ライフサイエンスコーパス: M-CSF

1 M-CSF (or CSF-1) and GM-CSF can regulate the development

2 M-CSF and IL-10, both released by T lymphocytes, may thu

3 M-CSF and IL-34 up-regulate the expression, by different

4 M-CSF and RANKL stimulation of myeloid cells that overex

5 M-CSF drives the generation of human monocyte-derived ma

6 M-CSF has myriad effects on mononuclear phagocytes but i

7 M-CSF is a cytokine present within atherosclerotic lesio

8 M-CSF is known to induce cytoskeletal reorganization in

9 M-CSF is overexpressed in breast cancer and is known to

10 M-CSF promoted the development of mature monocytes and t

11 M-CSF showed neuroprotective effects as a preventive tre

12 M-CSF treatment resulted in an increased production of m

13 M-CSF treatment showed no adverse effect on long-term li

14 M-CSF was identified in tumor-conditioned media and show

15 M-CSF was necessary for the expansion of lung mononuclea

16 M-CSF-activated AMPK is via M-CSF receptor-dependent rea

17 M-CSF-Mphi and IL-34-Mphi also express the hepatic stell

18 M-CSF-stimulated p21(ras)-GTP and Akt phosphorylation wa

19 al reduced the release of endothelial CSF-1 (M-CSF), which stimulates polarization of macrophages to

20 sed were treated with growth factors (IGF-1, M-CSF), angiogenic factors (VEGF, IL-8), and matrix prot

21 macrophage colony-stimulating factor (CSF-1; M-CSF) directly instructed myeloid commitment in HSCs.

22 F, and TNF-alpha, whereas IL-2, IL-4, IL-10, M-CSF, and IFN-gamma were not detected.

23 ession of IL-6, IL-1beta, cyclo-oxygenase 2, M-CSF, and IDO.

24 d with recombinant MCP-1/CCL2, whereas IL-6, M-CSF, G-CSF, GM-CSF, IL-8/CXCL8, SDF-1/CXCL12, and MGSA

25 ontains only 1 FMS-D1-D3 molecule bound to a M-CSF dimer, due to a weak, hydrophilic M-CSF:FMS interf

26 ally reduces but does not completely abolish M-CSF binding and signaling through its cognate receptor

27 Consequently, Syk(Y317F) abolishes M-CSF- and integrin-stimulated Syk ubiquitination.

28 Myc activation and sterol biosynthesis after M-CSF stimulation.

29 limited extent but in combination may alter M-CSF:FMS signaling dramatically.

30 IFN-gamma, and GM-CSF, and IL-4, IL-13, and M-CSF induce anti-inflammatory M2 macrophages.

31 y reveals an intense expression of IL-34 and M-CSF by hepatocytes around liver lesions.

32 enhance the in vitro production of IL-34 and M-CSF by hepatocytes.

33 ting factors tumor necrosis factor alpha and M-CSF was increased by BMSCs cultured on both micro- and

34 protegerin, tumor necrosis factor alpha, and M-CSF in cultured BMSCs at different time points were me

35 tion by ex vivo-cultured human aMvarphis and M-CSF-derived macrophages stimulated by either LPS or IF

36 BARF1 and M-CSF form a high-affinity, stable, ring-like complex in

37 Ser276 plays an important role in basal and M-CSF-stimulated NF-kappaB activation in human mononucle

38 We demonstrate a role for TGF-beta and M-CSF, but not CRP in generating these cells using monoc

39 F revealed that the combination of BMDMs and M-CSF was required to promote myotube growth (15%).

40 ment by the tumor-derived cytokines CCL2 and M-CSF expressed increased levels of the Notch ligand Dll

41 The latter were recruited in a CCR2- and M-CSF-mediated pathway at the necroinflammatory phase an

42 GM-CSF and M-CSF (CSF-1) induce different phenotypic changes in mac

43 G-CSF and M-CSF are two lineage-specific cytokines that play a dom

44 states of macrophages induced by GM-CSF and M-CSF in either cell culture or atherosclerotic plaques

45 n vitro system about the roles of GM-CSF and M-CSF in macrophage lineage biology.

