ライフサイエンスコーパス: serum-starved

1 urface of lysosomal membranes when cells are serum starved.

2 Treatment of IL-3 and serum-starved 32D cells with 1 muM imatinib mysylate inh

3 enerating stable, detyrosinated (Glu) MTs in serum-starved 3T3 cells.

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.

7 In serum-starved adherent cells, LPA induced transient Rho

8 ild-type ERK2 with MEK1 but not with MEK2 in serum-starved adherent cells.

9 t and MEK1/2 pathways as well as survival of serum-starved AML cell lines.

10 d on the surface of infected cells that were serum starved and had Akt activity inhibited.

11 Cultured rat goblet cells were serum starved and incubated with adenoviruses containing

12 Goblet cells were serum starved and incubated with an adenovirus containin

13 luent passage 2 HCECs from eight donors were serum starved and, at different times after growth facto

14 Here we show that st expression in serum-starved and density-arrested NHF specifically indu

15 hly attenuated replicative phenotype in both serum-starved and proliferating normal human astrocytes.

16 asts, ZO-1 was localized to nucleoli of both serum-starved and serum-treated cells.

17 nt study, we report that HB-EGF treatment of serum-starved at aortic SMCs can induce fibroblast growt

18 also stimulated DNA synthesis in quiescent, serum-starved Balb 3T3 transfectants.

19 Cells were serum starved by growth for 48 hours in DMEM/F12 with 0.

20 Angiopoietin-1 promoted survival of serum-starved C2C12, HSM, and NCM (MTT, trypan blue) and

21 PDGF-AA stimulation of serum-starved Cbl transfectants induced the in vivo asso

22 t (</=80% confluent) controls, as well as in serum- starved cells when compared with cells incubated

23 Zinc treatment of serum-starved cells activated extracellular signal-regul

24 ered Plk3-interfering RNA with lentivirus to serum-starved cells and found that, upon serum stimulati

25 This was found both in quiescent serum-starved cells and in cells expressing dominant-neg

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

28 xplore this, PIPKIalpha was overexpressed in serum-starved cells and stimulated with PDGF.

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

33 3) The p67 mRNA was synthesized in serum-starved cells by expression of a p67 cDNA.

34 ium and also after mitogen activation of the serum-starved cells cannot phosphorylate eIF-2 alpha-sub

35 Furthermore, LT induction in serum-starved cells demonstrated gamma-H2AX accumulation

36 ockdown leads to stalling at G0/G1 Moreover, serum-starved cells display reduced hRpn13 and Uch37 pro

37 dependent CDK2 complexes were activated; and serum-starved cells entered S phase.

38 In serum-starved cells estradiol further decreased cell 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

41 he presence of serum, and EGF stimulation of serum-starved cells induced invadopodium formation.

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,

44 In serum-starved cells or during serum stimulation, the Chi

45 content decreased by 42% in palmitate-loaded serum-starved cells overexpressing PGC-1alpha (P<0.05).

46 Also, the extracts from the serum-starved cells phosphorylated the eukaryotic initia

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,

54 Attachment of serum-starved cells to the immobilized anti-TM4SF mAbs i

55 at a similar rate in serum-treated cells and serum-starved cells treated with the phosphoinositide 3-

56 The appearance of p67 mRNA in the serum-starved cells was accompanied by the appearance of

57 at the loss of protein synthesis activity in serum-starved cells was due to loss of p67 mRNA.

58 Meanwhile, the metabolomic data showed serum-starved cells were clearly separated with control

59 Serum-starved cells were incubated for 24 h in Dulbecco'

60 Furthermore, when quiescent serum-starved cells were restimulated with serum, entry

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

63 Pretreatment of serum-starved cells with GSE resulted in 70% to almost c

64 Consistent with these results, serum-starved cells with high ST6Gal-I expression mainta

65 -I overexpression or knockdown, we find that serum-starved cells with high ST6Gal-I levels exhibit in

66 Treatment of serum-starved cells with silymarin resulted in a signifi

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

70 MAL is predominantly cytoplasmic in serum-starved cells, but accumulates in the nucleus foll

71 tected in the nuclear fraction of lysates of serum-starved cells, but ZO-1 was found in the nuclear f

72 In serum-starved cells, KSR contains two constitutive sites

73 In serum-starved cells, PIPKIalpha expression did not stimu

74 to have significant constitutive activity in serum-starved cells, which is not increased further by e

75 on of spoT decreased when serum was added to serum-starved cells.

76 53-dependent apoptosis, and proliferation of serum-starved cells.

77 vel is density-dependent and up-regulated in serum-starved cells.

78 r localization of ERK2-Delta19-25 mutants in serum-starved cells.

79 mulated cultured smooth muscle cells than in serum-starved cells.

80 The expressed p67 mRNA was stable in serum-starved cells.

81 d in growing NIH3T3 fibroblasts, relative to serum-starved cells.

