ライフサイエンスコーパス: RAW 264.7 cell

1 ha production by LPS-stimulated macrophages (RAW 264.7 cells).

2 anti-inflammatory factor (IL-10) in inflamed Raw 264.7 cells.

3 xpression of Kruppel-like factor 2 (KLF2) in RAW 264.7 cells.

4 gamma interferon (IFN-gamma) stimulation of RAW 264.7 cells.

5 vity in response to RANKL in both BM-MNC and RAW 264.7 cells.

6 e bone marrow mononuclear cells (BM-MNC) and RAW 264.7 cells.

7 ponsible for the delayed escape phenotype in RAW 264.7 cells.

8 in culture supernatants from A549 cells and RAW 264.7 cells.

9 atterns of HMGB1 release similar to those of RAW 264.7 cells.

10 ut has an inverse effect in undifferentiated RAW 264.7 cells.

11 ge of inhibitor of NF-kappaB(IkappaBalpha)in RAW 264.7 cells.

12 proteins present in cytoplasmic extracts of RAW 264.7 cells.

13 factor alpha production in HeNC2, THP-1, and RAW 264.7 cells.

14 during RANKL-supported osteoclastogenesis in RAW 264.7 cells.

15 clear extracts from hypoxic but not normoxic RAW 264.7 cells.

16 s (murine myeloid cells), or 3) OCCM-30 plus RAW 264.7 cells.

17 reas CAAX-Akt down-regulated phagocytosis in Raw 264.7 cells.

18 sitively regulates LPS-induced activation of Raw 264.7 cells.

19 tivation of Elk-1 and NF-kappaB reporters in RAW 264.7 cells.

20 aracterized p300 binding to iNOS promoter in RAW 264.7 cells.

21 e element binding protein phosphorylation in RAW 264.7 cells.

22 inding of PSG17 to CD9-transfected cells and RAW 264.7 cells.

23 ction in cultured murine mesangial cells and RAW 264.7 cells.

24 nuclear NF-kappa B translocation in PBMC and RAW 264.7 cells.

25 ulation of iNOS monomers in mouse macrophage RAW 264.7 cells.

26 ric-oxide synthase and interleukin-1alpha in RAW 264.7 cells.

27 (ROS) in pulmonary alveolar macrophages and RAW 264.7 cells.

28 enuate PGE2 production in response to LPS in RAW 264.7 cells.

29 ed the expression of the PGHS-1 isoenzyme in RAW 264.7 cells.

30 P-1-dependent reporter gene transcription in RAW 264.7 cells.

31 sis reaction when compared with the parental RAW 264.7 cells.

32 of IFNgamma, acemannan induced apoptosis in RAW 264.7 cells.

33 itrite production and IkappaB degradation by RAW 264.7 cells.

34 te nitrite production and iNOS expression by RAW 264.7 cells.

35 inhibit LPS-induced TNF-alpha production in RAW 264.7 cells.

36 vely expressed in skin and in LPS-stimulated RAW 264.7 cells.

37 uction of NO in rat resident macrophages and RAW 264.7 cells.

38 accharide, stimulated TNF-alpha expressed by RAW 264.7 cells.

39 hrs) of liposome-encapsulated hemoglobin by RAW 264.7 cells.

40 equences for theIfnbgene by XBP1 in infected RAW 264.7 cells.

41 so prevent the release of IL-1 activity from RAW 264.7 cells.

42 ma, greatly increased the synthesis of NO in RAW 264.7 cells.

43 Similar results were obtained with untreated RAW 264.7 cells.

44 d constitutively in murine NIH 3T3 cells and RAW 264.7 cells.

45 of ulvan to stimulate cytokine production in RAW 264.7 cells.

46 e nitric oxide synthase (iNOS) expression in RAW 264.7 cells.

47 ate their anti-inflammatory properties using RAW 264.7 cells.

48 h primary splenocytes or cultured macrophage RAW 264.7 cells.

49 on of IL6 in gingival fibroblasts, HSC-2 and RAW 264.7 cells.

