major regulator of anchorage-dependent and -independent growth of cancer ce
30 producing human MC line HMC-1 augmented both anchorage-dependent and -independent growth of human lun
31 ynergistically inhibited survival as well as anchorage-dependent and -independent growth of rhabdoid
32 ast cancer as a transducer and integrator of anchorage-dependent and -independent growth signals by u
33 hase primary melanoma cells 1) promotes both anchorage-dependent and -independent growth, 2) initiate
34 enic and tumor survival pathways, to inhibit anchorage-dependent and -independent growth, and to indu
35 nstrate that both RhoB-F and RhoB-GG inhibit anchorage-dependent and -independent growth, induce apop
36 beta2AR stimulation results in inhibition of anchorage-dependent and -independent growth, induction o
37 ed HER-2/neu transformed 3T3 cells including anchorage-dependent and -independent growth, metastasis-
38 ermore, S3I-1757, but not S3I-1756, inhibits anchorage-dependent and -independent growth, migration,
39 l-targeted ND2 mutants resulted in increased anchorage-dependent and -independent growth, which was a
40 t increased expression of PKC-delta inhibits anchorage-dependent and -independent growth, while induc
41 B-231 cell migration, Matrigel invasion, and anchorage-dependent and -independent growth.
42 ted in an additive decrease in PG levels and anchorage-dependent and -independent growth.
43        Expression of a DN p38 inhibited both anchorage-dependent and -independent proliferation of MD
44                                Inhibition of anchorage-dependent and -independent proliferation, colo
45 on caused a DLC1-dependent decrease in NSCLC anchorage-dependent and -independent proliferation.
46 anced the ability of TGFbeta to inhibit both anchorage-dependent and -independent tumor cell growth.
47                            In addition, both anchorage-dependent and anchorage-independent apoptotic
48 ore slowly than mock-transfected C6 cells in anchorage-dependent and anchorage-independent assays.
49 agonized TGFbeta activity and inhibited both anchorage-dependent and anchorage-independent cell growt
50 e report that HIN-1 is a potent inhibitor of anchorage-dependent and anchorage-independent cell growt
51 orced expression of RAB25 markedly increased anchorage-dependent and anchorage-independent cell proli
52 in reduced IGF-I-induced cell growth in both anchorage-dependent and anchorage-independent conditions
53 ays, direct cell counts, clonogenicity under anchorage-dependent and anchorage-independent conditions
54 the ability of CaP cells to form colonies in anchorage-dependent and anchorage-independent conditions
55 cell lung cancer-derived cell lines, both in anchorage-dependent and anchorage-independent conditions
56                                TPSF inhibits anchorage-dependent and anchorage-independent E(2)-ERalp
57  long-chain fatty acid activation, inhibited anchorage-dependent and anchorage-independent glioma cel
58 ivation of PPARgamma in MOSER cells inhibits anchorage-dependent and anchorage-independent growth and
59  broad range of human tumors inhibited their anchorage-dependent and anchorage-independent growth by
60 resulted in a significant inhibition of both anchorage-dependent and anchorage-independent growth in
61 emonstrated that PTPN13 negatively regulates anchorage-dependent and anchorage-independent growth in
62 ed the stimulation of DNA synthesis, and the anchorage-dependent and anchorage-independent growth ind
63 tively active myr-Akt rescued cells from the anchorage-dependent and anchorage-independent growth inh
64 y significant to complete inhibition of both anchorage-dependent and anchorage-independent growth of
65               siRNA to TUC338 decreased both anchorage-dependent and anchorage-independent growth of
66                            RRD-251 inhibited anchorage-dependent and anchorage-independent growth of
67 tion of contact inhibition and diminution of anchorage-dependent and anchorage-independent growth rat
68  either a vector control or EDG2 had similar anchorage-dependent and anchorage-independent growth rat
69 ranslational mechanisms, and suppresses PDAC anchorage-dependent and anchorage-independent growth.
70 upport of this, PRLrYDmut expression reduced anchorage-dependent and anchorage-independent growth.
71 hesion when the transcriptions of genes from anchorage-dependent and anchorage-independent HeLa cells
72 hanced the growth of prostate tumor cells in anchorage-dependent and anchorage-independent in vitro a
73 calize RhoB and prevent RhoB from inhibiting anchorage-dependent and anchorage-independent tumor grow
74 sion attenuates breast cancer cell growth in anchorage-dependent and independent colony formation ass
75 MIA PaCa-2 pancreatic cancer cells inhibited anchorage-dependent and independent growth in cell cultu
76               Ro-31-8220 suppressed both the anchorage-dependent and independent growth of NSCLC cell
77 skeleton organization, signaling, apoptosis, anchorage-dependent and independent growth, migration an
78 or Src-dependent, heregulin (HRG)-augmented, anchorage-dependent and independent growth.