82 IR) and specifically phosphorylates 53BP1 in serum-starved cells.

83 n numerous cancers, promotes the survival of serum-starved cells.

84 metabolites were identified between ADMA and serum-starved cells.

85 oma protein (pRb) are associated with Sp1 in serum-starved CHOC400 cells.

86 We show that serum-starved colon cancer cells differentially respond

87 n(-/-) RPE showed low VEGF-A secretion under serum-starved conditions compared with wild-type cells.

88 were examined in RAW 264.7 macrophages under serum-starved conditions that trigger apoptosis.

89 g the LDLR led to decreased cell survival in serum-starved conditions, associated with Caspase 3 clea

90 Analysis revealed that, under serum-starved conditions, EGFR-Y1086 residue was poorly

91 Under serum-starved conditions, TRE17 localized predominantly

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.

94 hed a maximum of approximately 15-fold above serum-starved controls.

95 responses of normal cultured keratocytes and serum-starved corneal fibroblasts to TGFbeta in the pres

96 ZO-1 was rarely detected in the nucleus of serum-starved corneal fibroblasts.

97 Here we report that cholesterol depletion of serum-starved COS-1 cells with MbetaCD or filipin caused

98 Epidermal growth factor stimulation of serum-starved COS-7 cells promoted the formation of a Cd

99 omodeoxyuridine incorporation experiments in serum-starved cultures revealed that myogenin-positive c

100 onstrate that treatment with LCI-4 protected serum-starved endothelial cells from apoptosis.

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

106 Treatment of serum-starved fibroblasts with cholera toxin promoted se

107 were performed using conditioned media from serum-starved fibroblasts, these data also highlight our

108 ced stress fiber formation when expressed in serum-starved fibroblasts.

109 captured onto collagen-coated biosensors and serum-starved, followed by exposure to agonistic compoun

110 Passage 1 cells were serum starved for 24 to 48 hours and were incubated with

111 Therefore, cells were serum starved for 48 h and then exposed to CGF, EGF, or

112 infected with HCMV for 3, 5, and 7 days were serum starved for 48 hours.

113 ol high passage confluent cultures that were serum starved for 72 h.

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

116 Serum release of serum-starved (G0) 5L rat hepatoma cells triggers transi

117 Ser64 and Thr189 phosphorylation was low in serum-starved (G0) cells but was strongly increased in m

118 Here, we report that serum-starved (G0) diploid human fibroblasts initiate DN

119 in E are not appropriately down-regulated in serum starved, G1 arrested, v-mos-transformed cells as c

120 Forced overexpression of FAK in serum-starved glioblastoma cells plated on recombinant (

121 Serum-starved, growth-arrested, near confluent rat mesan

122 -dependent manner in HC11 cells and enhanced serum-starved HC11 cell survival.

123 Expression of 75 kinases in cultures of serum-starved (HCF) were investigated using protein kina

124 Confluent serum-starved HCM cells were exposed to increasing conce

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

128 n nuclei as well as membranes and cytosol of serum-starved HepG2 cells.

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

131 e culture conditions, but were attenuated in serum-starved host cells and mice.

132 form of Akt stimulated HSC proliferation in serum-starved HSCs, whereas LY294002 and dominant-negati

133 Stimulation of serum-starved human embryonic kidney (HEK) 293 cells wit

134 We used a serum-starved human foreskin fibroblast model to determi

135 Optimal DNA synthesis by serum-starved human gingival fibroblasts required the pr

136 Serum-starved human microvascular endothelial cells (HME

137 Overexpression of c-Myc in serum-starved human or mouse embryonic cells leads to ap

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

140 Using quiescent (serum-starved) human WI-38 cells, camptothecin (CPT) was

141 The addition of VEGF to serum-starved HUVE cells led to a 5.2-fold induction of

142 n decrease of mRNA and protein expression in serum-starved islets compared with controls.

143 Serum-starved JB6 cells contain very little endogenous H

144 ed areas made within confluent monolayers of serum-starved LLC-PK1 cells.

145 of ADMA on gene expression and metabolism in serum-starved LoVo cells with gene microarray and metabo

146 Serum addition causes serum-starved M2 cells to extend flat protrusions transi

147 Furthermore, we show that in serum-starved MCA, expression of constitutively active A

148 In serum-starved MCAs, EGFR activation was associated with

149 Attachment of serum-starved MCF-10A cells to fibronectin, but not poly

150 and the intrinsic MAPK (ERK-1 and ERK-2) of serum-starved MCF-7 cells.

151 d increased the levels of c-MYC and c-JUN in serum-starved MCF10A cells in a p300-dependent manner.