50 ferase reporter transgene was transfected in RAW 264.7 cells.

51 ssion associated with LRP1 gene silencing in RAW 264.7 cells.

52 corresponds to the protein content of three RAW 264.7 cells.

53 oplasma pneumoniae in SP-A knockout mice and RAW 264.7 cells.

54 duced inflammatory mediators (NO, CCL-20) in RAW 264.7 cells.

55 in mouse microglia BV-2 cells and macrophage RAW 264.7 cells.

56 ffect in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells.

57 lls and mouse peritoneal macrophages than in RAW 264.7 cells.

58 fMIF)-mediated proinflammatory activities in RAW 264.7 cells.

59 ng to TBK1-dependent IRF3 phosphorylation in RAW 264.7 cells.

60 xide amounts were observed in LPS-stimulated RAW 264.7 cells.

61 eptor into Slamf8-deficient primary MPhis or RAW 264.7 cells.

62 ide synthase, and nitric oxide production in RAW 264.7 cells.

63 ng of A. baumannii by HL-60 cells but not by RAW 264.7 cells.

64 in primary mouse bone marrow macrophages and Raw 264.7 cells.

65 RAP) activity was evaluated in RANKL-treated RAW 264.7 cells.

66 ng and down-regulation of iNOS expression in RAW 264.7 cells.

67 duced by TcdA was further demonstrated using RAW 264.7 cells.

68 ed motility following uptake of B. mallei by RAW 264.7 cells.

69 tract on lipopolysaccharide (LPS)-stimulated RAW 264.7 cells.

70 (a lipopolysaccharide analog) of macrophage RAW 264.7 cells.

71 the glucosyltransferase activity of TcdA in RAW 264.7 cells.

72 r mg protein in unstimulated macrophage-like RAW 264.7 cells.

73 d repressed VEGF-3' UTR reporter activity in RAW-264.7 cells.

74 OC of both murine bone marrow monocytes and RAW 264.7 cells, a monocytic line, by down-regulating th

75 ss RANKL signaling and osteoclastogenesis in RAW 264.7 cells, a murine monocytic cell line.

76 tion of 28 DAG molecular species detected in RAW 264.7 cells after stimulation of a G-protein coupled

77 LPS treatment of RAW 264.7 cells also induced the activation of the cAMP

78 lso induced NO synthesis when incubated with RAW 264.7 cells, an activity which probably results from

79 We also report that in RAW 264.7 cells, an E(2) receptor-positive murine monocy

80 prevented LPS-stimulated M-CSF production in RAW 264.7 cells, an effect that was abrogated by a speci

81 Using TLR5-negative RAW 264.7 cells and a TLR5-enhanced yellow fluorescent p

82 did not inhibit Mtb-induced NO production in RAW 264.7 cells and AM phi.

83 The treatment of RAW 264.7 cells and bone marrow-derived macrophages with

84 pain activation was examined by using murine RAW 264.7 cells and bone marrow-derived monocyte/macroph

85 Treatment of RAW 264.7 cells and CD-1 mouse peritoneal macrophages wi

86 bsequently, transgene expression in vitro in RAW 264.7 cells and ex vivo in primary activated and res

87 length human chemotactic peptide receptor in RAW 264.7 cells and examined cytoskeletal alterations in

88 Inhibition of SPK sensitized RAW 264.7 cells and HMs to LPS-induced apoptosis.

89 re, lipopolysaccharide stimulation of murine RAW 264.7 cells and human CD14(+) monocytes up-regulated

90 broad anti-inflammatory effects in monocytic RAW 264.7 cells and in primary intraperitoneal macrophag

91 dsRNA- and virus-induced iNOS expression by RAW 264.7 cells and mouse macrophages.