46 al an important mechanism by which G-CSF and M-CSF instruct neutrophil versus monocyte lineage choice

47 in Ba/F3 cells expressing both the G-CSF and M-CSF receptors and in lineage-negative murine marrow ce

48 G-CSF and M-CSF serve as prototypes for additional cytokines that

49 ucing distinct activation states, GM-CSF and M-CSF stimulated progressive but similar levels of incre

50 ls in combination with TGFbeta1, GM-CSF, and M-CSF resulted in increased (33%; P<0.05) accumulation o

51 f the gene expression profile in GM-CSF- and M-CSF-polarized macrophages revealed that a high CCL2 ex

52 nistration in mice induced G-CSF, CXCL1, and M-CSF, but not GM-CSF.

53 that can be activated by VACV infection and M-CSF stimulation.

54 Serum levels of FLT3-L and M-CSF were highest in high risk patients with extensive

55 o critical cytokines, namely RANK ligand and M-CSF.

56 with receptor activator NF-kappaB ligand and M-CSF; and (ii) TNF-transgenic mice have a significant i

57 IL-34-Mphi and M-CSF-Mphi induce type I collagen synthesis by HSCs, the

58 tivated natural killer cells, IL-34-Mphi and M-CSF-Mphi prevent the IFN-gamma-induced killing of HSCs

59 atrix metalloproteinase 1, by IL-34-Mphi and M-CSF-Mphi, thereby enhancing collagen synthesis.

60 re that such NK cells express both RANKL and M-CSF and are frequently associated with CD14(+) monocyt

61 of monocytes into osteoclasts with RANKL and M-CSF induced Nox4 expression.

62 us signaling pathways activated by RANKL and M-CSF.

63 sential osteoclastogenic cytokines RANKL and M-CSF.

64 steoclasts, a process dependent on RANKL and M-CSF.

65 e OCs when they were cultured with RANKL and M-CSF.

66 This effect was blocked by neutralizing anti-M-CSF Ab, but protein analysis of CM suggested that M-CS

67 163-L1 increases when cultured monocytes are M-CSF stimulated to macrophages, and the expression is f

68 DEX specifically arrested M-CSF activation of RhoA, Rac, and Vav3, each of which r

69 differentiation induced by cytokines such as M-CSF, GM-CSF, and IL-3.

70 genes were differentially expressed between M-CSF- and CXCL4-induced macrophages; 206 of them overex

71 ast, mutation of c-Fms Tyr-559 to Phe blocks M-CSF-induced cytoskeletal reorganization by inhibiting

72 ke in murine atherosclerotic plaques by both M-CSF and GM-CSF.

73 of inflammatory and metabolic profiles, both M-CSF and GM-CSF generated comparable levels of glucose

74 cytokine interleukin-4 (IL-4), as well as by M-CSF, which also controls homeostatic levels of tissue

75 +)CD206(+)CD209(-)) cells, differentiated by M-CSF or glucocorticoids.

76 consequence of signaling events elicited by M-CSF and receptor activator of NF-kappaB ligand, acting

77 ibited the acquisition of CCL2 expression by M-CSF-polarized macrophages.

78 ition of ERK prevented induction of c-Fos by M-CSF and reduced C/EBPalpha phosphorylation and formati

79 Fluid-phase endocytosis of LDL by M-CSF human macrophages showed non-saturable uptake of L

80 tective program, similar to that mediated by M-CSF.

81 Finally, ATF4 was largely modulated by M-CSF signaling and the PI3K/AKT pathways in BMMs.

82 Signaling by M-CSF through CSF-1R induced the stabilization and nucle

83 differentiation and formation stimulated by M-CSF/RANKL were inhibited (IC(50) = 0.3 nM) by ATRA.

84 and 7 days of therapy, and levels of CCL23, M-CSF, and CXCL13 showed a statistically significant pos

85 f atherosclerosis (fractalkine/CX3CL1, CCL8, M-CSF, HGF), T-cell development/activation (CD40L, IL-7,

86 e and female chickens in recombinant chicken M-CSF (CSF1).

87 iver cells were cultured in media containing M-CSF for 7-10 d, resulting in populations of cells that

88 In contrast, M-CSF was essential to survival and antimicrobial functi

89 In contrast, M-CSF-derived MDM were readily infected by HIV-1.

90 tic properties by Mphi generated with M-CSF (M-CSF-Mphi) or IL-34 (IL-34-Mphi).