152 Treatment of serum-starved ME-180 cells with fetal bovine serum (FBS)

153 Addition of anastellin to serum-starved microvessel cells resulted in a time-depen

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

156 In serum-starved mouse NIH 3T3 fibroblasts cultured in 1.8

157 ived macrophages with conditioned media from serum-starved mouse proximal tubule cells.

158 Western blot analysis phosphorylated Akt in serum-starved MP1 cells (NIH 3T3 cells transformed by JS

159 AF was sufficient to downregulate p27Kip1 in serum-starved NHEM.

160 rylation of the activating T loop of CDK2 in serum-starved NHF stimulated with mitogens or ectopicall

161 We found that in serum-starved NHF, cyclin E forms inactive complexes wit

162 Furthermore, TPA treatment of serum-starved NIH 3T3 cells led to phosphorylation of SE

163 mutants to promote cell cycle progression in serum-starved NIH 3T3 cells were compared.

164 duced from 3 to 6 h after serum induction of serum-starved NIH 3T3 cells, suggesting that the cdc25A

165 r calpastatin increased cyclin D1 protein in serum-starved NIH 3T3 cells.

166 In serum-starved NIH 3T3 clone 7 fibroblasts, choline phosp

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

169 latory effect of insulin on DNA synthesis in serum-starved NIH 3T3 fibroblasts.

170 corporation, DNA amounts, and cell number in serum-starved NIH-3T3 fibroblasts transfected with 5-HT2

171 ed that the p65e3B1 was the most abundant in serum-starved NIH/EGFR cells.

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

175 Furthermore, in serum-starved NIH3T3 fibroblasts PTN prevents apoptosis

176 The FoxO1 protein level is high in serum-starved normal CEF, but platelet-derived growth fa

177 ed ONOO(-)), induced apoptosis in confluent, serum-starved NRVMs at 48 hours.

178 exhibited increased apoptosis when they were serum starved or subjected to hypoxia-reoxygenation, whe

179 Treatment of serum-starved or cycloheximide-treated cells with Z-VAD.

180 adapter protein Nck, remain constitutive in serum-starved or epidermal growth factor-stimulated cell

181 works extend to the entire cell periphery in serum-starved or nonmotile fibroblasts.

182 impairment in their ability to replicate on serum-starved or quiescent human lung fibroblasts.

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

185 cultures and the lower metabolic activity in serum-starved plateau cultures.

186 onectin (Fn) or adhesion by poly-L-Lysine in serum-starved precursor B leukemia cells.

187 Serum-starved primary African green monkey kidney (AGMK)

188 ecific ligands failed to promote survival of serum-starved primary human endothelial cells.

189 PI3K/AKT signaling was reduced in serum-starved Psen1-/- cells, and this was associated wi

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,

196 g1 and Ang2 mRNAs were expressed by cultured serum-starved RPE cells.

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

199 Serum-starved smooth muscle cells exposed to serum for v

200 any genes that are regulated by IFN-gamma in serum-starved Stat1-null mouse fibroblasts.

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

203 thesis, cell migration, and proliferation in serum-starved Swiss 3T3 cells.

204 oth forskolin-treated REF-52 fibroblasts and serum-starved Swiss 3T3 fibroblasts.

205 omeric actin, Cy3-actin, was introduced into serum-starved Swiss 3T3 fibroblasts.

206 ore the restriction point in nocodazole- and serum-starved synchronized HT29 cells, without affecting

207 e did find a marked increase in apoptosis of serum-starved TEL-expressing NIH 3T3 cells.

208 rowth factor-induced mitogenesis, HLECs were serum starved, then stimulated with 15 ng/ml epidermal g

209 causes cell death, an alternative to G0, in serum-starved THP1 cells.

210 ature oocytes and hastens early G0 arrest in serum-starved THP1 cells.

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

213 Serum-starved tumor cells became apoptotic when exposed

214 ch sufficient to suppress Bbc3 expression in serum-starved tumor cells.

215 -beta1-stimulation of primary astrocytes and serum-starved U-251MG malignant astrocytoma cells attach

216 Analysis of extracts from serum starved v-H-ras, v-src, and tpr-met transformed NI

217 high levels of AP-1 DNA binding activity in serum starved v-mos-transformed cells compared to very l

218 Furthermore, serum starved v-mos-transformed cells have elevated hist

219 cle arrest in NIH3T3 cells is not present in serum starved v-mos-transformed cells.

220 genes cdc2, DHFR, cyclin A, and E2F1 seen in serum starved v-mos-transformed cells.

221 In serum-starved vector control cells, both MeNH2 (1 mM) an

222 Moreover, c-fos overexpression in serum-starved VSMCs results in the induction of cyclin A

223 Incubation of confluent serum-starved VSMCs with thrombin or phenylephrine (PE)

224 Whereas PDGF treatment of serum-starved wild-type mouse embryo fibroblasts resulte

225 P levels and triggered MTOC reorientation in serum-starved wounded monolayers of 3T3 fibroblasts.