92 Lipid loading of RAW 264.7 cells and mouse peritoneal macrophages with ei

93 tor binding to these AREs after treatment of RAW 264.7 cells and mouse peritoneal macrophages with ox

94 by increased N-terminal GSDMD expression in RAW 264.7 cells and mouse primary peritoneal macrophages

95 h a subtype-specific antagonist (MRS 1191 in RAW 264.7 cells and MRS 1220 in THP-1 cells) reverses th

96 LPS and poly(I:C) induce HMGB1 release from RAW 264.7 cells and murine macrophages, the response is

97 LPS induced autophagy in RAW 264.7 cells and murine peritoneal M that was attenua

98 Assays on murine preosteoclastic RAW 264.7 cells and on primary bone marrow monocytes bot

99 not mRNA) was decreased in both LPS-treated RAW 264.7 cells and peritoneal macrophages isolated from

100 All extracts showed low cytotoxicity against RAW 264.7 cells and Petit Verdot pomace suppressed TNF-a

101 and Mtb-induced TNF-alpha production in both RAW 264.7 cells and primary human alveolar macrophages (

102 paBalpha induced apoptosis in macrophagelike RAW 264.7 cells and primary human macrophages.

103 TNF from mouse macrophages and of ROIs from RAW 264.7 cells and suppressed the rise in serum TNF lev

104 erved in response to stimulation with LPS in RAW 264.7 cells and to PMA and LPS in U937 cells.

105 taken-up into cultured macrophage (J774.1 or RAW 264.7) cells and accumulates at perinuclear sites (w

106 represses VEGF-3' UTR reporter expression in RAW-264.7 cells and in mouse bone marrow-derived macroph

107 posures also caused morphological changes in RAW 264.7 cells, and at sublethal doses (i.e., 10 mg/L)

108 e-activating protein domain, in a subline of RAW 264.7 cells, and challenged the transfected cells wi

109 greater TNF-alpha than free CpG ODN in mouse RAW 264.7 cells, and in human peripheral blood mononucle

110 (CAT) reporter gene, stably transfected into RAW 264.7 cells, and transfectants were assayed for CAT

111 pattern in the cytosol of the LPS-stimulated RAW 264.7 cells, and was occasionally seen in the cytoso

112 a on day 6 increased NF-kappaB activation in RAW(264.7) cells, and plasma-induced osteoclastogenesis

113 It was observed that RAW 264.7 cells are highly susceptible to the toxic effe

114 In these experiments, using RAW 264.7 cells as a model, LPS and poly(I:C) caused HMG

115 ammatory response of primary macrophages and RAW 264.7 cells as indicated by the expression of IL1bet

116 enously generated PN in endotoxin-stimulated RAW 264.7 cells as well as in dissociated cultures of hi

117 ms involved in lung inflammation, we exposed RAW 264.7 cells as well as mouse primary macrophages to

118 njection of sEVs derived from LPS stimulated RAW 264.7 cells attenuated mechanical hyperalgesia in th

119 ction of HNO in aqueous solution and in live RAW 264.7 cells, based on the soft nucleophilicity of th

120 Here, we show that murine myeloid RAW 264.7 cells became activated when infected with MYXV

121 ed activation of RANK-dependent signaling in RAW 264.7 cells but had no effect on M-CSF-induced activ

122 ure to silica induced TNFalpha production by RAW 264.7 cells, but not by IC-21.

123 bitor, blocked LPS-induced TLR4 signaling in RAW 264.7 cells by inhibiting activation of ERK1/2, MEK1

124 12-myristate 13-acetate, is also blocked in RAW 264.7 cells by o-ATP pretreatment.

125 The enhancement of PGE2 production in RAW 264.7 cells by tetracyclines was accompanied by the

126 he addition of an NO donor and rIFN-alpha to RAW 264.7 cells caused HMGB1 release.

127 rpose of cloning the receptor, we screened a RAW 264.7 cell cDNA expression library.

