ライフサイエンスコーパス: CSF receptor

1 BM HSC compartment by expression of CD114 (G-CSF receptor).

2 G-CSF signalling, we coexpressed exogenous G-CSF receptor.

3 through the isolated alpha subunit of the GM-CSF receptor.

4 n containing the first tyrosine residue of G-CSF receptor.

5 -CSF required the C-terminal region of the G-CSF receptor.

6 e differentiation, as well as mRNA for the M-CSF receptor.

7 mmediate early genes, and induction of the M-CSF receptor.

8 mutation inhibited the degradation of the M-CSF receptor.

9 active structures that could recognize the G-CSF receptor.

10 the association of these enzymes with the G-CSF receptor.

11 e surface required for dimerization of the G-CSF receptor.

12 n, but not Hck, was physically coupled to GM-CSF receptor.

13 nduction of gene transcription through the G-CSF receptor.

14 s blocked by inhibiting activation of the GM-CSF receptor.

15 ons in GM-CSF that reduced binding to the GM-CSF receptor.

16 differentiation and activation, including M-CSF receptor.

17 ing the ligand-binding alpha chain of the GM-CSF receptor.

18 al complex between alpha9beta1 and ligated G-CSF receptor.

19 ing the common beta chain (Beta c) of the GM-CSF receptor.

20 t is independent of signaling through the GM-CSF receptor.

21 n confers signal specificity for IL-3 and GM-CSF receptors.

22 stricted to cells or tissues that express GM-CSF receptors.

23 L-5 share a common ss-chain with IL-3 and GM-CSF receptors.

24 G- and GM-CSF receptors and no detectable M-CSF receptors.

25 ndicating that they express high-affinity GM-CSF receptors.

26 Abl bound to the betac chain of IL-3/IL-5/GM-CSF receptors.

27 an up-regulation of surface expression of GM-CSF receptors.

28 -stimulating factor (G-CSF) acting via the G-CSF receptors.

29 yte-macrophage colony-stimulating factor (GM-CSF) receptor.

30 the granulocyte colony-stimulating factor (G-CSF) receptor.

31 yte macrophage colony stimulating factor (GM-CSF) receptor.

32 the granulocyte colony-stimulating factor (G-CSF) receptor.

33 ts genetically engineered to express human M-CSF receptors (3T3-FMS cells) and human monocytes.

34 IH 3T3 fibroblasts expressing mutant human M-CSF receptors (3T3-FMS(Y809F)) that fail to activate Ras

35 he IL-3 receptor shares with the IL-5 and GM-CSF receptors a common signal transducing beta-chain.

36 the macrophage colony-stimulating factor (M-CSF) receptor, a highly related receptor tyrosine kinase

37 the Granulocyte-Colony-Stimulating Factor (G-CSF) receptor activates non-receptor protein tyrosine ki

38 line RAW264; 2) SHIP2 associated with the M-CSF receptor after M-CSF stimulation; and 3) SHIP2 assoc

39 al differences suggested that the IL-3 and G-CSF receptor agonist domains within the MPO chimera may

40 L-3 receptor agonists linked with a common G-CSF receptor agonist have been examined for their IL-3 r

41 quences to engineer chimeric dual IL-3 and G-CSF receptor agonists in which the relative spatial orie

42 and granulocyte colony-stimulating factor (G-CSF) receptor agonists that are superior in comparison t

43 and granulocyte colony-stimulating factor (G-CSF) receptor agonists.

44 Ablation of the GM-CSF receptor alleviated the monocyte response and inhibi

45 ulations of hematopoietic and endothelial GM-CSF receptor alpha (GM-CSFRalpha)-positive cells.