91 Macrophage CSF (M-CSF) regulates monocyte differentiation, activation, a

92 GFbeta, IL-1beta, IL-4, IL-6, IL-10, GM-CSF, M-CSF, IDO, fms-related tyrosine kinase 3 ligand, c-kit

93 age RNA: Emr1 (F4/80), Itgam (CD11b), Csf1r (M-CSF Receptor), Itgal (CD11a), Tnf, and Nos2 Additional

94 The anti-inflammatory cytokine M-CSF, but not DC growth factors, sustains CD33/LAIR-1 e

95 ylation of NF-kappaBp65 leading to decreased M-CSF-induced monocyte survival.

96 Placental-derived M-CSF and IL-10 induced macrophages that shared the CD14

97 vely induced, including SPP1 and CSF1 (i.e., M-CSF) by TREM-1 activation and IL-23 and CSF3 (i.e., G-

98 Syk(Y317F) in primary Syk(-/-) OCs enhances M-CSF- and alphavbeta3-induced phosphorylation of the cy

99 ing PAP in 16-wk-old mice, along with excess M-CSF gene expression and secretion.

100 ate, or macrophage colony-stimulated factor (M-CSF) significantly activated AMPK and promoted monocyt

101 VEGF, macrophage colony-stimulating factor (M-CSF) ] and chemokines (SDF-1, MCP-1).

102 d with macrophage colony-stimulating factor (M-CSF) alone (termed M0) did.

103 /mL of macrophage colony-stimulating factor (M-CSF) and 50 ng/mL of receptor activator of nuclear fac

104 d with macrophage colony-stimulating factor (M-CSF) and granulocyte-M-CSF (GM-CSF) and its implicatio

105 els of macrophage colony-stimulating factor (M-CSF) and interleukin (IL)-34 than HCV-infected patient

106 ted by macrophage-colony-stimulating factor (M-CSF) and receptor activator of NF-kappaB ligand (RANKL

107 etween macrophage colony-stimulating factor (M-CSF) and the tyrosine kinase receptor c-FMS play a key

108 lizing macrophage colony-stimulating factor (M-CSF) antibody.

109 L) and macrophage colony-stimulating factor (M-CSF) as well as BMSC CM from each of the 4 surfaces.

110 ole of macrophage colony-stimulating factor (M-CSF) in TAM differentiation and polarization in differ

111 d with macrophage colony-stimulating factor (M-CSF) induces expression of vascular endothelial cell (

112 Macrophage colony-stimulating factor (M-CSF) influences the proliferation and survival of mono

113 Macrophage colony-stimulating factor (M-CSF) is a hematopoietic growth factor that is responsi

114 ), and macrophage colony-stimulating factor (M-CSF) levels.

115 s with macrophage colony-stimulating factor (M-CSF) on muscle regrowth.

116 ted by macrophage colony-stimulating factor (M-CSF) or granulocyte macrophage colony-stimulating fact

117 m with macrophage-colony-stimulating factor (M-CSF) produced a macrophage phenotype demonstrating con

118 Macrophage colony-stimulating factor (M-CSF) promotes mononuclear phagocyte survival and proli

119 or the macrophage colony-stimulating factor (M-CSF) receptor c-Fms.

120 sed by macrophage colony-stimulating factor (M-CSF) receptor mutations.

121 s with macrophage colony-stimulating factor (M-CSF) resulted in mTORC1-dependent anabolic metabolism,

122 F) and macrophage colony-stimulating factor (M-CSF) signaling in Ba/F3 cells expressing both the G-CS

123 c), or macrophage colony-stimulating factor (M-CSF) to produce M-Mac.