128 s revealed that S-AS were avidly taken up by RAW 264.7 cells, confirming that their lack of efficacy

129 RAW 264.7 cells contained significant membrane-bound CPD

130 re added exogenously to CHO-K1, NIH-3T3, and RAW 264.7 cells correlates with their relative in vitro

131 Interestingly, LPS treatment of RAW 264.7 cells, cotransfected with pRA-294-luc and pRSV

132 ng RNA (siRNA)-mediated silencing of KLF2 in RAW 264.7 cells could restore the activation of NF-kappa

133 ition of either genistein or herbimycin A to RAW 264.7 cell cultures 1-6 It after stimulation with LP

134 In cultured RAW 264.7 cells, curcumin inhibited endotoxin-induced in

135 a beta-glucocerebrosidase inhibitor, treated RAW 264.7 cells demonstrated the practical utility of th

136 etic model for cytosolic calcium dynamics in RAW 264.7 cells developed in the companion article, the

137 Depletion of gangliosides in RAW 264.7 cells did not alter the concentration dependen

138 ffects on augmenting chemokine expression in RAW 264.7 cells did not require JAK2.

139 rmore, the levels of miR-155 and miR-125b in Raw 264.7 cells displayed oscillatory changes in respons

140 ion of a dominant-inhibitory Raf-1 mutant in RAW 264.7 cells does not inhibit LPS-induced MAPK activi

141 Murine macrophage RAW 264.7 cells either infected with C. pneumoniae or tr

142 filing shows that encounter between PAO1 and RAW 264.7 cells elicits an early inflammatory response,

143 identified that over-expression of pTRAIL in RAW 264.7 cells enhanced OCL differentiation.

144 LPS-stimulated RAW 264.7 cells exhibited increased protein and mRNA lev

145 Phagocytic activity in RAW 264.7 cells exposed to both liposome-encapsulated he

146 RAW 264.7 cells expressed PKCs alpha, betaI, delta, epsi

147 of the supernatant from sonoporation-treated RAW 264.7 cells expressing CD63-GFP demonstrated a delay

148 established LXR target genes is increased in RAW 264.7 cells expressing the LXRalpha S198A phosphoryl

149 ssion of dominant negative mutants of PKR in RAW 264.7 cells fails to attenuate dsRNA- and EMCV-induc

150 f anthrax lethal factor and protected murine RAW-264.7 cells from lethal toxin, a mixture of lethal f

151 ha, IL-6, IL-1, GM-CSF, MCP-1 and IL-10 from RAW 264.7 cells; IL-6, IL-8 and MCP-1 from HTR-8/SVneo c

152 vimentin cytoskeleton, whereas expression in RAW 264.7 cells impeded vimentin reorganization upon sti

153 vities in human endothelial cells and murine RAW 264.7 cells in a comparable concentration-dependent

154 OS protein levels and promoter activities in RAW 264.7 cells in a time- and concentration-dependent m

155 Protection against apoptosis in RAW 264.7 cells in response to silica was mediated by en

156 es in CD63-GFP intensity and distribution in RAW 264.7 cells in terms of response time and duration d

157 tive mutant MAPK (ERK2) cDNA or in wild type RAW 264.7 cells in the presence of the MAPK kinase (MEK1

158 stimulated the production of iNOS and NO by RAW 264.7 cells in the presence, but not the absence, of

159 ide- and interferon-gamma-stimulated iNOS in RAW 264.7 cells in vitro, as assessed by nitrite accumul

160 ion, MMP-12 caused the release of sCD14 from RAW 264.7 cells in vitro.

161 oned media from both activated microglia and RAW 264.7 cells increased the proportion of ChAT-positiv

162 S treatment and pRSV-Raf-BXB transfection of RAW 264.7 cells increases p42 MAPK activity.

163 nalyses of the EP4 receptor gene promoter in RAW 264.7 cells indicated that there is a constitutive n

164 PS-induced NO production dose-dependently in RAW 264.7 cell indicates the extract's potential anti-in

165 Forskolin treatment of RAW 264.7 cells induced both kappa B and cAMP response e

166 yte lysate and the secretion of TNF-alpha by RAW 264.7 cells induced by lipid A and four different en

167 ion showed no differences in colonization in RAW 264.7 cells infected with either Salmonella construc

168 ted in an NF-kappaB-dependent fashion in the RAW 264.7 cells infected with vMyx-M141KO.

