ライフサイエンスコーパス: BMM

1 BMM from mice deficient in all three FcgammaR or in gamm

2 BMM+SIM preserved the most interproximal bone height (P

3 BMMs are the major source of inflammatory factors and pr

4 BMMs from MCP-1(-/-) mice showed decreased multinucleate

5 IRF-1(-/-) BMMs demonstrated enhanced LPS-induced Il23a expression

6 pha [TNF-alpha] and interleukin-10 [IL-10]), BMMs were transfected with selected miRNA mimics and inh

7 bserved that H. pylori-infected miR-155(-/-) BMMs were significantly more susceptible to cisplatin DN

8 A total of 14 adult SM patients (10 ISM, 2 BMM, 1 SSM, and 1 ASM-AHN) received omalizumab with a me

9 ductase binding site on the hydroxylase of a BMM enzyme, soluble methane monooxygenase (sMMO) from Me

10 th either bone mineralized matrix (BMM) or a BMM+SIM conjugate.

11 ong transient ruffling in both LR5 cells and BMM.

12 Small nodal tumor infiltrates and BMM were found in a total of 21 patients (17.2%) and 46

13 ociation of SNTI in sentinel lymph nodes and BMM in patients with stage I to III colon cancer and the

14 Pathologic hemolysis induced loss of RPM and BMM due to excess heme but induced Spic in monocytes to

15 ed Spic in monocytes to generate new RPM and BMM.

16 However, both SNTI and BMM are independent negative prognostic factors regardin

17 sociation between the occurrence of SNTI and BMM as well as their prognostic relevance.

18 sociation between the occurrence of SNTI and BMM in patients with stage I to III colon cancer.

19 ) and the communication between OB/BMSCs and BMMs (i.e., RANKL expression) that controls osteoclastog

20 tracts from RANKL-treated RAW264.7 cells and BMMs, suggesting that the 12-bp sequence may be involved

21 process was required to inhibit ruffling as BMM from Fc gamma (-/-) mice that bound C. neoformans bu

22 Coculture of Atf4-/- BMMs with WT OBLs or a high concentration of RANKL faile

23 d reverse transcription-PCR showed that both BMM and RAW264.7 cells display high levels of Flt-1 but

24 , all nonmotile L. pneumophila mutants bound BMM less efficiently than the wild type, resulting in po

25 ted by centrifugation, all the mutants bound BMM similarly, but only those microbes that synthesized

26 nd CRP opsonized zymosan for phagocytosis by BMM from mice deficient in FcgammaRII or FcgammaRIII.

27 LPS-induced IL-6 and TNF-alpha production by BMM from MKP-1(-/-) mice was significantly reduced as co

28 it RANKL/M-CSF-induced osteoclastogenesis by BMMs derived from STAT6-, but not SHIP1-, knockout mice.

29 ty, dose-dependently prompt TNF secretion by BMMs.

30 ssion by CSF-1 is more rapid in MRL than C3H BMM phi.

31 vates SMAD-3, was induced in RAW264.7 cells, BMM, and SPM by TMEV.

32 ion and SMAD-3 activation in RAW264.7 cells, BMM, and SPM.

33 steoclastogenesis depends on RANKL to commit BMMs to the osteoclast lineage and RANKL regulates the l

34 f, which has been previously shown to commit BMMs to the osteoclast lineage in RANKL- and TNF alpha-m

35 tal role in osteoclastogenesis by committing BMMs to the osteoclast lineage.

36 rotrophic fungus Plectosphaerella cucumerina BMM (PcBMM), but not to the bacterium Pseudomonas syring

37 TNF and c-src expression, by cultured BMMs derived from LPS-injected mice, reflects duration o

38 ptive transfer of WT but not TIM-4-deficient BMM readily recreated local inflammation response/hepato

39 ed by WT (TIM-4+) but not by TIM-4-deficient BMM.

40 endent signals is enhanced in DJ-1-deficient BMMs as compared to wild-type BMMs.