124 entive macrophage colony-stimulating factor (M-CSF) treatment was also studied to highlight the effec

125 erived macrophage colony-stimulating factor (M-CSF) was found to contribute to the generation of such

126 Macrophage colony stimulating factor (M-CSF) was implicated as a contributing upstream activat

127 human macrophage-colony stimulating factor (M-CSF), a hematopoietic cytokine with pleiotropic functi

128 Macrophage colony stimulating factor (M-CSF), through binding to its receptor FMS, a class III

129 arkers macrophage colony-stimulating factor (M-CSF), tumor necrosis factor receptor superfamily membe

130 ers in macrophage colony-stimulating factor (M-CSF)- and CXCL4-induced macrophages demonstrated virtu

131 Cs and macrophage-colony stimulating factor (M-CSF)-dependent, CD14(+)CD11b(+)DC-SIGN(+) monocyte-der

132 erated macrophage colony-stimulating factor (M-CSF)-derived monocytes from the bone marrow of mice wi

133 is and macrophage colony-stimulating factor (M-CSF)-induced myeloid differentiation.

134 a3 and macrophage-colony stimulating factor (M-CSF)-induced signaling, c-Src is central to osteoclast

135 ng the macrophage colony-stimulating factor (M-CSF)-mediated quiescence-to-proliferation switch but s

136 M1 and macrophage colony-stimulating factor (M-CSF)-polarized M2, but not human AB serum-derived cell

137 mpairs macrophage colony-stimulating factor (M-CSF)-stimulated inside-out integrin activation and cyt

138 L) and macrophage colony-stimulating factor (M-CSF).

139 L) and macrophage colony-stimulating factor (M-CSF).

140 L) and macrophage-colony stimulating factor (M-CSF).

141 nce of macrophage colony-stimulating factor (M-CSF).

142 Macrophage colony-stimulating factor (M-CSF)/IL-4 induces differentiation of cord blood (CB) m

143 ism by macrophage colony-stimulating factor (M-CSF; inflammation resolving) and granulocyte-M-CSF (GM

144 uch as macrophage colony-stimulation factor (M-CSF), and chemokines, such as platelet factor 4 (CXCL4

145 /macrophages in the humanized mice following M-CSF expression provide a superior in vivo system to in

146 identifying the M-CSFM residues critical for M-CSF .

147 Furthermore, ATF4 was crucial for M-CSF induction of RANK expression on BMMs, and lack of

148 g PKCalpha as important upstream kinases for M-CSF-induced NF-kappaB transcriptional activation, NF-k

149 results demonstrate an unrecognized role for M-CSF in alternative differentiation of monocytes into a

150 uginosa and the fungus Aspergillus fumigatus M-CSF treatment during engraftment or after infection ef

151 (Csf1(op)/Csf1(op)) mice lacking functional M-CSF and having reduced levels of KCs, the levels of se

152 y-stimulating factor (M-CSF) and granulocyte-M-CSF (GM-CSF) and its implications for fluorine 18 ((18

153 CSF; inflammation resolving) and granulocyte-M-CSF (GM-CSF; proinflammatory) may contribute to the in

154 7) as well as STAT1 phosphorylation in human M-CSF-derived macrophages.

155 Expression of human M-CSF or GM-CSF by hydrodynamic injection of cytokine-en

156 o x-ray structure is available for the human M-CSF .

157 that are essential for binding of the human M-CSF to c-FMS.

158 to a M-CSF dimer, due to a weak, hydrophilic M-CSF:FMS interface, and probably a conformational chang

159 These results identify M-CSF and IL-34 as potent profibrotic factors in HCV liv

160 In this article, we identify M-CSF-derived DCs (M-DCs) after stimulation with IL-10 a

161 Importantly, M-CSF treatment of MDM restored pyrin levels and IL-1bet

162 Forced expression of the M-CSFR in M-CSF-dependent bone marrow macrophages from Dicer-defic

163 rculosis displayed a progressive decrease in M-CSF in contrast to increasing levels of GM-CSF.

164 Expression of CD7 decreases in M-CSF-differentiated macrophages and in melanoma-conditi

165 e marrow-derived macrophages (BMDM) grown in M-CSF (CSF-1) have been used widely in studies of macrop

166 paB) is a key regulator of genes involved in M-CSF-induced mononuclear phagocyte survival and this st

167 ge differentiation and activation, including M-CSF receptor.

168 itis, a condition characterized by increased M-CSF expression.