79  lengthening of G(1), and inhibition of both anchorage-dependent and independent growth.
80 y delivered small hairpin RNA decreased both anchorage-dependent and independent proliferation of hum
81 essing the transfected Tsc2 gene became more anchorage-dependent and lost their ability to form tumor
82              Active hirsutinolides inhibited anchorage-dependent and three-dimensional spheroid growt
83 used inhibition of tumor cell growth in both anchorage-dependent and, particularly, in anchorage-inde
84                 MUC4 promotes proliferation, anchorage-dependent and-independent growth of TNBC cells
85    Although the number of colonies formed in anchorage-dependent assays was only slightly decreased,
86            A similar result was also seen in anchorage-dependent assays.
87 t least in part, fibroblasts are mitogen and anchorage dependent, because integrin action allows for
88                              Loss of p120 in anchorage-dependent breast cancer cell lines strongly pr
89 stant to FTI-induced growth inhibition under anchorage-dependent but not anchorage-independent condit
90 gration of a wide range of surface sensitive anchorage dependent cell types.
91                                         This anchorage-dependent cell cycle arrest is linked to incre
92 such as matrix assembly, cell migration, and anchorage-dependent cell growth and survival.
93  of HDGF resulted in no detectable effect on anchorage-dependent cell growth as determined with a 3-(
94 rget genes, p21(waf1/cip1), as components of anchorage-dependent cell growth control.
95 s significantly decreased cell viability and anchorage-dependent cell growth of HRG-overexpressing ce
96 caveolin-1 and Fyn in integrin signaling and anchorage-dependent cell growth.
97          In agreement with findings on other anchorage-dependent cell lineages, aortic smooth muscle
98 on during scattering occurs independently of anchorage-dependent cell migration.
99 in maintaining the anchorage-independent and anchorage-dependent cell proliferation in ACC by using S
100  the literature, disruption of CDX2 enhanced anchorage-dependent cell proliferation.
101 trix (ECM) to survive, a phenomenon known as anchorage-dependent cell survival.
102 53 monitors survival signals from ECM/FAK in anchorage- dependent cells.
103                                              Anchorage-dependent cells (OV-90AD) were grown in tissue
104  to facilitate adherence to FHL-1 present on anchorage-dependent cells and in the extracellular matri
105 es the acquisition of AnR, a process whereby anchorage-dependent cells become resistant to cell death
106                                   As typical anchorage-dependent cells myocytes must balance contract
107                   Industrial applications of anchorage-dependent cells require large-scale cell cultu
108 CP) that facilitates digital mass culture of anchorage-dependent cells.
109  control domain-specific signaling events in anchorage-dependent cells.
110  initiates "outside-in" signals that mediate anchorage-dependent cellular responses.
111 pendent fashion and promotes mitogenesis and anchorage-dependent cloning.
112 h MLK4 expression impaired proliferation and anchorage-dependent colony formation.
113  survival of H226 and H460 cells grown under anchorage-dependent conditions is impaired by A12, demon
114 F1R) cross-talk) in non-transformed cells in anchorage-dependent conditions.
115 d by signals from cell-matrix interaction in anchorage-dependent conditions.
116 f WT IGF1 or R36E/R37E in cancer cells under anchorage-dependent conditions.
117  conditions (polyHEMA-coated plates) than in anchorage-dependent conditions.
118 oikis - a form of apoptosis that occurs when anchorage-dependent CRC cells go into suspension.
119 egulate growth factor-induced proliferation, anchorage-dependent DNA synthesis, and cytoskeletal reor
120 le in actin cytoskeleton organization and in anchorage-dependent DNA synthesis.
121 n the intestine and achieve this not through anchorage-dependent effects but by generating Hh express
122                                Withdrawal of anchorage-dependent epithelial cells from their associat
123 propagate through the cytoplasm and activate anchorage-dependent ERK signaling.
124 owly invade the basement membrane but remain anchorage dependent for growth and do not form tumors in
125 ore, the cortactin overexpressing cells were anchorage dependent for growth.
126 hat renders PDA cells more invasive and less anchorage-dependent for growth in vitro, as well as more
127 ependent and independent soft agar growth or anchorage dependent growth, and triggered apoptosis in a
128 tivity, doubling time, morphological change, anchorage dependent growth, tumorigenicity in nude mice,
129 ed in metabolic shift to glycolysis, loss of anchorage-dependent growth and acquired invasive phenoty
130 fficient focus formation, suggesting loss of anchorage-dependent growth and contact inhibition, respe
131 xpressing SKBR3 cells were impaired in their anchorage-dependent growth and exhibited reduced migrati
132 optosis in the MCF7 line, thereby inhibiting anchorage-dependent growth and survival.
