ライフサイエンスコーパス: CSFR

1 G-CSFR cytoplasmic tyrosine (Y) residues (Y704, Y729, Y744

2 G-CSFR is expressed on mature hematopoietic cells, HPCs, a

3 G-CSFR truncation mutants from these patients transduce hy

4 G-CSFR(-/-) mice are markedly susceptible to bronchopulmon

5 G-CSFR-deficient mice have decreased numbers of phenotypic

6 c compartments were wild-type, IL-10(-/-), G-CSFR(-/-), or combinations thereof we demonstrated that

7 dependently inhibited G-CSF-stimulated 32D-G-CSFR cell proliferation.

8 in murine myeloid progenitor cell line 32D-G-CSFR cells was markedly enhanced by alcohol exposure.

9 Cells expressing a G-CSFR form lacking Tyr764 exhibited hypersensitivity to G

10 We show here that a G-CSFR mutant in which tyrosine 729 had been mutated to ph

11 We show here that a G-CSFR mutant, d715, derived from an SCN patient inhibited

12 ned the neutropenia present in young adult G-CSFR-deficient mice; moreover, exogenous IL-6 stimulated

13 tion and up-regulation of C/EBPepsilon and G-CSFR, but not in STAT3 phosphorylation.

14 mice reconstituted with both wild type and G-CSFR-deficient bone marrow cells, treatment with CY or G

15 Anti-G-CSFR mAb also suppressed zymosan-induced inflammatory pa

16 arthritis symptom, the efficacy of an anti-G-CSFR mAb for arthritic pain and disease was compared wit

17 by both prophylactic and therapeutic anti-G-CSFR mAb treatment, whereas only prophylactic anti-Ly6G

18 epatoma cells by using transduced chimeric G-CSFR-gp130 receptor constructs demonstrates that SHP-2,

19 ncreased cell surface expression of CXCR4, G-CSFR affecting HSPC migration, and CD47 mediating protec

20 f Src family kinase activation by the d715 G-CSFR may contribute to its hyperproliferative phenotype.

21 Interestingly, d715 G-CSFR myeloid progenitors were resistant to the growth-st

22 edly impaired in G-CSF receptor-deficient (G-CSFR-deficient) mice.

23 urred in wild-type, but not Lyn-deficient, G-CSFR-transfected DT40 B cells.

24 xploited to selectively target deleterious G-CSFR-mediated signaling events such as aberrant Stat3 ac

25 Despite reduction of C/EBPalpha, G-CSFR and M-CSFR levels were maintained in total marrow a

26 nous C/EBPs 50-fold and reduced endogenous G-CSFR expression.

27 In 32D cl3 cells coexpressing exogenous G-CSFR, activation of KalphaER prevented and even reversed

28 neutrophil development in cells expressing G-CSFR Y729F.

29 se results explain the molecular basis for G-CSFR mutations in the pathogenesis of the dominant-negat

30 ACAM1 acted as a coinhibitory receptor for G-CSFR regulating granulopoiesis and host innate immune re

31 ed with wild-type PMNs, PMNs isolated from G-CSFR-deficient mice demonstrated markedly decreased chem

32 Neutrophils isolated from G-CSFR-deficient mice have an increased susceptibility to

33 Furthermore, G-CSFR d715 suppressed unfolded protein response and apopt

34 in G-CSF signaling we expressed the human G-CSFR in cell lines derived from DT40 B cells, which lack

35 Seven human G-CSFR mRNA isoforms exist, named class I through class VI

36 no acids in the distal tail of the class I G-CSFR down-modulates proliferative signaling, not only in

37 n 50% of AML samples, the class IV/class I G-CSFR mRNA ratio is aberrantly elevated compared to norma

38 we characterize the neutrophil response in G-CSFR(-/-) mice following intratracheal injection with Ps

39 eutrophil production and was attenuated in G-CSFR(-/-) mice.