41 r, LPS-stimulated MKK-6- and MKK-3-deficient BMMs had suppressed LPS-mediated interleukin-6 (IL-6) ex

42 ROS was increased in DJ-1-deficient ((-/-)) BMMs compared with wild-type.

43 In this study, bone marrow-derived (BMM) and splenic macrophages (SPM) from SJL/J mice, susc

44 ion of MAPKs was decreased in differentiated BMMs from cKO animals.

45 TAT-IkappaB efficiently enters BMMs, and the NF-kappaB-inhibitory protein, once intrace

46 Defect grafting, especially BMM+SIM, reduced inflammation and preserved bone.

47 utively phosphorylated in Myr-Akt-expressing BMMs.

48 ular endothelial growth factor also followed BMM delivery.

49 ess greater levels of miR-125a-5p than do GM-BMM macrophages (M1).

50 r level in M-BMM (M2 macrophages) than in GM-BMM (M1 macrophages).

51 We found that overexpression of let-7c in GM-BMM diminished M1 phenotype expression while promoting p

52 ion was decreased when M-BMM converted to GM-BMM, whereas it increased when GM-BMM converted to M-BMM

53 rted to GM-BMM, whereas it increased when GM-BMM converted to M-BMM.

54 ke by both wild-type (P<0.006) and Hca2(-/-) BMMs (P<0.03) in response to LPS was observed, which was

55 wild-type BMMs (P<0.04) but not in Hca2(-/-) BMMs.

56 ages (BMMs) but failed to do so in Hca2(-/-) BMMs.

57 h after LPS stimulation but not in Hca2(-/-) BMMs.

58 had no effect on the chemotaxis of Hca2(-/-) BMMs.

59 d matrix degradation are reduced in Hck(-/-) BMMs or Hck shRNA cells.

60 NP-IDV-BMMs administered to HIV-1-challenged humanized mice rev

61 h ns2(H126R) activated RNase L in Ifih1(-/-) BMM to a similar extent as in wild-type (WT) BMM, despit

62 evels of IFN-alpha/beta in wt and IFNAR(-/-) BMM, indicating that ns2 expression has no effect on the

63 n alpha/beta receptor-deficient (IFNAR(-/-)) BMMs.

64 blocking antibody, as well as in Ifnar1(-/-) BMM, both expressing low basal levels of Oas genes.

65 l as in IFN receptor-deficient (Ifnar1(-/-)) BMM.

66 o be constitutively associated with SHP-1 in BMM and in 293T cells, co-expressing p62(dok) and either

67 126R) failed to induce RNase L activation in BMM treated with IFNAR1-blocking antibody, as well as in

68 acrophages (BMM) and that Spic expression in BMM and RPM development was induced by heme, a metabolit

69 Moreover, in BMM from MKP1(-/-) mice, the inhibition of LPS-induced p

70 In BMMs committed to become osteoclasts by RANKL treatment,

71 In BMMs, spleen cells, and RAW264.7 cells, osteoclast diffe

72 identified known gene targets of miR-155 in BMMs during H. pylori infection that are proapoptotic.

73 the T4SS, in the up-regulation of miR-155 in BMMs.

74 ibited E. coli-induced TNF-alpha and IL-6 in BMMs of both TRIF(-/-) and TRIF(+/+) mice, suggesting th

75 -alpha and IL-6 production were abolished in BMMs of TRIF(-/-) mice.

76 ased and abbreviated NF-kappaB activation in BMMs triggered by TLR9.

77 transient RANKL-induced Ca(2+) amplitudes in BMMs by approximately 50% (p < 0.0001) and prevented pho

78 (BMMs) of TRIF(+/+) mice, but attenuated in BMMs of TRIF(-/-) mice.

79 -alpha and IL-6 production was attenuated in BMMs of TRIF(-/-) mice.

