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1 urface of lysosomal membranes when cells are serum starved.
4 ) on uptake of 2-deoxy-d-[1-(14)C]glucose by serum-starved 3T3-L1 adipocytes was measured in the pres
5 ,5-P3 accumulated in the plasma membranes of serum-starved 3T3-L6 myoblasts due to de novo synthesis
6 D1-CDK4 complexes are associated with p27 in serum-starved activated MEK1 or cyclin D1 cell lines.
13 luent passage 2 HCECs from eight donors were serum starved and, at different times after growth facto
15 hly attenuated replicative phenotype in both serum-starved and proliferating normal human astrocytes.
17 nt study, we report that HB-EGF treatment of serum-starved at aortic SMCs can induce fibroblast growt
22 t (</=80% confluent) controls, as well as in serum- starved cells when compared with cells incubated
24 ered Plk3-interfering RNA with lentivirus to serum-starved cells and found that, upon serum stimulati
26 hibiting low luminescence with extracts from serum-starved cells and increased luminescence using ext
27 site resulted in activation of expression in serum-starved cells and no further induction by serum tr
29 ry epithelial cells and is down-regulated as serum-starved cells are stimulated to reenter the cell c
30 urthermore, HRR was inhibited by caffeine in serum-starved cells arrested in G(0)/G(1), suggesting th
31 infection of live and UV-inactivated KSHV in serum-starved cells as well as in the presence of serum.
32 15 RhoGEF was found mainly in the cytosol of serum-starved cells but partially localized to membranes
34 ium and also after mitogen activation of the serum-starved cells cannot phosphorylate eIF-2 alpha-sub
36 ockdown leads to stalling at G0/G1 Moreover, serum-starved cells display reduced hRpn13 and Uch37 pro
39 PCNA mRNA levels transiently increased in serum-starved cells exposed to ionizing radiation, an ob
40 f the beta-AR agonist isoproterenol (ISO) to serum-starved cells induced DNA synthesis in a dose-depe
42 refore, suggest that the loss of p67 mRNA in serum-starved cells is due to loss of p67 transcription.
43 sulin stimulated de novo purine synthesis in serum-starved cells largely through PI3K/Akt signaling,
45 content decreased by 42% in palmitate-loaded serum-starved cells overexpressing PGC-1alpha (P<0.05).
47 l 12-myristate 13-acetate addition, the same serum-starved cells regained p67 mRNA, p67 protein, and
48 ntity of procaspase-12 is actually higher in serum-starved cells relative to that cultured in the pre
49 However, the luciferase mRNA was higher in serum-starved cells than in control cells, suggesting th
50 we observed that DHFR mRNA is less stable in serum-starved cells than in exponentially growing cells.
51 RK7 has appreciable constitutive activity in serum-starved cells that is dependent on the presence of
52 in progression from G(0)-G(1) to S phase in serum-starved cells that were serum stimulated to reente
53 the genome of these cells as well as forces serum-starved cells to enter S phase of the cell cycle,
55 at a similar rate in serum-treated cells and serum-starved cells treated with the phosphoinositide 3-
61 Also, the rates of protein synthesis in the serum-starved cells were restored nearly to the level ob
62 in the nucleoli of corneal fibroblasts after serum-starved cells were treated with 10% FBS, PDGF, or
65 -I overexpression or knockdown, we find that serum-starved cells with high ST6Gal-I levels exhibit in
67 ntrast, nucleolin was exclusively nuclear in serum-starved cells, and F3 did not bind to these cells.
68 s highly active in oocytes and quiescent and serum-starved cells, and injection of active PAK I into
69 lated eNOS phosphorylation were performed on serum-starved cells, and only the short term effect of H
71 tected in the nuclear fraction of lysates of serum-starved cells, but ZO-1 was found in the nuclear f
74 to have significant constitutive activity in serum-starved cells, which is not increased further by e
87 n(-/-) RPE showed low VEGF-A secretion under serum-starved conditions compared with wild-type cells.
89 g the LDLR led to decreased cell survival in serum-starved conditions, associated with Caspase 3 clea
92 n cycling HEp-2 and HeLa cells and quiescent serum-starved, contact-inhibited human lung fibroblasts.
93 ronectin mRNA that was detected in untreated serum-starved control cells was EDA and EDB negative.
