ライフサイエンスコーパス: interleukin-3

1 (Flt3L + thrombopoietin + stem cell factor + interleukin 3).

2 went apoptosis within 24 h in the absence of interleukin 3.

3 genous addition of stem cell factor (SCF) or interleukin 3.

4 light previously unexplored sensitivities to Interleukin-3.

5 -) bone marrow-derived mast cells exposed to interleukin-3.

6 stem cells in culture in vitro that contains interleukin-3.

7 survival and proliferation in the absence of interleukin-3.

8 IGF-I than in cells exponentially growing in interleukin-3.

9 ophage colony-stimulating factor (GM-CSF) or interleukin-3.

10 ponsible for the cell-specific expression of interleukin-3.

11 ulating expression of cytokine genes such as interleukin-3.

12 te known to regulate apoptotic cell death by interleukin-3.

13 tion from apoptosis induced by withdrawal of interleukin-3.

14 by growth/survival factors such as serum or interleukin-3.

15 response to the BPDCN growth/survival factor interleukin-3.

16 plating in methylcellulose supplemented with interleukin-3.

17 asone, erythropoietin, stem cell factor, and interleukin-3.

18 d in Ba/f3 cells, and most were modulated by interleukin-3.

19 undergo rapid apoptosis following removal of interleukin-3.

20 ring into dHSCs in the presence of exogenous interleukin 3, although in fewer numbers than the AGM re

21 sed and they develop a DC-like morphology in interleukin 3 and CpG.

22 egulated in these cells after the removal of interleukin 3 and exposure to granulocyte colony stimula

23 B/p65 pathway activity and expression of the interleukin 3 and granulocyte/macrophage-colony stimulat

24 reduced allergen-provoked concentrations of interleukin 3 and interleukin 4 and augmented levels of

25 processes and show here that the 2 cytokines interleukin 3 and thrombopoietin have the ability to exp

26 tect from apoptosis induced by withdrawal of interleukin 3 and/or serum and did not induce leukemia i

27 c-kit mutant Kit(W/W-v) mice indicated that interleukin-3 and c-Kit contribute to expulsion of the i

28 cell survival in 32D cells in the absence of interleukin-3 and EGF, we found that receptors lacking g

29 the endoplasmic reticulum and is induced by interleukin-3 and eotaxin-1.

30 ght be a critical downstream event following interleukin-3 and granulocyte-macrophage colony-stimulat

31 /-) cells were stimulated with the cytokines interleukin-3 and granulocyte-macrophage colony-stimulat

32 loid lineage commitment and differentiation (interleukin-3 and granulocyte-macrophage colony-stimulat

33 F, and a beta-chain (betac), shared with the interleukin-3 and interleukin-5 receptors.

34 express mutant ERBB2, became independent of interleukin-3 and sensitive to HKI-272.

35 n single cell suspensions in the presence of interleukin-3 and stem cell factor allowed expansion and

36 sequence to the 3'-end of nonpolyadenylated interleukin-3 and TNFalpha mRNAs.

37 specific cytokines (e.g., erythropoietin and interleukin-3) and that activation of the Jak kinase is

38 human granulocyte colony-stimulating factor, interleukin 3, and stem cell factor in a subset of AML a

39 growth, renders proliferation independent of interleukin-3, and blocks granulocytic differentiation.

40 cytokines, eg, tumor necrosis factor alpha, interleukin-3, and granulocyte-macrophage colony-stimula

41 Splenocyte proliferation and interleukin-2, interleukin-3, and interferon-gamma release were determi

42 biomarkers chemokine (C-C motif) ligand 22, interleukin-3, and macrophage migration inhibitory facto

43 with transgenic expression of human GM-CSF, interleukin-3, and stem cell factor in a NOD/SCID-IL2Rga

44 ietic stem cell cytokines: stem cell factor, interleukin-3, and stromal derived factor-1alpha, in con

45 yzed for total protein and levels of GM-CSF, interleukin-3, and tumor necrosis factor (TNF)-alpha.

46 glycolysis, translocates into the nucleus by interleukin-3, but not by epidermal growth factor, stimu

47 In the presence of survival factor interleukin-3, cells phosphorylate BAD on two serine res

48 yte macrophage colony-stimulating factor and interleukin-3, clonally expand, and differentiate to Ly-

49 the coexpression of c-Myc and CCL6 abrogated interleukin 3 dependence and produced a highly leukemoge

50 es alone did not affect the proliferation or interleukin 3 dependence of these cells.

51 Ba/F3, a murine interleukin-3 dependent pro-B cell line is increasingly

52 (IC(50) = 40 nM) but had a lesser effect on interleukin 3-dependent (IC(50) = 250 nM) or granulocyte

53 positive target of the L-Myc oncoprotein in interleukin 3-dependent 32D myeloid cells.

54 We found, when introduced into an interleukin 3-dependent cell line, TPR-MET induces facto

55 Expression of mutant EpoR in interleukin 3-dependent hematopoietic cells was associat

56 Interleukin 3-dependent murine 32D cells do not detectab

57 BAD phosphorylation and led to cell death in interleukin-3-dependent 32D cells.

58 homologs, Eya2, triggers rapid apoptosis in interleukin-3-dependent 32D.3 murine myeloid cells, whic

59 When expressed in the interleukin-3-dependent cell line Ba/F3, the chimeric re

60 rs (c-Kit and Flt-3) were coexpressed in the interleukin-3-dependent cell line Ba/F3.