80 n in migration due to p85alpha deficiency in BMMs is associated with reduced adhesion and directed mi

81 orylation of CREB and expression of c-fos in BMMs (p < 0.01), culminating in decreased NFATc1 protein

82 ptional regulator of osteoclastogenesis), in BMMs but can up-regulate its expression in the presence

83 In addition, deficiency of p85alpha in BMMs also results in defective phagocytosis of sheep red

84 Biochemically, loss of p85alpha in BMMs results in reduced activation of Akt and Rac, but n

85 M-CSF signaling and the PI3K/AKT pathways in BMMs.

86 Similar to what has been reported in BMMs, phagosomes containing Legionella matured into endo

87 Th cells were clearly increased by SOCS1 in BMMs.

88 nced compared to bacterial growth ex vivo in BMMs from heterozygous littermate controls.

89 Bacterial growth ex vivo in BMMs from MyD88-deficient mice was not enhanced compared

90 ontained a heat-labile factor that increased BMMs osteoclastogenesis.

91 microbes that synthesized flagellin induced BMM death.

92 ponent of orthopedic implant cement, induces BMM expression of TNF mRNA and protein in a time- and do

93 TNF-mediated, endotoxin sequentially induces BMM expression of TNF, followed by c-src.

94 In P. gingivalis-infected BMMs, mmu-miR-155-5p significantly decreased TNF-alpha s

95 graphy altered BMSC phenotype and influenced BMM osteoclastogenesis.

96 e impaired in NF-kappaB-inducing kinase(-/-) BMM.

97 PIP5K-gamma knockout BMM also have more RhoA and less Rac1 activation, and ph

98 gly, cell survival of wild-type and knockout BMMs is unaltered.

99 In contrast, nonactivated ATG5-knockout BMMs actually restricted C. neoformans growth more effic

100 omparison of RANKL-treated WT versus Cox2 KO BMMs, and RANKL induced Saa3 protein secretion only from

101 dium (CM) from RANKL-treated WT, but not KO, BMMs blocked PTH-stimulated cAMP production in POBs.

102 Likewise BMMs expressing Myr-Akt displayed enhanced phagocytic ab

103 A let-7c is expressed at a higher level in M-BMM (M2 macrophages) than in GM-BMM (M1 macrophages).

104 In contrast, knockdown of let-7c in M-BMM promoted M1 polarization and diminished M2 phenotype

105 S stimulation reduced let-7c expression in M-BMM.

106 In this study, we found that M-BMM macrophages (M2) express greater levels of miR-125a-

107 reas it increased when GM-BMM converted to M-BMM.

108 let-7c expression was decreased when M-BMM converted to GM-BMM, whereas it increased when GM-BM

109 BM-derived macrophage (BMM) delivery resulted in early chemokine up-regulation

110 KL)-activated murine bone marrow macrophage (BMM) cultures revealed unique upregulation of KCa3.1 dur

111 henotype in bone marrow-derived macrophages (BMM) despite the reduced LLO activity.

112 ation using bone marrow-derived macrophages (BMM) from wild-type and Nur77-knockout (Nur77(-/-)) mice

113 tenuated in bone marrow-derived macrophages (BMM) generated from wild-type (wt) mice but not in L2 fi

114 5K-gamma-/- bone marrow-derived macrophages (BMM) have a highly polymerized actin cytoskeleton and ar

115 titution of bone marrow-derived macrophages (BMM) with Rac2 restores the integrin-dependent migration

116 f activated bone marrow-derived macrophages (BMM) with WP1130 significantly augmented killing of the

117 appab1(-/-) bone marrow-derived macrophages (BMM), the formation of both multinucleated osteoclast an

118 n in murine bone marrow-derived macrophages (BMM), to regulate production of a melanin-like pigment,

119 s poorly in bone marrow-derived macrophages (BMM), while ns2(H126R) replicates to high titer in sever

120 and murine bone marrow-derived macrophages (BMM).

121 cells) and bone marrow-derived macrophages (BMM).

122 )-activated bone marrow derived-macrophages (BMM) was detected in 6-hour cultures.

