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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

17 ides a key brake on signaling through the GM-CSF receptor.

18 differentiation and activation, including M-CSF receptor.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

46 Wild-type and GM-CSF receptor alpha (Csf2ra)-deficient mice reconstituted

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

76 the granulocyte colony-stimulating factor (G-CSF) receptor and exhibited potent, but delayed, in vitr

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

122 G-CSF receptor deficiency and CXCL1 blockade suppressed my

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

155 11b(+) myeloid cells, is known to regulate G-CSF receptor (G-CSFR) signaling, we hypothesized that CE

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

172 8 through 400 of the alpha subunit of the GM-CSF receptor (GM-R alpha) [IL-3R alpha/GM-R alpha] or th

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

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

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

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

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

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

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

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

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

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

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

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

185 GM-CSF receptor immunoreactivity was found on neurons withi

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

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

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

189 e established the absence of a functional GM-CSF receptor in murine nociceptors, and suggest an indir

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

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

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

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

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

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

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

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

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

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

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

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

202 GM-CSF-receptor is increased on HSCs and multipotent progen

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

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

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

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

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

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

209 catenin-TCF/LEF complex directly regulates G-CSF receptor levels, and consequently controls proper di

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

211 ced granulocyte colony-stimulating factor (G-CSF) receptor levels, attenuation of downstream Stat3 ph

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

268 93T cells transfected with alpha and beta GM-CSF receptor subunits (alphaGMR and betaGMR), GM-CSF-ind

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

270 o mutations in CSF2RA or CSF2RB, encoding GM-CSF receptor subunits); secondary PAP results from vario

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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