95 responses of normal cultured keratocytes and serum-starved corneal fibroblasts to TGFbeta in the pres
97 Here we report that cholesterol depletion of serum-starved COS-1 cells with MbetaCD or filipin caused
99 omodeoxyuridine incorporation experiments in serum-starved cultures revealed that myogenin-positive c
101 ve Akt was sufficient to promote survival of serum-starved endothelial cells in transient transfectio
102 roblasts differentiated in vitro, but not in serum starved fibroblasts, suggesting that their express
103 rbed ends, stimulated stable MT formation in serum-starved fibroblasts and caused a redistribution of
104 imed target alone, in an experiment in which serum-starved fibroblasts responded to the reintroductio
105 ous times following the addition of serum to serum-starved fibroblasts transfected with the chimeric
107 were performed using conditioned media from serum-starved fibroblasts, these data also highlight our
109 captured onto collagen-coated biosensors and serum-starved, followed by exposure to agonistic compoun
114 tin assay on cultured goblet cells that were serum-starved for 2 hours before stimulation with VIP, V
115 ltures of rat corneal endothelial cells were serum-starved for 48 hours and incubated for 2 hours wit
117 Ser64 and Thr189 phosphorylation was low in serum-starved (G0) cells but was strongly increased in m
119 in E are not appropriately down-regulated in serum starved, G1 arrested, v-mos-transformed cells as c
123 Expression of 75 kinases in cultures of serum-starved (HCF) were investigated using protein kina
125 1 stimulated actin stress fiber formation in serum-starved HeLa cells in a Rho-dependent manner and r
126 servation and flow cytometry in non-mitotic, serum-starved, HeLa cells showed that RNAi-mediated vigi
127 report that BIG1 concentrated in nucleoli of serum-starved HepG2 cells prompted us to identify molecu
129 antibody against TRAIL, blocked apoptosis of serum-starved HMECs plated on the nonintegrin attachment
130 n as early as 30 min postinfection (p.i.) in serum-starved HMVEC-d, which was sustained throughout th
132 form of Akt stimulated HSC proliferation in serum-starved HSCs, whereas LY294002 and dominant-negati
138 ated rat retinal ganglion cells (RGC-5), and serum-starved human retinal pigment epithelial cells (AR
139 ions of recombinant ERK2 into the lysates of serum-starved human umbilical vein endothelial cells (HU
145 of ADMA on gene expression and metabolism in serum-starved LoVo cells with gene microarray and metabo
151 d increased the levels of c-MYC and c-JUN in serum-starved MCF10A cells in a p300-dependent manner.
154 d dephosphorylated pRB were expressed in all serum-starved MM patient cells and MM-derived cell lines
155 tivity that normally associates with p130 in serum-starved mouse embryo fibroblasts associated instea
158 Western blot analysis phosphorylated Akt in serum-starved MP1 cells (NIH 3T3 cells transformed by JS
160 rylation of the activating T loop of CDK2 in serum-starved NHF stimulated with mitogens or ectopicall
164 duced from 3 to 6 h after serum induction of serum-starved NIH 3T3 cells, suggesting that the cdc25A
167 ganization, we show that UNC-115 activity in serum-starved NIH 3T3 fibroblasts results in the formati
168 We examined these issues in wound-edge, serum-starved NIH 3T3 fibroblasts where MT stabilization
170 corporation, DNA amounts, and cell number in serum-starved NIH-3T3 fibroblasts transfected with 5-HT2
172 Cyclin D1 promoter reporter assays done in serum-starved NIH3T3 cells indicated that the constituti
173 ow that lysophosphatidic acid stimulation of serum-starved NIH3T3 cells resulted in relocalization of
174 ellular signal-regulated kinase 2) occurs in serum-starved NIH3T3 cells, and that this activation of
178 exhibited increased apoptosis when they were serum starved or subjected to hypoxia-reoxygenation, whe
180 adapter protein Nck, remain constitutive in serum-starved or epidermal growth factor-stimulated cell
183 not cyclin E-CDK2 activity, was increased in serum-starved p27(-/-) cells, and decreasing CDK2 activi
184 icantly reduced light chain 3-II (LC3-II) in serum-starved PC3; in contrast, treatment with LY294002
190 Immunoblotting of p85-associated proteins in serum-starved PTEN-deficient LNCaP and C4-2 PCa cells sh
191 omal pathways with bafilomycin A1 sensitized serum-starved quiescent cells to MG132-induced apoptosis
192 and the autophagy/lysosomal pathway protect serum-starved quiescent fibroblasts from proteasome inhi
193 50YS middle T antigen inhibited apoptosis in serum-starved Rat-1 cells at both permissive and restric
194 I bound to p130(cas), but not to paxillin in serum-starved rat-1 fibroblasts overexpressing the human
195 lling, cell morphology and actin dynamics in serum-starved rodent fibroblasts independently of Smad2,
197 e found that the addition of serum or LPA to serum-starved Schwann cells rapidly (10 min) induced the
198 ving three groups of human fibroblast cells (serum starved, serum stimulated, and a 50:50 mixture of
201 nstitutively active Cdc42/RhoA chimeras into serum-starved Swiss 3T3 cells showed that although prese
202 t the cytoplasmic stiffness and viscosity of serum-starved Swiss 3T3 cells transiently and locally en
206 ore the restriction point in nocodazole- and serum-starved synchronized HT29 cells, without affecting
208 rowth factor-induced mitogenesis, HLECs were serum starved, then stimulated with 15 ng/ml epidermal g
211 to reenter the cell cycle, fibroblasts were serum starved to stop DNA replication and cellular repli
212 ntaneous growth was examined in synchronized serum-starved tumor cell lines and a model of spontaneou
215 -beta1-stimulation of primary astrocytes and serum-starved U-251MG malignant astrocytoma cells attach
217 high levels of AP-1 DNA binding activity in serum starved v-mos-transformed cells compared to very l
225 P levels and triggered MTOC reorientation in serum-starved wounded monolayers of 3T3 fibroblasts.
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