46 ell line WT-19 transfected with the human GM-CSF receptor alpha and beta subunits (GM-CSFRalpha and b

47 The gene encoding the GM-CSF receptor alpha subunit (CSF2RA) is located on X and

48 mprising the extracellular domain of the hGM-CSF receptor alpha subunit (hGM Ralpha) fused to the int

49 tein of 198 amino acids, designated GRAP (GM-CSF receptor alpha subunit-associated protein), was isol

50 Variant and mutated GM-CSF receptor alpha subunits, along with the beta subunit

51 with protein kinase CbetaII (PKCbetaII), GM-CSF receptor alpha-chain, and two actin-associated prote

52 yte-macrophage colony-stimulating factor (GM-CSF) receptor alpha-chain (CSF2RA) deficiency is a rare,

53 and the role of the alpha subunit of the GM-CSF receptor (alpha GMR) in modulating transporter activ

54 d that an elevated proportion of immature GM-CSF receptor-alpha(R) subunit-expressing cells were pres

55 lular portion of the alpha subunit of the GM-CSF receptor (alphaGMR) to search for interacting protei

56 e late interactions occurring between the GM-CSF receptor and activated eosinophil signaling molecule

57 from impaired signaling downstream of the M-CSF receptor and alpha(v)beta3 integrin.

58 mice carrying targeted mutations of their G-CSF receptor and displaying markedly different G-CSF-ind

59 eral sympathetic nerve neurons express the G-CSF receptor and ex vivo stimulation of peripheral sympa

60 Oval cells were found to express G-CSF receptor and G-CSF was produced within the regenerat

61 ing, the data support the concept that the G-CSF receptor and gp130 are both structurally and functio

62 ng the interaction between ICAM-1 and the GM-CSF receptor and highlight the importance of targeting I

63 l of the G-CSF-expressing lines lacked the G-CSF receptor and injections of purified recombinant G-CS

64 ced expression of c-fms, which encodes the M-CSF receptor and is obligatory for macrophage differenti

65 herefore, the physical coupling of Lyn to GM-CSF receptor and its early activation are required for i

66 s chimera to bind human cells through the GM-CSF receptor and prevent apoptosis.

67 that resident spinal microglia express the G-CSF receptor and that G-CSF signaling mediates microglia

68 lism, which in turn promoted expression of M-CSF receptor and transcription factors PU.1 and IRF8, th

69 As encoding varying portions of the human GM-CSF receptor and/or beta chains.

70 Since bone marrow myeloid cells express G-CSF receptors and G-CSF rapidly reduces CXCR4 expression

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

72 ll cells had minimal expression of G- and GM-CSF receptors and no detectable M-CSF receptors.

73 w that the LNCaP cells express functional GM-CSF receptors and that prostatic carcinomas have promine

74 cell lines were transfected with the human G-CSF receptor, and stable transfectants were studied.

75 orms a complex with the beta-chain of the GM-CSF receptor, and this interaction involves the first pa

76 the granulocyte colony-stimulating factor (G-CSF) receptor, and the granulocyte-macrophage colony-sti

77 pl, granulocyte-colony-stimulating factor [G-CSF] receptor, and Flt-3) were inserted into mouse prima

78 Truncating mutations of the G-CSF receptor are found during disease course in nearly h

79 at two distinct cytoplasmic regions of the G-CSF receptor are involved in the regulation of the inten

80 he membrane-proximal 55 amino acids of the G-CSF receptor are sufficient for activation of Stat5, the

81 Although the GM-CSF and M-CSF receptors are unrelated, both couple to Ras-dependen

82 Truncation of the carboxyl terminus of the G-CSF receptor, as seen in patients with acute myeloid leu

83 uce a recombinant fusion toxin that kills GM-CSF receptor-bearing cells.

84 ceptor, such as monocytes, as well as for GM-CSF receptor-bearing myeloid cell lines, HL60 (promyelom

85 increased tyrosine phosphorylation of the GM-CSF receptor beta chain (betac), STAT5, and other signal

86 Mice that lack the GM-CSF receptor beta chain (GM-CSFRbeta) developed invasive

87 ative substrates SHPTP-2, Stat-5, and the GM-CSF receptor beta(c) subunit.

