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 known to induce cytoskeletal reorganization in

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

9 M-CSF permits macrophages to express CD122, and IFNs are

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

44 , we compared their modulation by GM-CSF and M-CSF in murine primary AMs and IMs.

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

46 wever, the comparative actions of GM-CSF and M-CSF on AMs are incompletely understood.

47 te that the activating actions of GM-CSF and M-CSF on primary AMs are not conserved in primary IMs.

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

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

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

51 RA, interleukin-6, interleukin-8, G-CSF, and M-CSF (p < 0.001).

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

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

54 Interestingly, G-CSF- and M-CSF-stimulated activation of Erk1/2 was augmented in l

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

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

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

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

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

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

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

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

63 rials for breast cancer, decreased RANKL and M-CSF, and subsequently RANKL and M-CSF-dependent osteoc

64 RANKL and M-CSF, and subsequently RANKL and M-CSF-dependent osteoclastogenesis of murine bone marrow

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

66 sential osteoclastogenic cytokines RANKL and M-CSF.

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

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

69 XCL2, CXCL5, CXCL9, G-CSF, GM-CSF, VEGF, and M-CSF) and chemokine receptors on MDSCs (CCR1, CCR5, and

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

71 163-L1 increases when cultured monocytes are M-CSF stimulated to macrophages, and the expression is f

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

94 , MCP-1, sVCAM-1, MIP-1alpha, IP-10, GM-CSF, M-CSF, TNF-alpha, IFN-gamma, VCAM-1, ICAM-1, PD-L1 and I

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

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

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

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

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

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

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

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

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

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

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

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

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

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

109 nce of macrophage colony stimulating factor (M-CSF) and receptor activator of nuclear factor-kappa B

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

111 ANKL), macrophage colony-stimulating factor (M-CSF) and transforming growth factor-beta 1 (TGF-beta1)

112 ion of macrophage-colony stimulating factor (M-CSF) and tumor necrosis factor-alpha (TNF-alpha) in vi

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

114 ess to macrophage colony-stimulating factor (M-CSF) in bone marrow macrophages.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

156 red the effect of calcitriol on homeostatic (M-CSF, TGF-beta-treated) and proinflammatory (GM-CSF-tre

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

186 GM-CSF, but not M-CSF, increased the expression of both M1 and M2 marker

187 GM-CSF, but not M-CSF, reinforced the cellular identity, as identified b

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 In vitro secretion of M-CSF by LPS-stimulated peripheral monocytes, but not TN

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

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

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

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

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

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

216 Under human serum AB or M-CSF, only monocytes from RA had a defect of differenti

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 ts, including increased expression of RANKL, M-CSF, and osteoprotegerin (OPG).

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

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

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

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

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

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

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

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

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

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

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

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

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

242 We also demonstrate that M-CSF-induced differentiation of myeloid progenitors int

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

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

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

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

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

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

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

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 ic cells) are controlled by signals from the M-CSF receptor (CSF1R).

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

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

256 within this time frame, S100A9 inhibited the M-CSF-mediated induction of RANK.

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

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

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

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

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

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

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

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

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

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

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

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

269 ates macrophage proliferation in response to M-CSF.

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

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

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

273 -HT(2B) and 5-HT(7) expression restricted to M-CSF-primed monocyte-derived macrophages (M-MO).

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

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

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

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

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

279 nce of AM functions throughout life, whereas M-CSF is broadly important for macrophage differentiatio

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

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

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

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

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

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

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

287 y human macrophages when differentiated with M-CSF.

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

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

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

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

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

293 erentiation of monocytes to macrophages with M-CSF or GM-CSF strongly up-regulated full-length Dicer.

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

295 d and differentiated toward osteoclasts with M-CSF and receptor activator of NF-kappaB (RANK) ligand

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

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

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

299 derived macrophages (MDMs) were treated with M-CSF, followed by IL-4/IL-13 to induce the M2a allergic

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