40 spleen progenitors (CFU-S) was detected in G-CSFR-deficient mice after cyclophosphamide administratio

41 e defects in PMN activation are present in G-CSFR-deficient mice and indicate that G-CSF plays an imp

42 rease in circulating CFU-C was detected in G-CSFR-deficient mice following interleukin-8 (IL-8) admin

43 r744, which also correlated with increased G-CSFR expression.

44 sive murine cell line 32Dcl3 with class IV G-CSFR cDNA.

45 hat aberrantly increased relative class IV G-CSFR expression seen in AML can uncouple G-CSFR prolifer

46 SF stimulation, clones expressing class IV G-CSFR had greater percentages of myeloblasts and promyelo

47 increased relative expression of class IV G-CSFR in AML uncouples proliferative and maturational G-C

48 s targeting inhibitory pathways that limit G-CSFR signaling may have promise in the treatment of pati

49 L uncouples proliferative and maturational G-CSFR signaling pathways.

50 kine signaling proteins also down-modulate G-CSFR signals.

51 omology 2 protein (CIS) in down-modulating G-CSFR signals and demonstrate that loss of their recruitm

52 Class IV/murine G-CSFR mRNA ratios after 24 hours of G-CSF stimulation for

53 The mutant G-CSFR allele is expressed in a myeloid-specific fashion a

54 w that the most frequently isolated mutant G-CSFR form from patients with SCN/AML (delta716) confers

55 than observed with the most common mutant G-CSFR form in patients with SCN/AML, prompting us to inve

56 igand internalization is deleted in mutant G-CSFR forms from patients with SCN/AML.

57 WT/mutant G-CSFR heterodimers appeared to be retained in the endopla

58 prolonged in cells with the SCN/AML mutant G-CSFR lacking Tyr729 and Tyr744, which also correlated wi

59 Furthermore, we show that two mutant G-CSFR proteins, a truncation mutant that deletes the carb

60 anulopoiesis in vivo and show that neither G-CSFR or IL-6 signals are required for the commitment of

61 into the pathophysiologic contribution of G-CSFR mutations to AML.

62 -8), we examined the effect of the loss of G-CSFR on IL-8-stimulated PMN function.

63 d granulopoiesis in vivo in the absence of G-CSFR signals.

64 hil accumulation into the infected lung of G-CSFR(-/-) mice was markedly reduced.

65 PMN emigration into the skin of G-CSFR-deficient mice in response to IL-8 was also impaire

66 the number of CFU-C in the bone marrow of G-CSFR-deficient mice was increased relative to wild-type

67 Chemoattractant-induced adhesion of G-CSFR-deficient PMNs was significantly impaired, suggesti

68 entiation using retroviral transduction of G-CSFR-deficient, primary hematopoietic progenitor cells.

69 of the G-CSF domain can alter the ratio of G-CSFR:IL-3R agonist activities, demonstrating that it is

70 Cells expressing truncated proximal G-CSFR, the tyrosine-null (Y4F) G-CSFR, or Y764F mutant re

71 The G-CSF receptor (G-CSFR) activates the Jak/STAT pathway, although little is

72 locyte-colony stimulating factor receptor (G-CSFR) and downregulation of interleukin-3 receptor (IL-3

73 locyte colony-stimulating factor receptor (G-CSFR) and erythropoietin receptor (EPOR).

74 runcation mutations of the G-CSF receptor (G-CSFR) are associated with the development of acute myelo

75 imal 87 amino acids of the G-CSF receptor (G-CSFR) are sufficient to mediate this response.

76 The G-CSF receptor (G-CSFR) belongs to the superfamily of the cytokine recepto

77 locyte colony-stimulating factor receptor (G-CSFR) distal to the conserved box 2 motif necessary for

78 locyte colony-stimulating factor receptor (G-CSFR) gene.

79 he cytoplasmic tail of the G-CSF receptor (G-CSFR) have been detected.

80 locyte colony-stimulating factor receptor (G-CSFR) in approximately 80% of patients.