88 eosinophils, we have identified that the GM-CSF receptor beta-chain (GMRbeta) interacted with ICAM-1

89 yte-macrophage colony-stimulating factor (GM-CSF) receptor-beta-deficient (Csf2rb(-/-)) mice that dev

90 CP-1), matrix metalloproteinase 9 (MMP-9), G-CSF receptor, beta2 integrins, or selectins responded to

91 ns displayed increased phosphorylation of GM-CSF receptor betac subunit in response to stimulation, a

92 (Gmcsf) or the beta common subunit of the GM-CSF receptor (betac) are inactivated display normal stea

93 We show that the common beta chain of the GM-CSF receptor (betac) is dispensable for Nras(G12D/+) HSC

94 Importantly, G-CSF receptor blockade did not adversely affect viral cle

95 describe for the first time the effect of G-CSF receptor blockade in a therapeutic model of inflamma

96 imals neutropenic, suggesting an effect of G-CSF receptor blockade on neutrophil homing to inflammato

97 Shp2-deficient cells transfected with the G-CSF receptor but intact in cells expressing phosphatase-

98 myeloid leukemia progenitors bearing the GM-CSF receptor, but not normal marrow progenitors.

99 r c-Jun could promote the induction of the M-CSF receptor by collaborating with PU.1.

100 partner CBF beta synergistically activate M-CSF receptor by more then 60 fold.

101 The CSF-1/M-CSF receptor c-fms and RAFTK appeared to associate in re

102 -regulating cell surface expression of the M-CSF receptor c-Fms by a matrix metalloprotease- and MAPK

103 n of Tyr-721, the PI3K binding site in the M-CSF receptor c-Fms, fails to suppress cytoskeletal remod

104 of STAT1:STAT3:STAT5 activated by various G-CSF receptor C-terminal deletion mutants.

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

106 by the kinetic appearance of mRNA for the M-CSF receptor, c-fms, at day 3 following culture initiati

107 eated them with a mAb directed against the M-CSF receptor, c-Fms.

108 he presence of at least 100 high affinity GM-CSF receptors/cell and the absence of overexpressed anti

109 y mapped the Lyn-binding site of the IL-5/GM-CSF receptor common beta (beta c) subunit.

110 osinophil peroxidase, CCR3, the IL-3/IL-5/GM-CSF receptor common beta-chain, and the transcription fa

111 s constitutively express higher levels of GM-CSF receptor compared with CD103(+) DCs and are thus sel

112 exhibited a higher level of expression of M-CSF receptor compared with normal controls.

113 the receptor by nearly 15 degrees C in the G-CSF/receptor complex.

114 The GM-CSF receptor consists of two subunits: GMRalpha, which b

115 yte-macrophage colony-stimulating factor (GM-CSF) receptor consists of 2 glycoprotein subunits, GMRal

116 tations in the extracellular domain of the G-CSF receptor (CSF3R) have been reported only in severe c

117 he membrane-proximal 55 amino acids of the G-CSF receptor cytoplasmic domain are sufficient for media

118 G-CSF receptor deficiency and CXCL1 blockade suppressed my

119 t not flt-3 ligand is markedly impaired in G-CSF receptor-deficient (G-CSFR-deficient) mice.

120 G-CSF- and G-CSF receptor-deficient mice are profoundly protected in

121 lar proteinosis in mice transplanted with GM-Csf-receptor-deficient progenitors.

122 and IL-6 or by retroviral transduction of G-CSF receptors, demonstrating that loss of both of these

123 M-CSF-activated AMPK is via M-CSF receptor-dependent reactive oxygen species productio

124 nism by which the carboxyl terminus of the G-CSF receptor down-regulates G-CSF-induced Stat activatio

125 SF monoclonal or polyclonal Abs or soluble M-CSF receptors, dramatically inhibited HIV-1 replication

126 Lyn-deficient DT40 cells that express the G-CSF receptor (DT40GR) do not demonstrate G-CSF-induced m

127 yte-macrophage colony-stimulating factor (GM-CSF) receptors, ectopically expressed in FDCP-mix multip

128 These M-CSF receptor events correlated with activation of the se

129 activation mediated by a carboxy truncated G-CSF receptor, expressed in patients with acute myeloid l

130 ependent coactivator of PU.1, resulting in M-CSF receptor expression and development of the monocytic

131 macrophage immune function by decreasing GM-CSF receptor expression and downstream PU.1 nuclear bind

132 The upregulation of M-CSF receptor expression by AML1-ETO may contribute to th

133 exhibited a significantly higher level of M-CSF receptor expression than U937 cells.