123 of F4/80(+)VCAM1(+) bone marrow macrophages (BMM) and that Spic expression in BMM and RPM development

124 esponses of primary bone marrow macrophages (BMM) from wild-type and SHP-1-deficient motheaten (me/me

125 Wild-type (WT) bone marrow macrophages (BMM) that overexpress the tandem Src homology 2 (SH2) do

126 tosis of zymosan by bone marrow macrophages (BMM) was enhanced by opsonization with SAP or CRP.

127 Bone marrow macrophages (BMM) were generated by culturing bone marrow with macrop

128 loaded into murine bone marrow macrophages (BMM, IDV-NP-BMM) after ex vivo cultivation.

129 row-derived dendritic cells and macrophages (BMMs).

130 G5-knockout bone marrow-derived macrophages (BMMs) also had decreased fungistatic activity against C.

131 n wild-type bone marrow-derived macrophages (BMMs) and partially restored in interferon alpha/beta re

132 type murine bone marrow-derived macrophages (BMMs) but failed to do so in Hca2(-/-) BMMs.

133 Using bone marrow-derived macrophages (BMMs) deficient in the expression of p85alpha-subunit of

134 mary murine bone marrow-derived macrophages (BMMs) during H. pylori infection and examined the downst

135 oblasts and bone marrow-derived macrophages (BMMs) from knockin mice expressing SUMO-free STAT1 to ex

136 oduction by bone marrow-derived macrophages (BMMs) in response to L. pneumophila infection requires t

137 f miRNAs in bone marrow-derived macrophages (BMMs) in which activity was induced by infection with Po

138 detected in bone marrow-derived macrophages (BMMs) of TRIF(+/+) mice, but attenuated in BMMs of TRIF(

139 in Hck(-/-) bone marrow-derived macrophages (BMMs) or in RAW/LR5 macrophages in which Hck expression

140 s (GMPs) or bone marrow-derived macrophages (BMMs) results in the robust production of BMHs.

141 nto carrier bone marrow-derived macrophages (BMMs) was developed.

142 uently, rat bone marrow-derived macrophages (BMMs) were cultured in media supplemented with soluble r

143 Bone marrow-derived macrophages (BMMs) were stimulated with lipopolysaccharide (LPS) and

144 mulation of bone marrow-derived macrophages (BMMs) with endotoxin resulted in increased DJ-1 mRNA and

145 t to murine bone marrow-derived macrophages (BMMs), we show that dendritic cells (DCs) restrict the g

146 E in murine bone marrow-derived macrophages (BMMs).

147 ogenesis in bone marrow-derived macrophages (BMMs).

148 inhibitor, we used bone marrow macrophages (BMMs) and primary osteoblasts (POBs) from WT and Cox2 kn

149 servations, primary bone marrow macrophages (BMMs) derived from S100A4(-/-) mice display defects in c

150 In vitro, bone marrow macrophages (BMMs) from MCP-1(-/-) and WT mice were cultured with M-C

151 gative CAAX-Akt and bone marrow macrophages (BMMs) from wild-type and transgenic mice expressing macr

152 7 cells and primary bone marrow macrophages (BMMs) in an electrophoretic mobility shift assay (EMSA).

153 Bone marrow macrophages (BMMs) isolated from cKO mice are severely inhibited in t

154 ls of RANKL or from bone marrow macrophages (BMMs) pretreated by RANKL.

155 Bone marrow macrophages (BMMs) share common progenitors with osteoclasts and are

156 nd that LPS induces bone marrow macrophages (BMMs) to express c-src, a protooncogene product that we

157 n of wild type (WT) bone marrow macrophages (BMMs) with RANKL, TAK1 deficiency in these cells leads t

158 uce c-src in murine bone marrow macrophages (BMMs), a protein specifically expressed when these cells

159 NF-kappaB in murine bone marrow macrophages (BMMs), is mediated, by c-Src, in a cell, and cytokine sp

160 nic anhydrase II in bone marrow macrophages (BMMs), RANKL renders these osteoclast genes responsive t

161 arrow cells (BMCs), bone marrow macrophages (BMMs), spleen cells, and RAW264.7 cells were evaluated b

162 eoclasts (OCs) from bone marrow macrophages (BMMs), we examined the capacity of this T cell-derived c

163 s, IkappaBalpha, in bone marrow macrophages (BMMs), which are osteoclast precursors, is tyrosine-phos

164 last (OC) precursor bone marrow macrophages (BMMs).