81 ns in the hematopoietic cytokine receptor (G-CSFR) in combination with the second mutations in the do

82 Mutations in the G-CSF receptor (G-CSFR) in patients with severe congenital neutropenia (SC

83 locyte colony-stimulating factor receptor (G-CSFR) in the pathogenesis of severe congenital neutropen

84 locyte colony-stimulating factor receptor (G-CSFR) occur in a subset of patients with severe congenit

85 locyte colony-stimulating factor receptor (G-CSFR) on C/EBPalpha(-/-) cell lines, and by our finding

86 locyte colony-stimulating factor receptor (G-CSFR) proliferative and maturational signaling pathways

87 of truncated forms of the G-CSF receptor (G-CSFR) protein.

88 locyte colony-stimulating factor receptor (G-CSFR) regulates the proliferation and differentiation of

89 locyte colony-stimulating factor receptor (G-CSFR) signal transducer and activator of transcription (

90 ells, is known to regulate G-CSF receptor (G-CSFR) signaling, we hypothesized that CEACAM1 would regu

91 ystem to study the role of G-CSF receptor (G-CSFR) signals in granulocytic differentiation using retr

92 targeted mutation of their G-CSF receptor (G-CSFR) such that the cytoplasmic (signaling) domain of th

93 locyte colony-stimulating factor receptor (G-CSFR) transduces intracellular signals for myeloid cell

94 f CSF3R, which encodes the G-CSF receptor (G-CSFR), are implicated in leukemic progression in patient

95 development via its cell surface receptor (G-CSFR), can play a role in inflammation, and hence in man

96 We use mixed G-CSF receptor (G-CSFR)-deficient bone marrow chimeras to show that G-CSF-

97 Because G-CSF receptor (G-CSFR)-deficient mice do not have the expected neutrophil

98 locyte colony-stimulating factor receptor (G-CSFR)-deficient mice have a severe quantitative defect i

99 ization was examined using G-CSF receptor (G-CSFR)-deficient mice.

100 locyte colony-stimulating factor receptor (G-CSFR)-gp130(S782A) receptors resulted in increased cell

101 arked by expression of the G-CSF receptor (G-CSFR).

102 locyte colony-stimulating factor receptor (G-CSFR); and were uniformly interleukin-7 receptor alpha (

103 idues in the G-CSFR to negatively regulate G-CSFR signaling by limiting proliferation and modulating

104 roliferative signaling by a representative G-CSFR truncation mutation (termed d715) has been document

105 Surprisingly, G-CSFR expression on neutrophils is neither necessary nor

106 lopoiesis in vivo, but also indicated that G-CSFR independent mechanisms of granulopoiesis must exist

107 sgenic mice are intact, demonstrating that G-CSFR signals in monocytic cells are sufficient to induce

108 Cs, and stromal cells, which suggests that G-CSFR signals in one or more of these cell types was requ

109 However, the data also suggest that G-CSFR-independent mechanisms of granulopoiesis must exist

110 These data suggest that G-CSFR/G-CSF targeting may be a safe therapeutic strategy

111 trend was found for the MPOs in which the G-CSFR agonist activity is mostly a property of the cpG-CS

112 recruitment and activation of Stat3 by the G-CSFR and reveal unique features of this interaction that

113 ard loop to transcriptionally activate the G-CSFR and sustain neuroblastoma CSCs.

114 corresponding to Tyr744 and Tyr764 in the G-CSFR and that Tyr764 is required for in vivo phosphoryla

115 generated by the cytoplasmic domain of the G-CSFR are not required for G-CSF-dependent granulocytic d

116 These data confirm a role for the G-CSFR as a major regulator of granulopoiesis in vivo and

117 These results confirmed a role for the G-CSFR as a major regulator of granulopoiesis in vivo, but

118 acellular and transmembrane domains of the G-CSFR fused to the cytoplasmic domain of the erythropoiet

119 demonstrate that ectopic expression of the G-CSFR in hematopoietic progenitor cells allows for multil

120 rt on the mechanistic contributions of the G-CSFR in neuroblastoma CSCs.