169 n the level of secreted TNF-alpha protein in RAW 264.7 cells is due primarily to activation of TNF-al

170 olysacharide/interferon-gamma stimulation of RAW 264.7 cells is largely divorced from production of r

171 nhibited LPS-induced degradation of IkB-a in RAW 264.7 cells, leading to inhibition of the NF-kB path

172 hibited TGF-beta1 expression by macrophages (RAW 264.7 cell line and bone marrow-derived macrophages)

173 f FS and PCS were compared using LPS treated RAW 264.7 cell line and lipoxygenase inhibition.

174 oidal gold and compared their binding to the RAW 264.7 cell line by electron microscopy.

175 om both mouse peritoneal macrophages and the RAW 264.7 cell line in vitro.

176 in cellular defenses against HNE toxicity, a RAW 264.7 cell line overexpressing human aldehyde dehydr

177 to the murine-derived, peritoneal monocytic RAW 264.7 cell line showed significantly reduced TNF-alp

178 led to death of the macrophages, but for the RAW 264.7 cell line this was not due to apoptotic pathwa

179 t an accepted sphingolipid model system, the RAW 264.7 cell line, and 61 sphingolipids were quantifie

180 In this report, using the macrophage-like RAW 264.7 cell line, we provide experimental evidence th

181 ma-stimulated peritoneal macrophages and the Raw 264.7 cell line.

182 acellular survivability assays in Caco-2 and Raw 264.7 cell lines as well as the determination of the

183 gestion and analysis of picogram loadings of RAW 264.7 cell lysate.

184 lied the system for triplicate analysis of a RAW 264.7 cell lysate; 2 +/- 1 and 7 +/- 2 protein group

185 We prepared triplicate RAW 264.7 cell lysates that contained 6, 30, 120, and 30

186 IFN-gamma-lipopolysaccharide (LPS)-activated RAW 264.7 cells (macrophages) with aqueous humor, aqueou

187 ble levels of 1-deoxyDHCers and ceramides in RAW 264.7 cells maintained in culture.

188 FP3 also increased NO synthesis by RAW 264.7 cells, mimicking an alpha2M activity that has

189 M-30 (immortalized murine cementoblasts), 2) RAW 264.7 cells (murine myeloid cells), or 3) OCCM-30 pl

190 LPS treatment of RAW 264.7 cells, murine bone marrow-derived macrophages,

191 Internalization of OmpA(+) E. coli by RAW 264.7 cells occurred by both actin- and microtubule-

192 s is not required for toxicity toward either RAW 264.7 cells or for alveolar macrophages.

193 Treatment of RAW 264.7 cells or mouse macrophages with dsRNA stimulat

194 from macrophages (Mphi) stimulated with LPS, RAW 264.7 cells or murine primary peritoneal Mphi were i

195 Infection of RAW 264.7 cells or peritoneal macrophages with either Sa

196 und to survive and replicate within infected RAW 264.7 cells over an 18-h period.

197 -green fluorescent protein-transfected mouse RAW 264.7 cells, oxLDL-IC-induced HSP70B' co-localized w

198 loride (AAPH) treatment of liposomes made of RAW 264.7 cell phospholipids were each labeled with the

199 on ET-induced CREB activity was examined in RAW 264.7 cells possessing a CRE-luciferase reporter.