134 Endogenous M-CSF receptor expression was examined in Kasumi-1 cells,

135 that prostatic carcinomas have prominent GM-CSF receptor expression.

136 orrelate with the reduction in bone marrow G-CSF receptor expression.

137 factor (TNF), and colony-stimulating factor (CSF) receptor expression suggest that the release of ext

138 o liver repopulation, as well as the G-CSF/G-CSF-receptor expression levels were evaluated.

139 nous macrophage colony-stimulating factor (M-CSF) receptor, Fms, we have analyzed the role of a new m

140 d by macrophage colony-stimulating factor (M-CSF), receptor for activation of NF-kappa B ligand (RANK

141 Defects in GM-CSF receptor function disrupt surfactant clearance, caus

142 of N-glycosylation of the beta subunit on GM-CSF receptor function.

143 ia (AML) associated with a mutation of the G-CSF receptor (G-CSF-R) developed in a patient with SCN m

144 The G-CSF receptor (G-CSFR) activates the Jak/STAT pathway, al

145 Truncation mutations of the G-CSF receptor (G-CSFR) are associated with the developmen

146 he membrane-proximal 87 amino acids of the G-CSF receptor (G-CSFR) are sufficient to mediate this res

147 The G-CSF receptor (G-CSFR) belongs to the superfamily of the

148 that truncate the cytoplasmic tail of the G-CSF receptor (G-CSFR) have been detected.

149 Mutations in the G-CSF receptor (G-CSFR) in patients with severe congenital

150 n the expression of truncated forms of the G-CSF receptor (G-CSFR) protein.

151 11b(+) myeloid cells, is known to regulate G-CSF receptor (G-CSFR) signaling, we hypothesized that CE

152 we describe a system to study the role of G-CSF receptor (G-CSFR) signals in granulocytic differenti

153 ted mice with a targeted mutation of their G-CSF receptor (G-CSFR) such that the cytoplasmic (signali

154 tion mutations of CSF3R, which encodes the G-CSF receptor (G-CSFR), are implicated in leukemic progre

155 We use mixed G-CSF receptor (G-CSFR)-deficient bone marrow chimeras to

156 Because G-CSF receptor (G-CSFR)-deficient mice do not have the exp

157 progenitor mobilization was examined using G-CSF receptor (G-CSFR)-deficient mice.

158 is known to be marked by expression of the G-CSF receptor (G-CSFR).

159 uman fibrosarcoma cell line expressing the G-CSF receptor, G-CSF induces the tyrosine phosphorylation

160 strate elevated risk with mutations in the G-CSF receptor gene and a specific mutation in the ELANE g

161 SCN patients with mutations in the G-CSF receptor gene are predisposed to acute myeloid leuke

162 sociation of auto-antibodies to GM-CSF or GM-CSF receptor gene mutations with PAP has implicated GM-C

163 has been shown to harbor mutations in the G-CSF receptor gene that resulted in the truncation of the

164 Palpha, and CBF, regulate the NE, MPO, and M-CSF Receptor genes.

165 and granulocyte colony-stimulating factor (G-CSF) receptor genes by 2.5-, 1.8-, and 1.6-fold, respect

166 proteins or the common beta chain for the GM-CSF receptor (GM-CSFR) are causal.

167 ing to the alpha and beta subunits of the GM-CSF receptor (GM-CSFRalpha and betac, respectively).

168 8 through 400 of the alpha subunit of the GM-CSF receptor (GM-R alpha) [IL-3R alpha/GM-R alpha] or th

169 ssion levels of uPA receptors (uPARs) and GM-CSF receptors (GM-CSFRs) as well as with total uPA level

170 yte-macrophage colony-stimulating factor (GM-CSF) receptor (GM-CSFr) and the intracellular domain of

171 -Cbl (henceforth referred to as Cbl) as a GM-CSF receptor (GMR) adaptor protein that targets Src for

172 xerts its effects by interaction with the GM-CSF receptor (GMR) on the surface of responsive cells.