121 reports of extracellular mutations in the G-CSFR in patients with SCN unresponsive to G-CSF suggest

122 data suggest that STAT-3 activation by the G-CSFR is critical for the transduction of normal prolifer

123 Thus, the G-CSFR is generating unique signals that are required for

124 the cytoplasmic (signaling) domain of the G-CSFR is replaced with the cytoplasmic domain of the eryt

125 These results show that the G-CSFR is required for mobilization in response to cycloph

126 transgenic mice in which expression of the G-CSFR is restricted to cells of the monocytic lineage.

127 tibility to apoptosis, suggesting that the G-CSFR may also regulate neutrophil survival.

128 but not flt-3 ligand and suggest that the G-CSFR may play an important and previously unexpected rol

129 esis in vivo and provide evidence that the G-CSFR may regulate granulopoiesis by several mechanisms.

130 These data demonstrate that the G-CSFR mutation found in patients with SCN is not sufficie

131 definitive evidence that expression of the G-CSFR on HPCs is not required for their mobilization by G

132 imeras demonstrated that expression of the G-CSFR on transplantable hematopoietic cells but not strom

133 Here we show that a critical domain in the G-CSFR that mediates ligand internalization is deleted in

134 and myeloid LGM-1 cells overexpressing the G-CSFR to G-CSF resulted in induction of differentiation a

135 ith distal phosphotyrosine residues in the G-CSFR to negatively regulate G-CSFR signaling by limiting

136 G-CSF stimulation of cells expressing the G-CSFR truncation mutant induces sustained activation of A

137 tation in the extracellular portion of the G-CSFR within the WSXWS motif in a patient with SCN withou

138 ains the Cfs3r gene, which encodes for the G-CSFR, and its NZM2410 allele carries a nonsynonymous mut

139 n and modulating surface expression of the G-CSFR, respectively.

140 or Stat3 recruitment and activation by the G-CSFR, the side chain of Stat3 R609, which interacts with

141 The G-CSFR-G-CSF pathway has been previously implicated in the

142 ther decreased (linkage at residue 39) the G-CSFR-mediated proliferative activity.

143 corresponding to Tyr729 and Tyr744 of the G-CSFR.

144 nsmembrane and cytoplasmic portions of the G-CSFR.

145 esting a loss of negative signaling by the G-CSFR.

146 tely regulate growth signaling through the G-CSFR.

147 Mice carrying a targeted mutation of their G-CSFR that reproduces the mutation found in a patient wit

148 Recombinant Stat3 bound to G-CSFR phosphotyrosine peptide ligands pY704VLQ and pY744L

149 e proliferation of wild-type and truncated G-CSFR-transfected Ba/F3 cells and enhanced their myeloid

150 er in proximal truncated than in wild-type G-CSFR cells, suggesting that Gab2 is dissociated from PI3

151 show that ectopic expression of wild-type G-CSFR in hematopoietic progenitor cells supports G-CSF-de

152 G-CSFR expression seen in AML can uncouple G-CSFR proliferative and maturational signaling pathways.

153 represent an important mechanism by which G-CSFR mutations contribute to leukemogenesis.

154 ether, these data suggest a model in which G-CSFR signals in bone marrow monocytic cells inhibit the

155 tion by G-CSF and suggest a model in which G-CSFR-dependent signals act in trans to mobilize HPCs fro

156 cellular trafficking of the wild-type (WT) G-CSFR by constitutively heterodimerizing with it.

157 -6) in granulopoiesis, we generated IL-6 x G-CSFR doubly deficient mice.

158 were detected in the bone marrow of IL-6 x G-CSFR-deficient mice and their ability to terminally diff

159 d proximal G-CSFR, the tyrosine-null (Y4F) G-CSFR, or Y764F mutant receptors had decreased phosphoryl

160 Thus, the truncated G-CSFRs associated with SCN/AML may protect myeloid precur

161 n the expression of C-terminally truncated G-CSFRs that promote strong cell proliferation and surviva

162 Conversely, granulocyte macrophage (GM)-CSFR had no effect on the mononuclear tumor infiltrate o

163 to the mitogenic receptors IL-3R, IL-5R, GM-CSFR, which assemble as alphabeta heterodimers.