200 t the TcdA-mediated glucosylation of Rac1 in RAW 264.7 cells, presaturation of FcgammaRI with anti-CD

201 IRF3 phosphorylation was not blocked in RAW 264.7 cells pretreated with the RNA polymerase III i

202 ells of established cell lines (MC3TC-E1 and RAW 264.7 cells), primary murine calvarial osteoblasts,

203 at- or urea-denatured proteins) for 6-300 ng RAW 264.7 cell protein analysis in terms of number of pe

204 ivity in RAW 264.7 cells, suggesting that in RAW 264.7 cells, Raf-1 kinase is not an activating compo

205 RAW 264.7 cells rapidly induce cyclooxygenase-2 (COX-2)

206 sly demonstrated that murine macrophage-like RAW 264.7 cells respond to CpG DNA with an increase in t

207 LPS treatment of RAW 264.7 cells resulted in a time- and dose-dependent a

208 s; knockdown of Neu1 in macrophage cell line RAW 264.7 cells resulted in enhanced LPS-induced toleran

209 Knockdown of siglec-1 in RAW 264.7 cells resulted in inhibiting the production of

210 Analysis of RAW 264.7 cell RNA demonstrated transcripts for CB2 but

211 Using this method we found that in RAW 264.7 cells RSNO formation occurs only at very low (

212 the tssE mutants were able to survive within RAW 264.7 cells, significant growth defects were observe

213 ve but not a kinase-inactive p70S6 kinase in Raw 264.7 cells significantly enhanced phagocytosis.

214 impacts EV production using mouse macrophage RAW 264.7 cells stably expressing CD63-GFP as a model sy

215 omplex kinetic model for calcium dynamics in RAW 264.7 cells stimulated by the C5a ligand.

216 Using a model of macrophages (RAW 264.7 cells) stimulated with bacterial lipopolysacch

217 cephalomyocarditis virus (EMCV) infection of RAW 264.7 cells stimulates COX-2 expression and PGE(2) a

218 human A549 alveolar carcinoma cells but not RAW 264.7 cells, suggesting that alternative pathways co

219 detect LPS-induced Raf-1 kinase activity in RAW 264.7 cells, suggesting that in RAW 264.7 cells, Raf

220 rexpression of AUF1 in mouse macrophage-like RAW-264.7 cells suppresses endogenous VEGF protein level

221 her level of osteoclast differentiation from RAW 264.7 cells than did nonimmune B cells that were not

222 ctor strain colonized to a greater extent in RAW 264.7 cells than in peritoneal macrophages.

223 pneumoniae D39 caused higher cytotoxicity to RAW 264.7 cells than the DeltaadhE strain under the etha

224 rbohydrate-decorated NPs were endocytosed by Raw 264.7 cells than the ones without carbohydrate modif

225 e mechanism of toxicity, we selected variant RAW 264.7 cells that resist PAO1.

226 In addition, in RAW 264.7 cells the activity of the distal gene 50/RTA p

227 Finally, in LPS- and IFN-gamma-activated RAW-264.7 cells, the association between NFAT and ICSBP

228 mented RANKL-supported osteoclastogenesis in RAW 264.7 cells, thereby implicating its pivotal role in

229 he presence of IFNgamma induces apoptosis in RAW 264.7 cells through a mechanism involving the inhibi

230 er hand, overexpression of MCPIP1 sensitized RAW 264.7 cells to apoptosis under stress, whereas MCPIP

231 as indicated by decreased transformation of RAW 264.7 cells to osteoclasts and reduced TRAP activity

232 lly, whole OSPW also impaired the ability of RAW 264.7 cells to perform phagocytosis.

233 nduced LKB1 degradation, whereas exposure of RAW 264.7 cells to S-nitroso-l-glutathione, a NO donor,

234 ent to induce a heightened susceptibility of RAW 264.7 cells to Salmonella-induced pyroptosis, and th

235 escue serum deprivation-induced apoptosis in RAW 264.7 cells transfected with a dominant-negative mut

236 following a mycobacterial infection, we used RAW 264.7 cells transfected with a TNF-alpha or NOS2 pro

237 RAW 264.7 cells treated with CpG ODN had a transient inc

238 ith IP10, both in lung after i.v. LPS and in RAW 264.7 cells treated with LPS or with IFN-gamma.