169 nduced differentiation is IL-10 independent, M-CSF-driven M2c polarization and related MerTK upregula

170 human macrophages at the sites of infection, M-CSF-treated humanized mice exhibited an enhanced prote

171 TLRs inhibited M-CSF signaling by rapidly down-regulating cell surface

172 ntrol of the circulating and effective local M-CSF concentration, perturbation of the receptor-bindin

173 pregulated in response to hypoxia only in M2(M-CSF) macrophages, and the hypoxia-mediated upregulatio

174 erentially expressed by anti-inflammatory M2(M-CSF) macrophages and was detected in vivo in liver Kup

175 es and transmembrane domain of DAP12 mediate M-CSF signaling.

176 gonist, pioglitazone, prevented LPS-mediated M-CSF induction.

177 We show that in an ex vivo model, M-CSF-differentiated monocyte-derived macrophages unifor

178 We further demonstrated that Cdc42 modulated M-CSF-stimulated cyclin D expression and phosphorylation

179 pressed a combinatorial library of monomeric M-CSF (M-CSFM) single mutants and screened this library

180 Furthermore, Cdc42 was required for multiple M-CSF- and RANKL-induced osteoclastogenic signals includ

181 Specifically, neutralizing M-CSF activity via a novel human monoclonal antibody red

182 HP2 reduces CFU-G and prevents G-CSF but not M-CSF activation of ERK.

183 ion reduced ERK activation in G-CSF, but not M-CSF, and reduced colony-forming unit-granulocytes, und

184 F-dependent gene expression, GM-CSF- but not M-CSF-dependent cell proliferation, surfactant clearance

185 ld lower than that of CLPs in the absence of M-CSF, the relative myeloid potential of both population

186 thy controls, which required the addition of M-CSF.

187 encourage potential clinical applications of M-CSF to prevent severe infections after HS/PC transplan

188 We show that binding of M-CSF to its receptor c-Fms generates a signaling comple

189 yperresponsive to limiting concentrations of M-CSF and receptor activator of NF-kappaB ligand (RANKL)

190 Also, the circulating concentrations of M-CSF were significantly higher in patients with CP than

191 ostasis, and that transcriptional control of M-CSF production is regulated by NF-kappaB and PPARgamma

192 Phorbol ester mimicked the effect of M-CSF, activating ERK independent of SHP2.

193 tudies show that the levels of expression of M-CSF and GM-CSF participate in the progression of macro

194 bolism, which in turn promoted expression of M-CSF receptor and transcription factors PU.1 and IRF8,

195 eveals overlapping and distinct functions of M-CSF and GM-CSF in human monocyte and macrophage develo

196 Genetic deletion or immunoneutralization of M-CSF resulted in reduced survival, increased bacterial

197 tiated from monocytes under the influence of M-CSF is a plausible mechanism to account for macrophage

198 macrophages generated under the influence of M-CSF, whereas CCR2 is expressed only by GM-CSF-polarize

199 ion of RANK transcription, and inhibition of M-CSF signaling that is required for RANK expression.

200 bone lesions had relatively higher levels of M-CSF and of stem cell factor.

201 tosis and therefore attenuated the number of M-CSF and RANKL-derived osteoclasts in vitro.

202 e into mature osteoclasts in the presence of M-CSF and receptor activator of NF-kappaB (RANK) ligand.

203 cytes were differentiated in the presence of M-CSF and then further treated with IL-12/IL-18, cells b

204 The production of M-CSF and RANKL (receptor activator of nuclear factor ka

205 he transcriptional and functional profile of M-CSF-dependent monocyte-derived human macrophages expos

206 proproliferative and survival properties of M-CSF, TNF-alpha enhanced osteoclast precursor number on

207 A potential regulator of M-CSF, peroxisome proliferator-activated receptor-gamma

208 However, the role of M-CSF in pulmonary infection with Mycobacterium tubercul

209 We report a 2.4 A crystal structure of M-CSF bound to the first 3 domains (D1-D3) of FMS.

210 turbation of the receptor-binding surface of M-CSF, and imposition of an unfavorable global orientati

211 to explain the biological effect of BARF1 on M-CSF:FMS signaling.

