ライフサイエンスコーパス: A549 cell

1 nhanced by DUSP1 overexpression in pulmonary A549 cells.

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

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

4 responsible for its efficient replication in A549 cells.

5 -F2 mutants colocalized with mitochondria in A549 cells.

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

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

8 esponse in human primary dendritic cells and A549 cells.

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

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

11 s the morphological and cytotoxic effects on A549 cells.

12 ane "rippling" along with nanoscale pores on A549 cells.

13 lation of mitochondrial transcripts in human A549 cells.

14 ing chloride permeability in F508-expressing A549 cells.

15 rom healthy donors and patients with IPF and A549 cells.

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

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

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

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

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

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

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

23 intact Ag-Phen and Ag(+), in the presence of A549 cells.

24 ctivity and an increased replication rate in A549 cells.

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

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

27 in invasion when Deltasan1518 was used with A549 cells.

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

29 markers (CD44 and CD87) in both BEAS-2B and A549 cells.

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

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

32 atment suppressed acute acrolein toxicity in A549 cells.

33 unaltered appearance of human lung carcinoma A549 cells.

34 h the regulation of STAT1 phosphorylation in A549 cells.

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

36 inhibitory activity) in human adenocarcinoma A549 cells.

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

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

39 alization in AD32 cells relative to parental A549 cells.

40 tures in bovine aortic endothelial cells and A549 cells.

41 ive to the parental discodermolide-sensitive A549 cells.

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

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

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

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

46 zation was necessary for robust signaling in A549 cells.

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

48 4 interaction and inhibited proliferation of A549 cells.

49 o the formation of the SET-FTY720 complex in A549 cells.

50 g ability in human bronchoalveolar carcinoma A549 cells.

51 leads to impairment in the proliferation of A549 cells.

52 ffects of RNase L on ZIKV infection in human A549 cells.

53 Rab5-GTP levels in FAK-null fibroblasts and A549 cells.

54 and reduced proliferation in PC9 but not in A549 cells.

55 ical inhibitor of FAK, PF562,271, in resting A549 cells.

56 and inhibited Rab dephosphorylation in human A549 cells.

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

58 uble thioglycosylated zinc(II) porphyrins in A549 cells.

59 iated with increased metastatic potential of A549 cells.

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

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

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

63 sing chromatin immunoprecipitation (ChIP) in A549 cells.

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

65 HEJ appears lower in U2OS than in HEK293 and A549 cells.

66 of human telomerase activity, extracted from A549 cells.

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

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

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

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

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

72 Here, we confirm that H1299 and A549 cells, 2 lung cancer cell lines, relay on aerobic g

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

74 biological determinants of MCPyV entry into A549 cells, a highly transducible lung carcinoma cell li

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

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

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

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

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

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

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

82 afficking of fluorescently labeled HAdV26 in A549 cells and A549-derived cell clones with stably incr

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

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

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

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

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

88 nd an increase of reactive oxygen species in A549 cells and fibroblasts, but fibroblasts were less af

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

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

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

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

93 reased bacterial adherence and invasion into A549 cells and increased A549 cell viability.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

110 Both in vitro and in human A549 cells, appending a 3'-end single-stranded pyrimidin

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

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

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

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

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

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

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

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 Doxycycline slowed proliferation of A549 cells by 35%.

121 resulting in a further decrease of surviving A549 cells by 59% and of fibroblasts by 24% compared to

122 After confirming GBA knockout of HEK 293 and A549 cells by both Western blotting and lipid mass spect

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

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

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

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

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

128 tion in H460 and H1975, but not in HCC827 or A549 cells, by decreasing SLC2A1 (GLUT1) mRNA and protei

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

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

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

132 s proteolytic processing of core proteins in A549 cells consistent with higher infectious virus titer

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

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

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

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

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

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

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

140 1, degraded interleukin 8 (IL-8) secreted by A549 cells during coculture with strain K279a.

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

142 While overexpression of LY6E in C3A and A549 cells efficiently inhibited the infection of HCoV-O

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

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

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

146 A549 cell exposure to cigarette smoke condensate increas

147 Furthermore, human A549 cells expressing codon-optimized C16L/B22R and C12L

148 A549 cells expressing FDH showed a much slower recovery

149 tionally, using SARS-CoV-2-Nluc infection of A549 cells expressing human ACE2 receptor (A549-hACE2),

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

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

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

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

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

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

156 005, virus Wb/AH82) in human lung epithelial A549 cells (however, the reassortant virus did not repli

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

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

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

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

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

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

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

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

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

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

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

168 cific proteins in human lung adenocarcinoma (A549) cells in which eEF2K had been depleted by an induc

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

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

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

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

173 Transcriptome analysis of BEAS-2B and A549 cells incubated with TGF-beta were analyzed through

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

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

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

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

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

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

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

181 NSCLC A549 cells lacking ANXA2 exhibited defects in tumor grow

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

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

184 In an A549 cell line carrying the rs189256251 variant CT genot

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

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

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

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

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

190 he metabolism with established NSCLC PC9 and A549 cell lines in vitro Surprisingly, [(13)C(6)]glucose

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

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

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

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

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

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

197 inesterase concentration and activity in the A549 cell media but not in the media of either HFL1 or H

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

199 own of endogenous Rab5 prevented FAK-induced A549 cell migration, whereas expression of WT or GTP-bou

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

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

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

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

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

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

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

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

208 This was confirmed in A549 cells, plus submersion, and ALI culture of HBE cell

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

210 ters of m(6)A display reduced replication in A549 cells, primary well differentiated human airway epi

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 antibody to the bacteria prior to adding to A549 cells reduced internalization of QT7 2-fold compare

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

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

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

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

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

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

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

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

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

225 A549 cells selected in vivo to give brain metastases exh

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

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

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

229 P2-6R accumulated in A549 cells significantly faster and produced 50-fold hig

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

235 Key effects of doxycycline observed in A549 cells, such as the decrease of mitochondrial-encode

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

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

238 red human non-small cell lung cancer (NSCLC) A549 cells take up the precursor, which is extended by c

239 and more effectively inhibited viability of A549 cells than viability of either H1299 or HFL1 cell l

240 the replication and amplification of DVGs in A549 cells that are deficient in a variety of innate int

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

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

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

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

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

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

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

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

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

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

251 s were diminished upon the same treatment of A549 cells transfected with either p53 siRNA or acetylch

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

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

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

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

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

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

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

259 functions, we deleted DNA-PKcs from HeLa and A549 cells using CRISPR/Cas9.

260 time series of IL1B-induced inflammation in A549 cells, using cytokine production as outputs and tes

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

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

263 e and invasion into A549 cells and increased A549 cell viability.

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

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

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

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

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

269 ovement of GFP-labeled RNP particles in live A549 cells was recorded within 3 to 4 h postinfection at

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

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

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

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

274 ion and in situ proximity ligation assays in A549 cells, we observed that beta-arrestin-1 and unligan

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

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

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

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

279 A549 cells were infected and analyzed for global transcr

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

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

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

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

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

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

291 Pretreatment of A549 cells with MAb against CD9 and CD9-EC2 significantl

292 cription and replication during infection of A549 cells with parainfluenza virus type 2 (PIV2), PIV3,

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

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

299 , we found that in TRIM6 knockout (TRIM6-KO) A549 cells, WNV replication is significantly increased a

300 Finally, by means of an A549 cell xenograft mouse model, we demonstrate that the