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 set enrichment analysis of Notch2(tm1.1Ecan) BMMs cultured in the presence of macrophage colony stimu

9 by TNFalpha was greater in Notch2(tm1.1Ecan) BMMs than in control cells, possibly contributing to the

10 data of pooled control and Notch2(tm1.1Ecan) BMMs treated with M-CSF or M-CSF and receptor activator

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

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

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

14 ong transient ruffling in both LR5 cells and BMM.

15 bserved in achieving mRS 0-2 between EVT and BMM (adjusted OR 1.00, 95% CI 0.67 to 1.50, p>0.99).

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

17 ored IL-12 and IFN-gamma cytokine levels and BMM -T cell interaction.

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

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

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

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

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

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

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

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

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

27 As BMMs progress, the ER reduction and endocrine resistance

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

29 6 BMMs compared to those in the untreated B6 BMM controls.

30 sed the concentrations of R. australis in B6 BMMs compared to those in the untreated B6 BMM controls.

31 Compared to B6 BMMs, TLR4(-/-) BMMs failed to secrete a significant lev

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

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

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

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

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

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

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

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

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

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

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

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

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

45 II (LC3-II) and LC3 puncta in Atg5-competent BMMs but not in Atg5-deficient BMMs, while no p62 turnov

46 cleared PMNs in lungs compared with control BMM s.

47 osis of apoptotic PMNs compared with control BMM s.

48 hages (BMMs) than in Atg5(flox/flox) Lyz-Cre BMMs in vitro was abolished by exogenous treatment with

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

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

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

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

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

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

55 tg5-competent BMMs but not in Atg5-deficient BMMs, while no p62 turnover was observed.

56 e L. monocytogenes killing in P2X5-deficient BMMs is substantially rescued by exogenous IL-1beta or I

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

58 Adoptive transfer of Gas6-depleted BMM s failed to clear PMNs in lungs following LPS challe

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

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

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

62 EZH2 drives ER(+) BMMs toward a basal and stem-like state.

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

64 utively phosphorylated in Myr-Akt-expressing BMMs.

65 ular endothelial growth factor also followed BMM delivery.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

83 In BMM, Kava-205Me also reduced secretion of other cytokine

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

85 f progressions in typical ISM group, 1.7% in BMM, and 9.4% in SSM).

86 126R) failed to induce RNase L activation in BMM treated with IFNAR1-blocking antibody, as well as in

87 hibition of IL-6 by its blocking antibody in BMM-OB cocultures diminishes the increase of osteoclasto

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

89 the SOCS1 level remains consistently high in BMM s and SOCS3 expression is pronounced and long lastin

90 th decreased IgG (P = .008) plasma levels in BMM cases.

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

92 ni activates IDO/kynurenine/AHR signaling in BMM s to maintain prolonged SOCS1 expression.

93 In BMMs committed to become osteoclasts by RANKL treatment,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

110 Th cells were clearly increased by SOCS1 in BMMs.

111 ice were significantly greater than those in BMMs of B6 controls, highlighting the important role of

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

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

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

115 microbes that synthesized flagellin induced BMM death.

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

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

118 Later, PGE2, secreted from infected BMM s induces cAMP-PKA pathway by binding to the EP2/EP4

119 promoter for its early induction in infected BMM s.

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

121 graphy altered BMSC phenotype and influenced BMM osteoclastogenesis.

122 urvival (EFS) were found when comparing ISM, BMM, and SSM.

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

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

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

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

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

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

129 Likewise BMMs expressing Myr-Akt displayed enhanced phagocytic ab

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

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

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

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

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

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

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

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

138 Using bone marrow-derived macrophages (BMM s) and CD4(+) T cells, we observed that L. donovani

139 priming of bone marrow-derived macrophages (BMM s) with IL-4 or TSG6 also induced M transition and e

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

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

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

143 5K-gamma-/- bone marrow-derived macrophages (BMM) have a highly polymerized actin cytoskeleton and ar

144 nfection of bone marrow-derived macrophages (BMM) with lethal Ehrlichia polarized M0 macrophages into

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

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

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

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

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

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

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

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

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

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

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

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

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

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

159 ti-inflammatory effects, murine macrophages (BMM) and THP-1 cells were infected with P. gingivalis (M

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

161 Depletion of BM macrophages (BMMs) increased AML growth in vivo.

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

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

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

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

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

167 5-deficient bone marrow-derived macrophages (BMMs) exhibit defective cytosolic killing of L. monocyto

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

169 cultures of bone marrow-derived macrophages (BMMs) from Notch2(tm1.1Ecan) mice when compared with the

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

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

172 ustralis in bone marrow-derived macrophages (BMMs) of TLR4(-/-) and ASC(-/-) mice were significantly

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

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

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

176 (flox/flox) bone marrow-derived macrophages (BMMs) than in Atg5(flox/flox) Lyz-Cre BMMs in vitro was

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

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

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

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

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

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

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

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

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

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

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

188 7 cells and primary bone marrow macrophages (BMMs) in an electrophoretic mobility shift assay (EMSA).

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

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

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

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

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

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

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

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

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

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

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

200 lastogenesis of rat bone-marrow macrophages (BMMs).

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

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

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

204 with typical ISM, bone marrow mastocytosis (BMM), and smoldering SM (SSM), 4.1% of disease progressi

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

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

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

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

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

210 f cells of the bone marrow microenvironment (BMM), such as mesenchymal stem cells (MSCs) and macropha

211 gnals from the bone marrow microenvironment (BMM).

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

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

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

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

216 ltures of bone marrow macrophages/monocytes (BMMs) and OBs after treatment with the conditioned mediu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

238 iated osteoclastogenesis requires priming of BMMs by RANKL.

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

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

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

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

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

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

245 Adoptive transfer of TSG6- or IL-4-primed BMM s i.t.

246 TSG6- or IL-4-primed BMM s induced efferocytosis of apoptotic PMNs compared w

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

248 analysis, 1713 received EVT and 412 received BMM.

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

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

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

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

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

254 egative regulator of Il23a in LPS-stimulated BMMs.

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

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

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

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

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

260 Conversely, B-ALL conditions the BMM to induce hepatic generation of plasminogen, the pla

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

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

263 ophages and, to a lesser extent, MSCs of the BMM and integrin beta3-AKT signaling in HSCs as at least

264 t impairs HSC function via impairment of the BMM and the periostin/integrin beta3 axis, possibly asso

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

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

267 ng published examples that alteration of the BMM can lead to hematological malignancies in mice, we d

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

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

270 ible effect of VKAs on hematopoiesis via the BMM.

271 vivo neovascularization was studied with the BMM plug assay.

272 aining double-membrane-bound vacuoles in the BMMs of B6 mice.

273 Compared to B6 BMMs, TLR4(-/-) BMMs failed to secrete a significant level of IL-1beta a

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

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

276 Treating BMMs with the SMAD inhibitor dorsomorphin confirms the r

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

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

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

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

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

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

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

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

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

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

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

288 Finally, in vitro BMM killing and in vivo L. monocytogenes infection exper

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

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

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

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

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

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

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

296 induced Saa3 protein secretion only from WT BMMs.

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

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

299 PS-induced Il23a expression compared with WT BMMs.

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