173 of mature host defense cells through the GM-CSF receptor (GMR), which is composed of alpha (alphaGMR

174 ation between the tyrosine phosphorylated GM-CSF receptor (GMR)-beta c chain and Shc in vivo.

175 yte-macrophage colony-stimulating factor (GM-CSF) receptor (GMR) consists of an alpha (GMRalpha) and

176 yte-macrophage colony-stimulating factor (GM-CSF) receptor (GMR) is a heterodimeric receptor expresse

177 yte-macrophage colony-stimulating factor (GM-CSF) receptor has several isoforms that result from alte

178 Because patients with a truncated G-CSF receptor have a high risk of developing acute myeloi

179 mice with the ubiquitous transgenic human GM-CSF receptor (hGM-CSFR) were used for the analysis.

180 d by IL-3 and granulocyte-macrophage CSF (GM-CSF) receptors (IL-3R and GM-CSFR).

181 GM-CSF receptor immunoreactivity was found on neurons withi

182 ntly decreased membrane expression of the GM-CSF receptor in alveolar macrophages.

183 es the actin-linkage of integrins and the GM-CSF receptor in dendritic cells.

184 coding the alpha and beta subunits of the GM-CSF receptor in LNCaP cells, and the presence of the alp

185 we have restored expression of the G- and M-CSF receptors in PU.1-deficient cells using retroviral v

186 yte-macrophage colony-stimulating factor (GM-CSF) receptor in the human prostate carcinoma cell line

187 ivated by G-CSF in cells expressing the wt G-CSF receptor, in addition to the previously reported STA

188 used a retroviral vector to transduce the G-CSF receptor into MO7e cells, which are known to express

189 Indeed, the human GM-CSF receptor is a good target because it is overexpresse

190 The GM-CSF receptor is composed of two subunits, alpha and beta

191 The transduced G-CSF receptor is functionally active, and the resultant M

192 However, the G-CSF receptor is not expressed on osteoblasts; accordingl

193 First, myeloid-specific expression of the M-CSF receptor is regulated transcriptionally by three fac

194 onstrate that the carboxyl terminus of the G-CSF receptor is required for SHP-1 down-regulation of St

195 The granulocyte colony-stimulating factor (G-CSF) receptor is expressed exclusively in myeloid cells

196 the macrophage colony-stimulating factor (M-CSF) receptor is regulated by three transcription factor

197 that the chimeric protein binds the human GM-CSF receptor, is endocytosed, and appears to reach the c

198 e RNA: Emr1 (F4/80), Itgam (CD11b), Csf1r (M-CSF Receptor), Itgal (CD11a), Tnf, and Nos2 Additionally

199 signaling through the KGF receptor/GM-CSF/GM-CSF receptor/JAK-STAT axis.

200 odel of hematopoietic deficiency, T(-) and G-CSF-receptor knock-out (GR(-)) mice were crossed, and F1

201 g a granulocyte-colony stimulating factor (G-CSF) receptor knockout mouse model in combination with b

202 cells of wild-type mice, activation of the G-CSF receptor leads to upregulation of cyclin D3.

203 d in HIV-1-infected donors despite normal GM-CSF receptor levels.

204 t SHIP-1 was involved in the regulation of M-CSF receptor (M-CSF-R)-induced Akt activation.

205 the level of receptor expression and that M-CSF receptor (M-CSFR) may be used as an early marker of

206 or 1 (CSF-1) receptor (CSF-1R, or macrophage CSF receptor [M-CSFR]) is the primary regulator of the p

207 ains, domains with the L1 linker had lower G-CSF receptor-mediated proliferative activities and confo

208 or functional importance and redundancy of G-CSF receptor-mediated signaling in human granulopoiesis.

