ライフサイエンスコーパス: A549 cell

1 ing chloride permeability in F508-expressing A549 cells.

2 sion of the tumor suppressor gene RASSF1A in A549 cells.

3 of CDK9 and by a selective CDK9 inhibitor in A549 cells.

4 translocated to the nucleus in TCRV-infected A549 cells.

5 mice and silica-induced IL-8 generation from A549 cells.

6 olipids in H596 cells was 4-fold higher than A549 cells.

7 ouse strains enhanced HAdV-5 transduction of A549 cells.

8 ed to adherence to and efficient invasion of A549 cells.

9 lipase A2 (cPLA2) in H596 cells than that of A549 cells.

10 ctivity and an increased replication rate in A549 cells.

11 nes, and increased the invasive potential in A549 cells.

12 nce to, invasion of, and plaque formation in A549 cells.

13 in invasion when Deltasan1518 was used with A549 cells.

14 were down-regulated in IFN-alpha-treated HEV-A549 cells.

15 addition of exogenous dNs to virus-infected A549 cells.

16 reased in HEV-A549 cells compared with naive A549 cells.

17 atment suppressed acute acrolein toxicity in A549 cells.

18 unaltered appearance of human lung carcinoma A549 cells.

19 h the regulation of STAT1 phosphorylation in A549 cells.

20 e of Rhodamine 123 or DMP-PNBS in SF-295 and A549 cells.

21 and evaluated the protease's activity toward A549 cells.

22 inhibitory activity) in human adenocarcinoma A549 cells.

23 nce to and invasion of human lung epithelial A549 cells.

24 taken up by CT26 and PC-3M cells but not by A549 cells.

25 elial Beas-2B cells and human lung carcinoma A549 cells.

26 alization in AD32 cells relative to parental A549 cells.

27 tures in bovine aortic endothelial cells and A549 cells.

28 ive to the parental discodermolide-sensitive A549 cells.

29 tion was observed in 293 cells compared with A549 cells.

30 luate the effect of silencing hnRNP A2/B1 in A549 cells.

31 le arrest and apoptosis in human lung cancer A549 cells.

32 e THP-1 cells but not respiratory epithelial A549 cells.

33 zation was necessary for robust signaling in A549 cells.

34 actor (HGF)-dependent scattering response of A549 cells.

35 a rapid Ca(2+)-dependent release of ATP from A549 cells.

36 timulated nSMase2 translocation to the PM in A549 cells.

37 ously identified as downstream of nSMase2 in A549 cells.

38 tumor necrosis-alpha (TNF-alpha)-stimulated A549 cells.

39 s K209D mutant protected this degradation in A549 cells.

40 teins for their ability to stimulate TLR5 in A549 cells.

41 bits oxidant-induced loss of syndecan-1 from A549 cells.

42 uces invasive behavior in C2C12 myocytes and A549 cells.

43 ch do not express any endogenous Sp3, and in A549 cells.

44 y enhanced tumor formation and metastasis by A549 cells.

45 effect on COX-1 mRNA in xenograft tumors or A549 cells.

46 non-small-cell lung cancer (NSCLC) A427 and A549 cells.

47 -filled capillaries on fluorescently labeled A549 cells.

48 sing chromatin immunoprecipitation (ChIP) in A549 cells.

49 ption and cell death as observed in U937 and A549 cells.

50 of human telomerase activity, extracted from A549 cells.

51 lular replication of L. pneumophila Corby in A549 cells.

52 nhanced by DUSP1 overexpression in pulmonary A549 cells.

53 and viral RNAs from IAV PR8DeltaNS1-infected A549 cells.

54 iated with increased metastatic potential of A549 cells.

55 [Ck/TY31]) to grow in human lung epithelial A549 cells.

56 responsible for its efficient replication in A549 cells.

57 -F2 mutants colocalized with mitochondria in A549 cells.

58 lock Xps-mediated rounding and detachment of A549 cells.

59 anced the growth capability of this virus in A549 cells.

60 esponse in human primary dendritic cells and A549 cells.

61 t is not induced by either stimulus in human A549 cells.

62 rus (JUNV), induced an IFN response in human A549 cells.

63 s the morphological and cytotoxic effects on A549 cells.

64 cant increase of ROS in human lung carcinoma A549 cells.

65 plication in both rodent (BHK-21) and human (A549) cells.

66 nce microscopy in human lung adenocarcinoma (A549) cells.