212 macrophage lineage branches are dependent on M-CSF during inflammation, and thus the potential for th

213 hp2 deletion, however, has minimal effect on M-CSF-dependent survival and proliferation of OC precurs

214 ling in RAW 264.7 cells but had no effect on M-CSF-induced activation of some of the same signaling e

215 both colony stimulating factor-1 (CSF-1, or M-CSF) and receptor activator of NF-kappaB ligand (RANKL

216 ration of macrophages in response to IL-4 or M-CSF.

217 one marrow-derived macrophages (BMDM) and/or M-CSF revealed that the combination of BMDMs and M-CSF w

218 hages generated in the presence of GM-CSF or M-CSF are considered as proinflammatory (M1) or anti-inf

219 phenotypes under the influence of GM-CSF or M-CSF, denoted as GM-Mvarphi and M-Mvarphi, respectively

220 mmatory Mvarphis upon culture with GM-CSF or M-CSF, respectively (subsequently referred to as GM14, M

221 s, derived from human monocytes by GM-CSF or M-CSF, were compared with the differences between the re

222 ived macrophages differentiated by GM-CSF or M-CSF.

223 nerated in the presence of GM-CSF (GM-MO) or M-CSF (M-MO), which do not release pro- or anti-inflamma

224 as lost with fetal bovine serum, 20% oxygen, M-CSF, higher concentrations of cytokines, or premature

225 A RF fractions purified from RA serum pools, M-CSF-generated macrophages skewed their cytokine respon

226 Restoring pulmonary M-CSF levels during infection resulted in a significant

227 esorption for 18 h in the presence of RANKL, M-CSF, and native bone particles.

228 PCI-32765 blocked RANKL/M-CSF-induced phosphorylation of Btk and downstream PLC-

229 Each prong may reduce M-CSF:FMS signaling to a limited extent but in combinati

230 ine phosphatase, is implicated in regulating M-CSF and receptor activator of nuclear factor-kappaB li

231 ound that PPARgamma is capable of regulating M-CSF through transrepression of NF-kappaB binding at th

232 More specifically, M-CSF promoted the anti-inflammatory macrophage phenotyp

233 sRANKL/M-CSF treatment of nonadherent Cx37(-/-) bone marrow cel

234 ession of PPARgamma prevented LPS-stimulated M-CSF production in RAW 264.7 cells, an effect that was

235 In summary, M-CSF activates ERK more potently than G-CSF, and thereb

236 ters showed higher expression in CXCL4- than M-CSF-induced macrophages, resulting in lower low-densit

237 increased proinflammatory activity and that M-CSF plays a central role in this process by increasing

238 We conclude that M-CSF is critical to host defenses against bacterial pne

239 In addition, these studies demonstrate that M-CSF may have a role in the adaptive immune response to

240 Here, we demonstrate that M-CSF stimulated NF-kappaB transcriptional activity in h

241 We therefore tested the hypothesis that M-CSF is required for mononuclear phagocyte-mediated hos

242 Calorimetric data indicate that M-CSF cannot dimerize FMS without receptor-receptor inte

243 -type alveolar macrophages, we observed that M-CSF itself is capable of inducing foam cell formation

244 Thus, we propose that M-CSF drives CD14(++)CD16- monocyte differentiation into

245 derived from Csf-1(-/-) op/op mice show that M-CSF is required "before" developing such osteoclastoge

246 We also show that M-CSF, but not G-CSF, stimulated strong and sustained ac

247 We previously showed that M-CSF is important for developing tolerogenic dendritic

248 Taken together, these data suggest that M-CSF is an important mediator of alveolar macrophage ho

249 nto anti-inflammatory M-DCs and suggest that M-CSF-induced DCs may be of use for suppressing unwanted

250 b, but protein analysis of CM suggested that M-CSF alone was not manifesting enhanced expansion of my

251 Although the M-CSF and monocyte chemoattractant protein 1 (MCP-1) mRN

252 fact, activin A receptor blockade during the M-CSF-driven differentiation of CD16(+) monocytes, or ad

253 Here we show DAP12 deficiency impaired the M-CSF-induced proliferation and survival of macrophages

254 ion of Tyr-721, the PI3K binding site in the M-CSF receptor c-Fms, fails to suppress cytoskeletal rem

255 s with the ability to sterically occlude the M-CSF.c-FMS binding interface.

256 the basis for a deeper understanding of the M-CSF .

