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

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

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

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

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

7 proteins present in cytoplasmic extracts of RAW 264.7 cells.

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

9 during RANKL-supported osteoclastogenesis in RAW 264.7 cells.

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

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

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

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

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

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

16 e element binding protein phosphorylation in RAW 264.7 cells.

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

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

19 h primary splenocytes or cultured macrophage RAW 264.7 cells.

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

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

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

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

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

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

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

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

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

29 itrite production and IkappaB degradation by RAW 264.7 cells.

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

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

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

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

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

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

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

37 Similar results were obtained with untreated RAW 264.7 cells.

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

39 ferase reporter transgene was transfected in RAW 264.7 cells.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

58 the glucosyltransferase activity of TcdA in RAW 264.7 cells.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

111 12-myristate 13-acetate, is also blocked in RAW 264.7 cells by o-ATP pretreatment.

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

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

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

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

116 RAW 264.7 cells contained significant membrane-bound CPD

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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