67 ks (DSBs) in normal (HFS) and cancer (LNCaP, A549) cells.

68 of human-BDMs and human alveolar epithelial (A549) cells.

69 With human A549 cells, 4-MCHM mainly induced DNA damage-related bio

70 In this study, A549 cells, a human cell line with a robust innate respo

71 nduce the rounding, detachment, and death of A549 cells, a human lung epithelial cell line.

72 A549 cells aberrantly exited mitosis, following a prolon

73 abs and PFU determined by titration on human A549 cells, according to standard procedures.

74 grew significantly slower than the wild-type A549 cells after cisplatin treatment (P = 0.008).

75 ntial splicing events in lung adenocarcinoma A549 cells after downregulation of the oncogenic serine/

76 We found that Vero and A549 cells already infected by JUNV were fully competent

77 The SP isolated from TIMP-2-overexpressing A549 cells also demonstrated impaired migratory capacity

78 studied changes to the keratin IF network in A549 cells (an alveolar epithelial cell line) exposed to

79 was found that CNPs exert marked effects in A549 cells and also contribute to increases in global DN

80 y (HEK293), Lewis lung carcinoma (LLC1), and A549 cells and are devoid of cytotoxicity.

81 ain within the endoplasmic reticulum (ER) of A549 cells and are not secreted into the culture medium.

82 endogenous GAPDH gene activity in MCF-7 and A549 cells and compared this with plasmid DNA delivery.

83 sing constructs for their overexpressions in A549 cells and confirmed that enzymatic activities of bo

84 -induced interleukin-8 (CXCL8) production in A549 cells and decreased the ability of dexamethasone to

85 chanism by which StmPr1 induces the death of A549 cells and found that StmPr1 induces A549 IL-8 secre

86 totoxicity, but it enhanced proliferation of A549 cells and had antibacterial activity.

87 induced epithelial-mesenchymal transition in A549 cells and HCC827 cells.

88 of the surfactant protein A2, SP-A2, in both A549 cells and in primary type II alveolar epithelial ce

89 increased viral replication and apoptosis in A549 cells and increased virulence and host inflammatory

90 CCR4 was expressed by BEAS-2B and A549 cells and internalized after ligation with CCL17.

91 vault RNAs (vtRNAs) were greatly induced in A549 cells and mouse lungs after infection with IAV.

92 Analysis of model cell lines, such as A549 cells and primary airway epithelial cells, infected

93 nd F-actin content in the cortical region of A549 cells and primary human lung epithelial cells was o

94 ) were measured in culture supernatants from A549 cells and RAW 264.7 cells.

95 normal human bronchial epithelial (NHBE) and A549 cells and secondhand cigarette smoke-induced, ovalb

96 are critical for EGFR-mediated signaling in A549 cells and suggest that up-regulation of Rin1 in A54

97 account for all Xps-mediated effects toward A549 cells and that StmPr1 contributes the most to Xps-m

98 aining the 85I mutation grew faster in human A549 cells and the 336M mutation most significantly enha

99 ected with genotype 3 HEV, designated as HEV-A549 cells and the effects HEV has on IFN-alpha-mediated

100 th the induction of senescence in PM-exposed A549 cells and was unrelated to PM-mediated loss of cell

101 r effects on IL-8 and TGF-beta1 release from A549 cells and were all cytotoxic for small airway epith

102 -inhibitory effects of ceramide both against A549 cells and xenograft-driven tumors in situ and in vi

103 in 0.5% Nonidet P-40 lysates of transfected A549 cells, and demonstrate greater protein instability

104 T cells, human lung adenocarcinoma cell line A549 cells, and human and mouse primary airway epithelia

105 at TGF-beta up-regulated CDH11 expression on A549 cells, and inhibition of CDH11 expression using siR

106 nt PsrP(SRR1-BR) (rPsrP(SRR1-BR)) adhered to A549 cells, and moreover, preincubation of cells with rP

107 ing of AD32-resistant cells versus sensitive A549 cells, and subsequent unbiased gene ontology analys

108 to stimulate IL-8 and TGF-beta1 release from A549 cells, and to serve as ART1 substrates.