164 tinct from those used for IL-3R alpha and GM-CSFR alpha.

165 ting alpha-chain mRNAs for both IL-3R and GM-CSFR as well as the beta-chain mRNA.

166 ifaceted and opposing roles of M-CSFR and GM-CSFR signaling in governing the phenotype of macrophage

167 rophage CSF (GM-CSF) receptors (IL-3R and GM-CSFR).

168 o increased expression of both GM-CSF and GM-CSFR, triggering an autocrine loop that further enhances

169 Neither CCL2/CCR2 nor GM-CSF/GM-CSFR signaling pathways were required for macrophage inf

170 Both depressed GM-CSFR expression and increased Mphi iDC apoptosis, as wel

171 However, GM-CSFR signaling played an important role in fine-tuning t

172 gion fused to the extracellular domain of GM-CSFR alpha-chain (GMER).

173 sociated with specific down-regulation of GM-CSFR alpha-chain, but not beta-chain expression.

174 bolished the increased phosphorylation of GM-CSFR betac in cells expressing CBL mutants, whereas trea

175 tor dasatinib resulted in equalization of GM-CSFR betac phosphorylation signal between wild type CBL

176 he hypothesis that the down-regulation of GM-CSFR is a critical event in producing cells with a lymph

177 ed enhanced kinase activity downstream of GM-CSFR.

178 ing beta subunit (beta common receptor or GM-CSFR beta [beta(c)]).

179 als synergized with those through TLR2 or GM-CSFR to promote RALDH activity in undifferentiated DC.

180 ommon beta chain for the GM-CSF receptor (GM-CSFR) are causal.

181 phage colony-stimulating factor receptor (GM-CSFR) is a potential target for toxin-directed therapy,

182 phage-colony-stimulating factor receptor (GM-CSFR) ligands.

183 phage colony-stimulating factor receptor (GM-CSFR) results in proliferation only.

184 ivity is mediated by a cellular receptor (GM-CSFR) that is comprised of an alpha-chain (GM-CSFRalpha)

185 to-Mac differentiation by down-regulating GM-CSFR expression and increasing DC apoptosis.

186 it further investigation in CMML and that GM-CSFR expression on myeloid progenitors may be a biomarke

187 n result from a genetic deficiency of the GM-CSFR alpha chain, encoded in the X-chromosome pseudoauto

188 ial cell preparations at levels equal to (GM-CSFR) or lower than those seen on monocytes.

189 stimulation, although expression of total GM-CSFR betac was lower.

190 nificant surface expression of IL-3Rs and GM-CSFRs, as well as ERK1/2 phosphorylation in response to

191 A receptors (uPARs) and GM-CSF receptors (GM-CSFRs) as well as with total uPA levels.

192 hGM-CSFR transgenic mice were crossed with mice deficient in

193 mon lymphoid progenitors (CLPs) and >20% hGM-CSFR+ pro-T cells gave rise to granulocyte, monocyte, an

194 Strikingly, >50% hGM-CSFR+ common lymphoid progenitors (CLPs) and >20% hGM-CS

195 In cultures with hGM-CSF alone, hGM-CSFR-expressing (hGM-CSFR+) granulocyte/monocyte progeni

196 with hGM-CSF alone, hGM-CSFR-expressing (hGM-CSFR+) granulocyte/monocyte progenitors (GMPs) and megak

197 uitous transgenic human GM-CSF receptor (hGM-CSFR) were used for the analysis.

198 n of hGM-CSF into mice transplanted with hGM-CSFR+ CLPs blocked their lymphoid differentiation, but i

199 M-CSFR antibody blocking experiments demonstrated that inc

200 M-CSFR down-modulation was inhibited by treating cells in

201 M-CSFR expression was stimulated in C/EBPepsilon-expressin

202 M-CSFR mRNA and protein levels were also increased in brai

203 M-CSFR overexpression increased the mRNA for macrophage sc

204 M-CSFR overexpression resulted in microglial proliferation

205 M-CSFR signaling blockade shifted the MHC-II(lo)/MHC-II(hi

206 bers of microglia strongly labeled with an M-CSFR antibody near Abeta deposits.