209 To investigate the role Gab2 plays in G-CSF receptor-mediated signaling, we have analyzed its ac

210 ith rGM-CSF via the upper airway restored GM-CSF receptor membrane expression as well as PU.1 protein

211 This phenotype is distinct from that of G-CSF receptor-/- mice, suggesting that other genes are li

212 Bone marrow G-CSF receptor mRNA levels and G-CSF-stimulated proliferat

213 n was associated with the up-regulation of G-CSF receptor mRNA, and the combination of GM-CSF and G-C

214 hat granulocyte colony-stimulating factor (G-CSF) receptor mRNA was undetectable and granulocyte matu

215 n of the myeloperoxidase, lactoferrin, and G-CSF receptor mRNAs.

216 d by macrophage colony-stimulating factor (M-CSF) receptor mutations.

217 the granulocyte-colony-stimulating factor (G-CSF) receptor, neutrophil elastase, and myeloperoxidase.

218 GM-CSF-receptor occupancy at 0.7 nmol/L GM-CSF-ligand conce

219 he induction of apoptosis correlates with GM-CSF-receptor occupancy at low ligand concentrations.

220 n receptor-binding affinity, induction of GM-CSF receptor oligomerization and signaling capacity.

221 tively inhibited binding of GM-CSF to the GM-CSF receptor on HL-60 cells and demonstrated antagonist

222 that recombinant GM-CSF-Bcl-XL binds the GM-CSF receptor on human monocyte/macrophage cells and bone

223 easurements of the number and affinity of GM-CSF receptors on cells from the same samples showed no c

224 ecules that bind and activate the IL-3 and G-CSF receptors on hematopoietic cells.

225 up-regulates the expression of functional M-CSF receptors on monocytes.

226 his may reflect the presence of functional G-CSF receptors on other cell types and tissues, as well a

227 o be explained by an increased density of GM-CSF receptors on these cells.

228 ls stably expressing either wild-type (wt) G-CSF receptor or a series of C-terminal deletion mutants.

229 SF, although some may have had defects in GM-CSF receptor or signal-transduction mechanisms.

230 from macrophage colony-stimulating factor (M-CSF) receptors or Fc receptors to the actin cytoskeleton

231 G-CSF receptor positive (aka G-CSFr(+) or CD114(+)) cells

232 uman macrophage colony-stimulating factor (M-CSF) receptor presents an excellent model with which we

233 Cells expressing the truncated G-CSF receptor produced more ROSs than those with the full

234 -O-tetradecanoylphorbol-13-acetate-induced M-CSF receptor promoter activity during monocytic differen

235 o found two regions that are important for G-CSF receptor promoter activity.

236 s the ability of PU.1 to transactivate the M-CSF receptor promoter as well as a minimal thymidine kin

237 c-Jun does not directly bind to the M-CSF receptor promoter but associates via its basic domai

238 differentiation, but the monocyte-specific M-CSF receptor promoter has no AP-1 consensus binding site

239 hown that AML1 and C/EBPalpha activate the M-CSF receptor promoter in a synergistic manner.

240 A 1,391-bp fragment of the G-CSF receptor promoter is both active in myeloid cell lin

241 other functionally important region of the G-CSF receptor promoter is in the 5' untranslated region,

242 DNA binding to and transactivation of the M-CSF receptor promoter, a direct PU.1 target gene, were d

243 s interacting with critical regions of the M-CSF receptor promoter, including PU.1 and AML1.PU.1 is e

244 work synergistically to transactivate the M-CSF receptor promoter, thus exhibiting a different activ

245 the macrophage colony-stimulating factor (M-CSF) receptor promoter.

246 Anti-G-CSF receptor rapidly halted the progression of establish

247 uman lymphocytes expressing high affinity GM-CSF receptors responded to alpha GMR antibody with incre

248 p30 repressed expression of the endogenous G-CSF receptor several-fold.