109 can increase amiloride-sensitive current in A549 cells as well as in freshly isolated type II alveol

110 The effect of AP301 in A549 cells as well as in human embryonic kidney cells an

111 ation apparatus, was dramatically reduced in A549 cells as well as in the lung, spleen, and thymus of

112 stimulation in a human epithelial cell line (A549 cells) as well as in primary human astrocytes and b

113 crotubule dynamics as compared with parental A549 cells, as assessed by live-cell confocal microscopy

114 s used to analyze the miRNA content of human A549 cells at steady state and following infection with

115 Retroviral expression of PU.1 in A549 cells blocked endosomal escape, nuclear translocati

116 gh less than that of wild-type virus) in DKO A549 cells but not in DKO HAP1 cells where a smaller inc

117 function showed that EGR-1 was functional in A549 cells but not in H460 cells.

118 o localized to the nucleus when expressed in A549 cells, but did not confer any significant protectio

119 d the internalization of S. aureus RN6390 by A549 cells, but the dependence on CD36 was reduced in QT

120 P-induced harmful effect of beta-carotene in A549 cells by downregulating the expression of CYP1A1/1A

121 ated epithelial-to-mesenchymal transition of A549 cells by inhibiting both Smad-dependent signaling a

122 replication of influenza A viruses in human A549 cells by preventing transport of the viral genome t

123 PAR3 was the only PAR subtype detected in A549 cells by reverse transcription-PCR.

124 kely induces cell rounding and detachment of A549 cells by targeting cell integrin-extracellular matr

125 eria to bind to fibronectin and to adhere to A549 cells by uncharacterized mechanisms.

126 nt NS1 and NS2, expressed in lung epithelial A549 cells, can form homo- as well as heteromers.

127 STAT1 levels were markedly increased in HEV-A549 cells compared with naive A549 cells.

128 ysiological processes: Depletion of USP21 in A549 cells compromises the reestablishment of a radial a

129 that purified SV5 virions derived from human A549 cells contained CD46, a plasma membrane-expressed r

130 response in RSV infection using an in vitro A549 cell culture model.

131 Hypoxia-treated A549 cells deficient in mitochondrial DNA or A549 cells

132 In vitro cotransfection experiments in A549 cells demonstrated that AMCase and EGFR physically

133 range in Pf lines and low toxicity in human A549 cells, demonstrating that these ANbPs are excellent

134 studies revealed that cell entry of LCMV in A549 cells depended on actin remodeling and Pak1, sugges

135 ally, deletion of the human IFIT1 protein in A549 cells did not affect IAV replication or infection,

136 d nanoparticles (NPs) on cultured human lung A549 cells directly from the gas phase.

137 1, degraded interleukin 8 (IL-8) secreted by A549 cells during coculture with strain K279a.

138 sis, and in vitro analyses were performed on A549 cells during the process of epithelial to mesenchym

139 n of progeny virus production in primary and A549 cells enriched in G(0)/G(1) using a specific CDK4/6

140 gly, H596 cells produced much less PGE3 than A549 cells even though the expression of COX-2 was simil

141 in degradation of keratin proteins in human A549 cells exposed to 0-24 h of shear stress (7.5-30 dyn

142 ime-dependent and dose-dependent dynamics of A549 cells exposed to doxorubicin are evaluated by monit

143 A549 cell exposure to cigarette smoke condensate increas

144 A549 cells expressing FDH showed a much slower recovery

145 In A549 cells expressing increased levels of TIMP-2, a sign

146 verexpression of Suv4-20h1 in human U2OS and A549 cells expressing integrated and endogenous GR, resp

147 The actin immunoblot from A549 cells from Fig 5A was reused as the actin blot from

148 ntified 19 antiviral VHHs that protect human A549 cells from lethal infection with influenza A virus

149 In A549 cells, global translation was increased, while in H

150 leton of cultured human alveolar epithelial (A549) cells have been investigated.

151 colonization after DAS181 treatment of human A549 cells, healthy mice, and mice challenged with a let

152 005, virus Wb/AH82) in human lung epithelial A549 cells (however, the reassortant virus did not repli

153 d inflammatory responses in human epithelial A549 cells, human innate immune primary cells, and murin

154 ary human bronchial epithelial cells, and in A549 cells IL1B-induced IRF1 protein was only modestly a

155 .g. Rac1, p22(phox), p67(phox), and NOXO1 in A549 cells impaired TPA-induced MnSOD expression.

156 nd significantly suppresses proliferation of A549 cells in a nude mice tumor xenograft model in terms

157 nd released peptide product from BEAS-2B and A549 cells in a time- and concentration-dependent fashio

158 tment also augments the invasive capacity of A549 cells in an SNCG-dependent manner.