257 and probably a conformational change of the M-CSF dimer in which binding to the second site is rende

258 of an unfavorable global orientation of the M-CSF dimer.

259 wn-regulating cell surface expression of the M-CSF receptor c-Fms by a matrix metalloprotease- and MA

260 n-dependent macropinocytosis of LDL by these M-CSF-differentiated macrophages.

261 h a BARF1 hexameric ring surrounded by three M-CSF dimers in triangular array.

262 for increases in serum enzyme levels through M-CSF regulation of tissue macrophage homeostasis withou

263 The binding of BARF1 to M-CSF dramatically reduces but does not completely aboli

264 last differentiation markers when exposed to M-CSF and receptor activator of nuclear factor kappaB (R

265 ow that BMMs from SHIP1 null mice respond to M-CSF, but not receptor activator of NF-kappaB ligand, b

266 In response to M-CSF, alveolar macrophages also increased their T cell-

267 iferation and differentiation in response to M-CSF, leading to an enlargement of the marrow OCP pool.

268 NA reduced NF-kappaB activity in response to M-CSF.

269 n osteoclast precursors (OcP) in response to M-CSF.

270 ates macrophage proliferation in response to M-CSF.

271 o organize their cytoskeleton in response to M-CSF.

272 expense of monocyte formation in response to M-CSF.

273 hil over monocyte development in response to M-CSF.

274 nt myeloid cells show increased responses to M-CSF and RANKL stimulation, and, through mechanisms of

275 tical regulator of myeloid cell responses to M-CSF and RANKL stimulation.

276 is necessary but not sufficient to transduce M-CSF-dependent cytoskeletal reorganization.

277 naling and metabolic reprogramming underlies M-CSF-induced myelopoiesis.

278 Here, we show that HCMV infection, unlike M-CSF treatment, does not induce caspase 8 activity to p

279 ough the Vav pleckstrin homology domain upon M-CSF stimulation.

280 murine bone marrow-derived macrophages upon M-CSF withdrawal in more detail.

281 ated in vitro from classical monocytes using M-CSF and GM-CSF, which is increased in viremic patient'

282 M-CSF-activated AMPK is via M-CSF receptor-dependent reactive oxygen species product

283 ulated factor 4 (IRF4) than of IRF5, whereas M-CSF induced IRF5 but not IRF4.

284 varphis in a self-autonomous manner, whereas M-CSF-treated CD16(+) monocytes generate Mvarphis with a

285 hosphatase 2 (SHP2) phosphorylation, whereas M-CSF preferentially activated phospholipase Cgamma2, an

286 We examined the mechanism by which M-CSF regulates the cytoskeleton and function of the ost

287 nalyses evidenced that genes associated with M-CSF-driven Mvarphi differentiation (including FOLR2, I

288 was not reversed by treatment of cells with M-CSF.

289 erexpressed in IL-12/IL-18 MDM compared with M-CSF MDM, and degradation of SAMHD1 by RNA interference

290 om MCP-1(-/-) and WT mice were cultured with M-CSF, RANKL and/or MCP-1.

291 y human macrophages when differentiated with M-CSF.

292 Differentiation with M-CSF produces macrophages that are highly phagocytic, H

293 rofibrotic properties by Mphi generated with M-CSF (M-CSF-Mphi) or IL-34 (IL-34-Mphi).

294 tes, or monocytes-macrophages generated with M-CSF, was instituted within 48 h of cytokine exposure,

295 s muscles were injected intramuscularly with M-CSF, we observed a 1.6-fold increase in macrophage den

296 of treatment of bone marrow macrophages with M-CSF and RANKL, corresponding to the onset of preosteoc

297 signature of CXCL4-induced macrophages with M-CSF-induced macrophages or macrophages polarized with

298 ages (MPhi0) and macrophages stimulated with M-CSF (MPhiM-CSF) or GM-CSF (MPhiGM-CSF).

299 t differentiation assays by stimulating with M-CSF and receptor activator of NF-kappaB ligand bone ma

300 therosclerotic aortas after stimulation with M-CSF or GM-CSF by using quantitative autoradiography.

301 rentiated into macrophages by treatment with M-CSF, whereas Egr2 was minimally induced and Egr4 was n