165 This method, Bayesian mutational mapping (BMM), assigns mutations to the branches of the evolution

166 from macrophage progenitors in bone marrow (BMMs) as a consequence of signaling events elicited by M

167 on was assessed on basement membrane matrix (BMM).

168 grafted with either bone mineralized matrix (BMM) or a BMM+SIM conjugate.

169 n levels were similar in wild-type and me/me BMM, except for the constitutive hyperphosphorylation of

170 niches in the bone marrow microenvironment (BMM) and may be the cause of relapse following chemother

171 M cells in the bone marrow microenvironment (BMM) context.

172 gnals from the bone marrow microenvironment (BMM).

173 lymph nodes and bone marrow micrometastases (BMM) were independently described as prognostic factors

174 y decreased in Atf4-/- bone marrow monocyte (BMM) cultures and bones.

175 RAW264.7) and bone marrow-derived monocytes (BMM), revealed that VEGF(121)/rGel was selectively cytot

176 ortus induced bone marrow-derived monocytes (BMMs) to undergo osteoclastogenesis.

177 pacity of FBLP-1 null bone marrow monocytes (BMMs) to differentiate into multinucleated OCLs in respo

178 by bacterial multicomponent monooxygenases (BMMs) requires the interplay of three or four protein co

179 of bacterial multicomponent monooxygenases (BMMs), particularly the syn disposition of the nitrogen

180 mice proliferate similarly to CSF-1; 2) MRL BMM phi proliferate more vigorously to CSF-1 than normal

181 pendent pathway in Dectin-1-triggered murine BMMs and influences TLR cross talk and T cell priming.

182 vidually in nfkappab1(-/-) or nfkappab1(+/+) BMM enhanced both giant osteoclast and MNG formation.

183 IDV-NP-BMM treatment led to robust IDV levels and reduced HIV-1

184 IDV-NP-BMM was administered i.v. to mice resulting in continuou

185 murine bone marrow macrophages (BMM, IDV-NP-BMM) after ex vivo cultivation.

186 Conversely, NUMBL-null BMMs, show increased osteoclast differentiation and mRNA

187 tination of NUMBL is diminished in TAK1-null BMMs compared to elevated K48-poly-ubiquitination in WT

188 Nur77(-/-) BMM exhibit changed expression of M2-specific markers an

189 alpha expression in nonstimulated Nur77(-/-) BMM is repressed by Nur77 and the chemoattractive activi

190 d the chemoattractive activity of Nur77(-/-) BMM is abolished by SDF-1alpha inhibiting antibodies.

191 NO synthesis in (non)-stimulated Nur77(-/-) BMM cells.

192 ity and a loss of contact-dependent death of BMM.

193 The occurrence of BMM was not associated with the presence of SNTI by stan

194 e sensitive than wt virus to pretreatment of BMM, but not L2 fibroblasts or primary astrocytes, with

195 on average, half a point higher than that of BMM phagosomes.

196 Furthermore, failure of BMMs derived from mice deleted of both the p55 and p75 T

197 We find that although pretreatment of BMMs with IL-4 does not alter M-CSF signaling, it revers

198 iated osteoclastogenesis requires priming of BMMs by RANKL.

199 alone or IFN-gamma alone, B7.2 expression on BMM was moderately up-regulated and was further increase

200 al for M-CSF induction of RANK expression on BMMs, and lack of ATF4 caused a shift in OCL precursors

201 ot in L2 fibroblasts, primary astrocytes, or BMM generated from type I interferon receptor-deficient

202 for regulating electron transfer, and other BMM enzymes are likely to adopt the same mechanism.