239 his method was applied in studies of TAGs in RAW 264.7 cells treated with the toll-like receptor 4 li

240 Infection of RAW 264.7 cells triggers an early response (2 to 6 h pos

241 Oxidation states were measured in living RAW 264.7 cells under varying electron flux and membrane

242 y GSH to form a GSH conjugate (GS-6-DHSG) in RAW 264.7 cells, via a potential mechanism involving the

243 Production of NO by H. pylori-stimulated RAW 264.7 cells was dependent on the L-Arg concentration

244 location of B. pseudomallei within infected RAW 264.7 cells was determined, and as expected, the bsa

245 The resulting substrate from RAW 264.7 cells was Histone H1.2, an isoform protein of

246 LPS induction of icIL-1Ra transcription in RAW 264.7 cells was regulated by strong positively actin

247 Inhibition of LPS binding to RAW 264.7 cells was reversed with anti-C1INH Ab and was

248 pIC4525.Luc in transfected but unstimulated RAW 264.7 cells was under the control of a weak inhibito

249 itro culture model of murine macrophage-like RAW 264.7 cells, we demonstrate that S. aureus biofilm-c

250 Using both murine peritoneal macrophages and RAW 264.7 cells, we demonstrated a significant, time-dep

251 Through the use of these biosensors on live RAW 264.7 cells, we found that changes in the overall ch

252 Using RAW 264.7 cells, we found that the presence of L-cystine

253 om CaR-/- mice as well as DN-CaR-transfected RAW 264.7 cells, we provide evidence that expression of

254 nd quantification of TNF-alpha production in RAW 264.7 cells were conducted.

255 RAW 264.7 cells were exposed to endotoxin (4 ng/mL or 10

256 Murine primary macrophages and RAW 264.7 cells were exposed to saliva and lipopolysacch

257 The IC-21 cell line was permissive, whereas RAW 264.7 cells were not.

258 rmore, the fluorescence images of Cys/Hcy in Raw 264.7 cells were obtained after adding this probe to

259 Zymosan-treated RAW 264.7 cells were shown to have an approximately 6-fo

260 (THP-1, U937, and MM6) or murine macrophage RAW 264.7 cells were stimulated with picomolar concentra

261 When RAW 264.7 cells were transfected with a panel of plasmid

262 Furthermore, macrophages cell line RAW 264.7 cells were treated with curcumin followed by s

263 ated replication kinetics in MDCK, A549, and RAW 264.7 cells when inoculated at a multiplicity of inf

264 ed production of nitric oxide in LPS-induced RAW 264.7 cells, whereas the ethanol extract mitigated s

265 ements that regulate CTSK gene expression in RAW 264.7 cells, which can be differentiated to osteocla

266 how here that CO increases ROS generation in RAW 264.7 cells, which is inhibited by antimycin A and i

267 sed decreased cell migration and motility of RAW 264.7 cells, which was rescued by transfection of Ga

268 RAW 264.7 cells with decreased expression of GBP-5 mRNA

269 Preincubation of RAW 264.7 cells with herbimycin A or genistein (but not

270 Stimulation of RAW 264.7 cells with LPS in the presence of inducible ni

271 In other experiments, treating RAW 264.7 cells with LPS induced citrullination in the i

272 hese experiments reveal that pretreatment of RAW 264.7 cells with o-ATP attenuates the LPS stimulatio

273 In additional studies, cotransfection of RAW 264.7 cells with pRA-294-luc and increasing amounts

274 We demonstrate that treatment of monocyte RAW 264.7 cells with RANKL induces dose-dependent growth

275 Sublines of RAW 264.7 cells with reduced GPI-PLD expression exhibite

276 Using stably transfected RAW 264.7 cells with the kinase-deleted dominant-negativ

277 Treatment of RAW 264.7 cells with the same LPS preparations induced l

278 Knocking down XBP1 expression by transducing RAW 264.7 cells with the short hairpin XBP1 lentiviral v

279 Treatment of mouse macrophages or RAW-264.7 cells with dsRNA or infection with EMCV stimul

280 a and TNF-alpha) levels in the LPS-activated Raw 264.7 cells without showing any enzyme-inhibition ac