207 espite reduction of C/EBPalpha, G-CSFR and M-CSFR levels were maintained in total marrow and in linea

208 munofluorescence measurements with an anti-M-CSFR antibody showed that 44% +/- 5% of CD34hi cells exp

209 of tumor-bearing mice with a blocking anti-M-CSFR monoclonal antibody resulted in a reduction of matu

210 lystyrene microspheres was not enhanced by M-CSFR overexpression.

211 ressor of cytokine signaling 1, and CD115 (M-CSFR) were functional targets of miR-155.

212 sed expression of CD126 (IL-6R) and CD115 (M-CSFR), were detected in APC-defective patient Mphi.

213 ed from myeloid precursors (CD56(-)CD117(+)M-CSFR(+)) showed more expression of killer immunoglobulin

214 cytotoxicity compared with CD56(-)CD117(+)M-CSFR(-) precursor-derived NK cells and thus resemble the

215 We found that the protease cleaving M-CSFR is a transmembrane enzyme and that its expression i

216 of the PGE(2) analog misoprostol decreased M-CSFR expression in bone marrow cells and reduced the num

217 the CD34hiM-CSFRhi cells had downmodulated M-CSFR (29% to 38%).

218 f these findings, we transiently expressed M-CSFR on murine BV-2 and human SV-A3 microglial cell line

219 for macrophage colony stimulation factor (M-CSFR) blocked splenic macrophage maturation, reduced spl

220 for macrophage-colony-stimulating factor (M-CSFR).

221 hages, indicating that repression of c-fms/M-CSFR is likely the dominant mechanism responsible for Fo

222 Enforced overexpression of c-Fms/M-CSFR reversed the cytokine production and phagocytosis d

223 acrophage colony-stimulating factor (c-Fms/M-CSFR), impaired migratory capacity, and diminished accum

224 nd identified the protease responsible for M-CSFR cleavage and down-modulation.

225 that TACE is the protease responsible for M-CSFR shedding and down-modulation in mononuclear phagocy

226 CD34+ cells that were positive for M-CSFR, CD64, or both gave rise exclusively to granulo-mon

227 These results show that increased M-CSFR expression induces microglial proliferation, cytoki

228 ggesting that in APP(V717F) mice increased M-CSFR on microglia could be an important factor in Abeta-

229 that TACE is required for the TPA-induced M-CSFR cleavage.

230 these cells TPA is unable to down-modulate M-CSFR expression.

231 ystrophic neurites and astroglia showed no M-CSFR labeling in the transgenic animals.

232 ver the multifaceted and opposing roles of M-CSFR and GM-CSFR signaling in governing the phenotype of

233 Simultaneous overexpression of M-CSFR and its ligand in AbetaPP(V717F) animals could resu

234 Increased expression of M-CSFR causes microglia to adopt an activated state that r

235 The shedding of M-CSFR elicited by phorbol esters (tetradecanoylphorbol my

236 ese results suggest that overexpression of M-CSFR in APPV717F mice may prime microglia for phagocytos

237 ation and function with down-regulation of M-CSFR levels.

238 Increased expression of M-CSFR on cultured microglia results in proliferation and

239 Biolistic overexpression of M-CSFR on microglia endogenous to the organotypic culture

240 ta in mouse and human microglia because of M-CSFR overexpression that was time- and concentration-dep

241 loperoxidase, and included a population of M-CSFR+ monocyte-lineage committed cells.