249 yte-macrophage colony-stimulating factor (GM-CSF) receptors share a common beta chain (beta(c)), and

250 with normal, hPAP-iPS-Mphis had impaired GM-CSF receptor signaling and reduced GM-CSF-dependent gene

251 Restoration of GM-CSF receptor signaling corrected the surfactant clearanc

252 Abrogation of GM-CSF receptor signaling in adoptive transfer recipients o

253 investigate the actions of blocking G-CSF/G-CSF receptor signaling in inflammatory disease, and as a

254 lopoiesis-specific mechanism downstream of G-CSF receptor signaling that leads to LEF-1 downregulatio

255 Despite abundant lung GM-CSF and intact GM-CSF receptor signaling, PPAR-gamma was not sufficiently

256 thereby inhibits STAT3 phosphorylation and G-CSF receptor signaling.

257 tact STAT3 upregulation, characteristic of G-CSF receptor signaling.

258 correlated that with wild-type and mutant G-CSF receptors stably expressed in the murine factor-depe

259 terns by Gr-1 antigen expression and their G-CSF receptor status.

260 ab2, Gab3 is tyrosine phosphorylated after M-CSF receptor stimulation and associates transiently with

261 93T cells transfected with alpha and beta GM-CSF receptor subunits (alphaGMR and betaGMR), GM-CSF-ind

262 hat depended on the ectopic expression of GM-CSF receptor subunits by tumors.

263 moattractant for native cells bearing the GM-CSF receptor, such as monocytes, as well as for GM-CSF r

264 hematopoietic growth factor receptor, the M-CSF receptor, suggesting a mechanism of how the AML1 fus

265 blocking neutrophil trafficking with anti-G-CSF receptor suppressed local production of proinflammat

266 This leads to increased GM-CSF receptor/Syk signalling, and to the induction of a t

267 nic mice with a targeted mutation of their G-CSF receptor (termed d715F) that abolishes G-CSF-depende

268 f the biochemical properties of mammalian GM-CSF receptors that are required for efficient binding of

269 the macrophage colony-stimulating factor (M-CSF) receptor, the granulocyte colony-stimulating factor

270 m an inflammatory phenotype following anti-G-CSF receptor therapy in collagen Ab-induced arthritis.

271 the expression and internalization of the M-CSF receptor, thus overriding the IL-6/M-CSF pathway.

272 the requirement for signaling through the GM-CSF receptor to initiate and sustain this MPD by generat

273 We conducted dynamic kinetic analyses of GM-CSF receptors to define the role of GMRbeta in the inter

274 We show here that the G-CSF receptor transcription start site is identical in ea

275 We established a G-CSF receptor-transduced promyelocytic cell line, EPRO-Gr

276 The G-CSF receptor transduces signals that regulate the prolif

277 in the blood and arthritic joints of anti-G-CSF receptor-treated mice showed alterations in cell adh

278 in granulocyte colony-stimulating factor (G-CSF) receptor-triggered granulopoiesis, is downregulated

279 M-CSF treatment induced M-CSF receptor tyrosine phosphorylation and recruitment of

280 sion of the common beta-chain of the IL-3/GM-CSF receptor was down-regulated in Stat-5-activated myel

281 at the interaction between ICAM-1 and the GM-CSF receptor was essential for GM-CSF-induced eosinophil

282 The extracellular domain of the murine G-CSF receptor was required for the activity of SB 247464,

283 ion, the common beta subunit of IL-3/IL-5/GM-CSF receptor was tyrosine phosphorylated in the clones i

284 l3 cells and FDCP1 cells expressing mutant G-CSF receptors was examined and it was found that G-CSF u

285 pDC that expressed the GM-CSF receptor were increased in breast tumors compared wi

286 lation of c-Kit and the beta-chain of the GM-CSF receptor were not observed, SCF and GM-CSF in combin

287 Binding studies indicated that human GM-CSF receptors were present on all of the human GI and le

288 instead, mutations of CSF3R, encoding the G-CSF receptor, were common.

289 developed a neutralizing mAb to the murine G-CSF receptor, which potently antagonizes binding of muri

290 expressing a carboxyl-terminally truncated G-CSF receptor, which supports proliferation but not diffe

291 ific macrophage colony-stimulating factor (M-CSF) receptor, which is critical for monocytic cell surv

292 netics, the MPOs were found to bind to the G-CSF receptor with low nanomolar affinities, similar to t