133 of these adjuvant drugs was investigated via anchorage-dependent growth assays, anchorage-independent
134 that (i) VPA affects GSC lines viability and anchorage-dependent growth by inducing differentiative p
135 d samples and between Cdc6 and total Chk1 in anchorage-dependent growth derived protein samples.
136 fers resistance to the proapoptotic and anti-anchorage-dependent growth effects of GGTI-2417.
137        In contrast, HRG had little effect on anchorage-dependent growth in any of the cell lines test
138 -induced cell cycle arrest and inhibition of anchorage-dependent growth in breast cancer cells.
139 , migration, invasion, colony formation, and anchorage-dependent growth in HCC cell lines.
140 xamined cell growth, plating efficiency, and anchorage-dependent growth in soft agar.
141 t signaling in tumor cells and inhibited the anchorage-dependent growth of a variety of tumor cell li
142       PL inhibited anchorage-independent and anchorage-dependent growth of multiple breast cancer cel
143                                          The anchorage-dependent growth of these cells was decreased
144  3T3 cells and influenced the morphology and anchorage-dependent growth of wild type Ras-transformed
145 termined that activated Wrch-1 also promoted anchorage-dependent growth transformation of NIH 3T3 fib
146 ivity, and we determined that although NSCLC anchorage-dependent growth was ROCK-independent, both an
147                    However, these effects on anchorage-dependent growth were transient, suggesting ce
148 ession levels in OSCC cells with a decreased anchorage-dependent growth, invasion and wound healing.
149 skeletal localization or ability to suppress anchorage-dependent growth.
150 wever, they did not lose the requirement for anchorage-dependent growth.
151 ft agar, underscoring its role in regulating anchorage-dependent growth.
152 breast carcinoma cells without affecting the anchorage-dependent growth.
153 e clones exhibited a significant decrease in anchorage-dependent growth.
154           Similarly, CCK treatment inhibited anchorage-dependent growth.
155 h the Rb checkpoint, entry into S phase, and anchorage-dependent growth.
156 ltered cellular proliferation, apoptosis and anchorage-dependent growth.
157 ENP7S exhibit greater cell proliferation and anchorage-dependent growth.
158  also showed a loss of density-dependent and anchorage-dependent growth.
159 clear ERK substrate, Elk-1 at serine 383, is anchorage dependent in response to growth factor treatme
160                            Addition of st to anchorage-dependent keratinocytes, expressing either LT
161 ned for their ability to activate MAPK in an anchorage-dependent manner.
162                                              Anchorage-dependent MDCK cells were converted to anchora
163 increased saturation density, and an unusual anchorage-dependent morphological transformation.
164 attached to a live cell membrane revealed an anchorage-dependent nonlinear response of the membrane.
165 )-initiated transformation of MYP3 cells, an anchorage-dependent nontumorigenic rat bladder epithelia
166 ibition of prostate cancer cells grown under anchorage-dependent or -independent conditions.
167 ificity of the cell lines, as well as on the anchorage-dependent or -independent growth conditions an
168 ta3 integrin complexes, but had no effect on anchorage-dependent or -independent growth in vitro.
169 ase in NF-kappaB activity but did not affect anchorage-dependent or -independent growth.
170 transformed fibroblasts revert to a flat and anchorage-dependent phenotype that persists for many day
171 ted with this induction of migration was the anchorage-dependent phosphorylation of p130CAS (Crk-asso
172                                              Anchorage-dependent proliferation and xenograft growth i
173 specific inhibitor of NFkappaB, inhibits the anchorage-dependent proliferation of antiestrogen-resist
174 D1-mediated anchorage-independent growth and anchorage-dependent proliferation of different tumor cel
175 haptotactic cell migration without affecting anchorage-dependent proliferation.
176 hese events can be uncoupled from effects on anchorage-dependent proliferation.
177 at significant differences in the control of anchorage-dependent regulation of apoptosis exist in mel
178 t that cross-talk between growth factor- and anchorage-dependent signaling pathways are essential for
179           Thus, there seems to be a distinct anchorage-dependent step between Ras and Raf in the sign
180 ing molecules downstream of FAK required for anchorage-dependent survival of primary fibroblasts.
181                  Most nonmalignant cells are anchorage-dependent; they require substrate attachment f

 
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