242 Monocytes also decreased the expression of M-CSFR, and low numbers of cells underwent differentiation

243 (+) BM monocytes expressed high amounts of M-CSFR/CD115 in steady state and 72 h following sublethal

244 When we silenced either VCAM-1 or M-CSFR in mice with myocardial infarction or in ApoE(-/-)

245 2 and human SV-A3 microglia to overexpress M-CSFR and examined microglial phagocytosis of fluorescein

246 otective role for microglia overexpressing M-CSFR in our coculture system and suggest under certain c

247 of the coculture, microglia overexpressing M-CSFR proliferated at a higher rate than nontransfected c

248 ng the expression of the cytokine receptor M-CSFR and the chemokine receptor CXCR4, without altering

249 ophage colony-stimulating factor receptor (M-CSFR or CSF1-R), which is a tyrosine kinase growth facto

250 ophage-colony-stimulating factor receptor (M-CSFR) and Fms-like thyrosine kinase 3 (Flt3) ligands.

251 ophage colony-stimulating factor receptor (M-CSFR) are closely linked through a positive feedback loo

252 ophage colony-stimulating factor receptor (M-CSFR) in both the blood and the peritoneal cavity.

253 ceptor expression and that M-CSF receptor (M-CSFR) may be used as an early marker of monocyte lineage

254 ophage colony-stimulating factor receptor (M-CSFR), encoded by the c-fms protooncogene, is overexpres

255 ophage colony-stimulating factor receptor (M-CSFR), encoded by the proto-oncogene c-fms.

256 ophage colony-stimulating factor receptor (M-CSFR)-positive macrophages.

257 imulating factor (M-CSF) and its receptor (M-CSFR).

258 ophage colony-stimulating factor receptor (M-CSFR; c-fms) are found surrounding plaques in Alzheimer'

259 ophage colony-stimulating factor receptor [M-CSFR]) could also differentiate into NK cells in the pre

260 eptor (CSF-1R, or macrophage CSF receptor [M-CSFR]) is the primary regulator of the proliferation, su

261 found in the CD64- subset, indicating that M-CSFR appears earlier than CD64 during monocyte developme

262 fic regulation of the M-CSFR and show that M-CSFR is a useful marker to discriminate between monocyti

263 In this study, we showed that M-CSFR is shed from macrophage surface and identified the

264 linked immunosorbent assay, we showed that M-CSFR overexpression on exogenous microglia induced expre

265 ated upon M-CSFR blockade, indicating that M-CSFR signaling shapes the MHC-II(lo) TAM phenotype.

266 2 microglia transfected to overexpress the M-CSFR and hippocampal organotypic slices treated with NMD

267 ined by lineage-specific regulation of the M-CSFR and show that M-CSFR is a useful marker to discrimi

268 Forced expression of the M-CSFR in M-CSF-dependent bone marrow macrophages from Dic

269 The M-CSFR is also increased on microglia after experimental b

270 y miRNA-223, which regulates NFI-A and the M-CSFR levels.

271 h as LPS, IL-2, and IL-4 down-modulate the M-CSFR via a mechanism involving protein kinase C and phos

272 The M-CSFR was present on progenitor cells that were positive

273 uptake depended on the interaction of the M-CSFR with its ligand.

274 age colony-stimulating factor (M-CSF), the M-CSFR, and neurotrophin receptors in the NMDA-treated sli

275 levels is important for expression of the M-CSFR, which is critical for osteoclast differentiation a

276 dy neutralization of M-CSF showed that the M-CSFR-induced proinflammatory response was dependent on M

277 ht into the mechanism of action underlying M-CSFR blockade.

278 of MHC-II(lo) TAMs were downregulated upon M-CSFR blockade, indicating that M-CSFR signaling shapes t

279 To determine whether M-CSFR-induced microglial activation affects neuronal surv

280 sG-CSFR, but not sEPOR, was able to synergize with SF or FL

281 Therefore, we tested the effects of sG-CSFR and sEPOR on primitive progenitors.

282 ire extracellular domain of the receptor (sG-CSFR).

283 The sG-CSFR exhibited a weak self-association into a dimer with

284 The sG-CSFR was purified from CHO cell conditioned media with a

285 However, when sG-CSFR was purified by conventional means, i.e., without a