159 pression, also suppressed lung metastasis of A549 cells in nude mice and tumorigenesis of Line 1 cell

160 on data generated from human lung epithelial A549 cells in response to A/Mexico/InDRE4487/2009 (H1N1)

161 n addition, Fas receptor was up-regulated in A549 cells in response to monastrol.

162 proteins inhibits IFN-beta mRNA induction in A549 cells in response to RNA bearing 5' phosphates (5'p

163 Further, ectopic miR-1 induced apoptosis in A549 cells in response to the potent anticancer drug dox

164 of lung cancer using tail vein injection of A549 cells in SCID mice.

165 r cells and suppresses the tumorigenicity of A549 cells in severe combined immunodeficiency mice.

166 We show the arrest of A549 cells in the G(1) phase of cell cycle in the presen

167 RC-3940-II on the proliferation of H460 and A549 cells in vitro was assessed by 3-(4,5-dimethylthiaz

168 re the autophagy gene ATG5 is dispensable in A549 cells in vitro, yet promotes tumorigenesis in mice.

169 MK-2206 promoted metastasis of KRAS-mutated A549 cells in vivo.

170 ells and was as potent as irinotecan against A549 cells in xenograft models.

171 creased adherence to human epithelial cells (A549 cells) in vitro.

172 els of IFNs and barely grow in IFN-competent A549 cells, in sharp contrast to the wild-type (WT) viru

173 We show that A549 cells increase glucose uptake during EMT, but inste

174 her levels of type I/III interferon (IFN) in A549 cells, increased IFN-alpha and tumor necrosis facto

175 double knockout (DKO) of PKR and RNase L in A549 cells, indicating that both pathways decreased repl

176 g activation of the IFN induction cascade in A549 cells infected with a variety of influenza A viruse

177 hange in the abundances of D-type cyclins in A549 cells infected with HRSV.

178 Transcriptional profiles of A549 cells infected with recombinant RSVs show significa

179 In addition, A549 cells infected with rLCMV/NP*(D382A), but not with

180 Stable knockdown of CD59 in A549 cells inhibited experimental metastasis.

181 show that the reduced bystander response in A549 cells is due to activation of NF-kappaB signaling b

182 el of miR-200c in non-small-cell lung cancer A549 cells is low in contrast to normal human bronchial

183 ADAR1 deletion in human lung adenocarcinoma A549 cells is rescued by CRISPR/Cas9 mutagenesis of the

184 NSCLC A549 cells lacking ANXA2 exhibited defects in tumor grow

185 knocking down either of the PKM isoforms in A549 cells lacking LKB1, a serine/threonine protein kina

186 o this end, we created a stable B1 knockdown A549 cell line (B1-KD) to investigate B1's role in micro

187 A549 cell line showed to be sensitive to CPD100 and the

188 tion in vitro, especially of lung epithelial A549 cell line.

189 man alveolar type II epithelial cells of the A549 cell line.

190 h effects are not observed in the P16 mutant A549 cell line.

191 rom homogenates prepared from a lung cancer (A549) cell line, on the basis of capillary sieving elect

192 tly reduced levels of adherence to HEp-2 and A549 cell lines in the mclS mutant strains compared to w

193 ls and suggest that up-regulation of Rin1 in A549 cell lines may contribute to their proliferative na

194 We report here the generation of A549 cell lines persistently infected with genotype 3 HE

195 Transfection of COS-7 or A549 cell lines with a construct in which green fluoresc

196 diating gene silencing in adherent MCF-7 and A549 cell lines, primary human umbilical vein endothelia

197 ractions was also evaluated against HeLa and A549 cell lines.

198 in breast cancer (MCF-7) and lung carcinoma (A549) cell lines.

199 osensor was applied to detect miRNA-215 from A549 cell lysate directly without complex sample treatme

200 BDP-PCZ concentrated within A549 cell membranes, and in particular within the endopl

201 achieved thus far for the targeting specific A549 cells on a selective area of patterned SiNWs, is de

202 We used wild-type A549 cells or cells depleted of PARP1.

203 cytotoxicity was observed after treatment of A549 cells or control cells with saporin or Pseudomonas

204 rols, knockdown of Ogg1 (using Ogg1 shRNA in A549 cells or primary alveolar type 2 cells from ogg1(-/

205 that four human lung cancer cells, including A549 cells, overexpress PRL-2 when compared with normal

206 ions occur independent of MMP inhibition, as A549 cells overexpressing Ala+TIMP-2 exhibited identical