203 Furthermore, p85alpha-/- BMMs demonstrate a significant reduction in migration in

204 : 1) glomerular M phi and bone marrow M phi (BMM phi) from MRL-lpr mice proliferate similarly to CSF-

205 ediated osteoclastogenesis from RANKL-primed BMMs by up-regulating the expression of the osteoclast m

206 S100A4(-/-) BMMs form unstable protrusions, overassemble myosin-IIA,

207 demonstrated robust lung, liver, and spleen BMMs and drug distribution.

208 ent, is substantially diminished in c-src-/- BMMs.

209 is markedly delayed and reduced in c-src-/- BMMs.

210 In stimulated BMMs, DJ-1 inhibited ROS production by binding to p47(ph

211 egative regulator of Il23a in LPS-stimulated BMMs.

212 CM from RANKL-stimulated BMMs with Saa3 knockdown did not inhibit PTH-stimulated

213 CSF-1-TEC + BMM phi caused a greater accumulation of M phi in the im

214 Furthermore, CSF-1-TEC + BMM phi caused a lesion consisting of M phi in MRL +/+ m

215 importantly, we show for the first time that BMM-supplied CTSK may be involved in CCL2- and COX-2-dri

216 In this study, we show that BMMs from SHIP1 null mice respond to M-CSF, but not rece

217 udies have shown that Wnt signaling from the BMM contributes to preservation of CML LSC following TKI

218 CML LSCs, but a role for TGF-beta1 from the BMM has not been defined.

219 Here, we show that alteration of the BMM by osteoblastic cell-specific activation of the para

220 distinct and suggest that modulation of the BMM by PTH may be a feasible strategy to reduce LSCs, a

221 ulated coevolutionary data indicate that the BMM method can successfully detect nearly all coevolving

222 in vitro and homing of WM tumor cells to the BMM in vivo.

223 vivo neovascularization was studied with the BMM plug assay.

224 SAP binding to BMM from gamma-chain-deficient mice was also greatly red

225 sine-phosphorylated protein in CSF-1-treated BMM.

226 Treating BMMs with the SMAD inhibitor dorsomorphin confirms the r

227 tinic acid significantly inhibited wild-type BMM chemotaxis (P<0.001), but had no effect on the chemo

228 stingly, knockdown of nfkappab2 in wild-type BMM dramatically enhanced both osteoclast and MNG format

229 ly suppressed by nicotinic acid in wild-type BMMs (P<0.04) but not in Hca2(-/-) BMMs.

230 tivation levels by 43% (P<0.03) in wild-type BMMs 6 h after LPS stimulation but not in Hca2(-/-) BMMs

231 damage-induced apoptosis than were wild-type BMMs.

232 DJ-1-deficient BMMs as compared to wild-type BMMs.

233 Unlike BMM, L. monocytogenes growth in DC was minimal after 5 h

234 Using BMMs of TNF receptor-deleted mice, we demonstrate that T

235 By using BMMs from tumor necrosis factor receptor p55 knockout mi

236 conclude that a single dose of NP-IDV, using BMMs as a carrier, is effective and warrants considerati

237 Experiments on in vitro BMM cultures revealed that KCa3.1(-/-) and TRAM-34 treat

238 role for this pathway in invasion, WASP(-/-) BMMs do not invade into tumor spheroids with the same ef

239 When BMM contact by each nonmotile strain was promoted by cen

240 up-regulated and was further increased when BMM were treated with both CT and IFN-gamma together.

241 F-1 (CSF-1-TECs) and placed these cells with BMM phi under the renal capsule.

242 brogated when these cells were cultured with BMMs from IL-17 receptor knockout mice.

243 former, NP-IDV formulation contained within BMMs was adoptively transferred.

244 mor spheroids with the same efficiency as WT BMMs and cells expressing phospho-deficient WASP have re

245 induced Saa3 protein secretion only from WT BMMs.

246 , however, was not different from that of WT BMMs.

247 In contrast to WT BMMs cultured in the presence of a p38alpha/beta inhibit

248 PS-induced Il23a expression compared with WT BMMs.

249 BMM to a similar extent as in wild-type (WT) BMM, despite the lack of IFN induction in the absence of