207 le of DNA repair (mt-hOgg1-Mut) each blocked A549 cell oxidant-induced mtDNA damage, mitochondrial p5

208 D and PcpA caused a decrease in adherence to A549 cells (P < 0.05).

209 A549 cell pretreatment with WRW4, an antagonist of the t

210 Silencing PPT by small interfering RNA in A549 cells prevents FDH modification, indicating the lac

211 bition of PKCbetaII with enzastaurin reduced A549 cell proliferation by >60% (48 h) and migration by

212 Neferine markedly inhibited A549 cell proliferation in a dose dependent manner.

213 nt with these findings, knockout of Rab29 in A549 cells reduces endogenous LRRK2-mediated phosphoryla

214 Finally, autophagy-deficient A549 cells regain tumorigenicity upon SMAD4 knockdown.

215 We show that B1-KD rendered A549 cells resistant to paclitaxel (PTX), phenocopying c

216 Rin1 depletion from A549 cells resulted in a decrease in cell proliferation

217 Overexpressing TMX in A549 cells resulted in a dramatic increase of ricin or a

218 Gene silencing of GILZ in A549 cells resulted in secretion of significantly higher

219 modification of the protein in vitro and in A549 cells, resulting in further increase in the cytotox

220 pression of PB1-F2 in U937 cells, but not in A549 cells, results in the presence of a specific beta-a

221 n blot analysis of IFN-alpha2a-treated human A549 cells revealed that phospho-STAT1 (Y701) levels pea

222 Expressing full-length GFP-Myo19 in A549 cells reveals a remarkable gain of function where t

223 AT2 and IFN regulatory factor 9 knockdown in A549 cells reversed IFN-gamma-mediated IFN-stimulated re

224 and StmPr2 are predominantly responsible for A549 cell rounding, extracellular matrix protein degrada

225 Additionally, adherence to A549 cells selected for longer chains within the wild-ty

226 A549 cells selected for resistance to GA overexpressed P

227 N2 virus with the PA-K356R mutation in human A549 cells showed increased nuclear accumulation of PA a

228 Gene expression microarray of transfected A549 cells showed that PTGS2 (prostaglandin-endoperoxide

229 Functional analysis of A549 cells showed that TIMP-2 overexpression increased c

230 Importantly, silencing vtRNA in A549 cells significantly inhibited IAV replication, wher

231 Silencing eIF4B expression in A549 cells significantly promoted IAV replication, and c

232 The stable knockdown of PK isoforms in A549 cells significantly reduced the cellular ATP level,

233 show here that knockdown of ERCC6L2 in human A549 cells significantly reduced their viability upon ex

234 RCM-mediated apoptosis was observed in both A549 cells stably expressing small interfering RNA EGR-1

235 protein levels in human lung adenocarcinoma A549 cells stably over-expressing TP receptor alpha isof

236 apoptosis in H1155 and H23 cells, but not in A549 cells, suggesting a correlation between drug sensit

237 hibited mouse serum-enhanced transduction in A549 cells, suggesting a potential role for CAR.

238 ivate AMPK in mitochondrion-deficient rho(0)-A549 cells, suggesting that mitochondrial ROS play an es

239 ed after restoration of ARLTS1 expression in A549 cells, suggesting that various pathways involved in

240 bryonic fibroblasts (MEFs), or in human lung A549 cells that contain mutant Keap1, by inhibition of t

241 (ZFN)--mediated homologous recombination in A549 cells that express aberrantly activated STAT3.

242 niaturized luciferase gene reporter assay in A549 cells that measures IFN-beta induction by viral dsR

243 ide microarray in intact and MDFIC-deficient A549 cells that were treated with glucocorticoids.

244 er membrane protein of A. baumannii binds to A549 cells through platelet-activating factor receptor (

245 A lack of tet38 reduced bacterial uptake by A549 cells to 36% of that of the parental strain RN6390.

246 s were validated in single human lung cancer A549 cells to demonstrate applicability in single-cell e

247 PM2.5 or PM10 deregulated the ability of the A549 cells to express the antimicrobial peptides human b

248 Supernatants from the THP-1 cell line prime A549 cells to release CXCL8 at levels similar to cocultu

249 al reorganization because the KIF network in A549 cells transfected with a dominant negative PKC zeta

250 H441 and A549 cells transfected with M2 showed higher levels of r

251 In A549 cells, transfection of EGFP/proSP-C21 constructs co

252 s, whereas EGF stimulation of EGFR wild-type A549 cells transiently increased Fn14 expression.

253 A549 cells deficient in mitochondrial DNA or A549 cells treated with a small interfering RNA against

254 nal gel electrophoresis of human lung cancer A549 cells treated with radiolabeled PEITC and SFN revea

255 nofluorescence in human alveolar epithelial (A549) cells treated with TGF-beta1 and CXCL9, with Smad2

256 We have further demonstrated that in A549 cells two GTPases, RhoA and Rac1, but not Cdc42, ar

257 und that two-disulfide Trx1 was generated in A549 cells under oxidative stress.

258 We find that MFN2 knockout from MCF7 and A549 cells via Crispr/Cas9 greatly promotes cell viabili

259 gest that thrombin promotes ATP release from A549 cells via Rho- and Ca(2+)-dependent activation of c

260 In vitro, FPR2 expressed on A549 cells was activated by IAV, which harbors its ligan

261 rest in both HRSV-infected primary cells and A549 cells was confirmed using dual-label flow cytometry

262 , replication of the DeltasfaA mutant within A549 cells was decreased 3.0-fold.

263 luciferase reporter activities in human lung A549 cells was dramatically different.

264 -NPs) to promote survivin MB uptake in human A549 cells was investigated.

265 reading frame (ORF)3 protein to STAT1 in HEV-A549 cells was observed.

266 The proliferation of A549 cells was significantly reduced by ITCs, with relat

267 ronchial epithelial and pulmonary epithelial A549 cells, we confirm that interleukin-1beta (IL1B) ind

268 fluorescent reporter construct expressed in A549 cells, we directly observed activation of PKC activ

269 he broad-spectrum HDACi Vorinostat (SAHA) in A549 cells, we find that combination with ATXN3 depletio

270 In the case of A549 cells, we found that GBS VII invasion and adherence

271 Using human lung adenocarcinoma (A549) cells, we provide evidence for the metabolic activ

272 We demonstrated that virus-infected A549 cells were efficiently killed in the presence of a

273 A549 cells were exposed to DEA at the ALI and under subm

274 A549 cells were exposed to the thiol-reactive dye Thiogl

275 A549 cells were found to be more resistant to radiation-

276 Stable lines of IL-18Ralpha-depleted human A549 cells were generated using shRNA, resulting in an i

277 Human HAP1 and A549 cells were genetically modified by clustered regula

278 A549 cells were infected and analyzed for global transcr

279 A549 cells were pre-incubated with beta-carotene (BC) al

280 s (H596, IMR-90) or dicoumarol-exposed NQO1+ A549 cells were resistant (LD50, >40 microM) to ROS form

281 the DeltamgrA and DeltatetR21 mutants within A549 cells were similar, while no growth was observed fo

282 MC3T3 and A549 cells were successfully encapsulated, demonstrating

283 A549 cells were treated with fullerene (C60), long or sh

284 Human pulmonary epithelial A549 cells were used to study the role of the mitogen-ac

285 Xrn1 KO A549 cells were viable but nonpermissive for VACV; howev

286 ation-conditioned medium (RCM) obtained from A549 cells when compared with the H460 exposed to RCM pr

287 In A549 cells, which are resistant to geldanamycin and stro

288 and yet had reduced growth in human alveolar A549 cells, which were found to have a higher endosomal

289 how enhanced replication of the 66S virus in A549 cells, while studies of BALB/c and DBA/2 mice and f

290 Treatment of HEV-A549 cells with 250, 500, and 1000 U/mL of IFN-alpha for

291 ng cancer H69 and non-small cell lung cancer A549 cells with a concomitant increase in the level of a

292 Treating RSV-infected A549 cells with antioxidants significantly inhibited RSV

293 Moreover, co-culture of A549 cells with RAW 264.7 macrophages induced expression

294 Infection of A549 cells with recombinant viruses deficient in the exp

295 r response was seen for quantifying captured A549 cells with respect to loaded cells.

296 Both viruses infected A549 cells with similar efficiencies, executed DNA repli

297 Treatment of A549 cells with the chemotherapeutic agents gemcitabine

298 Pre-treatment of Keap1(-/-) MEFs or A549 cells with the LY294002 PI3K inhibitor or the MK-22

299 In contrast, coculture of A549 cells with the macrophage-like THP-1 cell line, dif

300 ed prostaglandin E(2) in IL-1beta-stimulated A549 cells without affecting COX-2 expression, showing t