61 y proteins and the induction of apoptosis in interleukin-3-dependent control and bcl-xL-overexpressin

62 dependent cell survival was undertaken using interleukin-3-dependent FL5.12 cells.

63 phosphatase activity dephosphorylated BAD in interleukin-3-dependent FL5.12 lymphoid cells.

64 ion mutants of CRKL were transfected into an interleukin-3-dependent hematopoietic cell line, Ba/F3,

65 man erythroid progenitors and a multilineage interleukin-3-dependent hematopoietic cell line.

66 but not the wild-type ALK cDNA, transformed interleukin-3-dependent murine haematopoietic Ba/F3 cell

67 was expressed with wild-type GMRalpha in the interleukin-3-dependent murine hematopoietic cell line,

68 ytic differentiation of 32D IGF-IR cells, an interleukin-3-dependent murine hemopoietic cell line dev

69 f several different cell types including the interleukin-3-dependent murine myeloid cell line 32Dcl3,

70 o the wild-type EPOR when tested in a murine interleukin-3-dependent myeloid cell line (FDC-P1).

71 e with loss of its antiapoptotic activity in interleukin-3-dependent myeloid H7 cells.

72 pendent derivatives but had no effect on the interleukin-3-dependent parental BaF3 cells.

73 okine-dependent cell line 32D inhibited both interleukin-3-dependent proliferation and granulocyte co

74 actively undergoing apoptosis as a result of interleukin 3 deprivation for 24 h.

75 d the susceptibility to apoptosis induced by interleukin-3 deprivation, suppressed granulocytic diffe

76 optotic cell death in FL5.12 cells following interleukin-3 deprivation.

77 BCR domain (p185DeltaBCR) failed to protect interleukin 3-deprived 32Dcl3 myeloid precursor cells fr

78 t, despite abundant extracellular nutrients, interleukin-3-deprived hematopoietic cells begin to cata

79 re representative of this state than are the interleukin 3-derived mast cells.

80 A cDNA was isolated from interleukin 3-developed, mouse bone marrow-derived mast

81 e to the protein kinase-activating cytokines interleukin 3, erythropoietin, or granulocyte-macrophage

82 ombinant pig cytokines (stem cell factor and interleukin 3) for 2 weeks, whereas the other received o

83 Removal of interleukin-3 from the Fes(act)-expressing cells was fol

84 haracterized a silencer element in the human interleukin-3 gene promoter that is responsible for the

85 In an in vitro hematopoiesis assay, interleukin-3, granulocyte colony-stimulating factor, an

86 rossing transgenic founders carrying porcine interleukin-3, granulocyte macrophage-colony stimulating

87 e engineered to constitutively produce human interleukin-3, granulocyte-macrophage colony-stimulating

88 tential]) and lineage-committed (CFU-IL3/GM [interleukin 3/granulocyte macrophage]) allogeneic donor

89 ergistically with LNK deficiency to increase interleukin 3/granulocyte-macrophage colony-stimulating

90 immunogenicity, and toxicity of PIXY321 (an interleukin-3/granulocyte-macrophage colony-stimulating

91 not affect the production of erythropoietin, interleukin-3, growth hormone, or of full-length TPO.

92 assessed the effect that erythropoietin and interleukin-3 have on cisplatin-treated hematopoietic ce

93 hosphorylation of MAP kinase induced by both interleukin 3 (IL-3) and GM-CSF in HL-60 cells.

94 kemia (CML) express aberrant transcripts for interleukin 3 (IL-3) and granulocyte colony-stimulating

95 Activation of human interleukin 3 (IL-3) and granulocyte-macrophage colony-s

96 efore induction, all cells were dependent on interleukin 3 (IL-3) for growth and survival.

97 We evaluated the expression of the interleukin 3 (IL-3) receptor alpha subunit (CD123), an

98 Interleukin 3 (IL-3) stimulates the proliferation and di

99 phage colony-stimulating factor (GM-CSF) and interleukin 3 (IL-3) that was dependent on SHP-2 catalyt

100 en, and bone marrow were increased by either interleukin 3 (IL-3) treatment or by adoptive basophil t

101 age, and the levels of SWA- and SEA-specific interleukin 3 (IL-3) were weakly correlated with schisto

102 ophage colony-stimulating factor (GM-CSF) or interleukin 3 (IL-3), GM-CSF(-/-) or IL-3(-/-) mice were

103 day culture of CD34(+) cells stimulated with interleukin 3 (IL-3), granulocyte-macrophage colony-stim

104 TEL/TRKC, BCR/FGFR1, and NPM/ALK as well as interleukin 3 (IL-3), granulocyte-macrophage colony-stim

105 a), tumor necrosis factor-alpha (TNF-alpha), interleukin 3 (IL-3), IL-4, IL-5, IL-13, IL-2 receptor a

106 at transducing bone marrow HSCs cultured in interleukin 3 (IL-3), IL-6, and stem cell factor for 96

107 observed in response to cocktails containing interleukin 3 (IL-3), IL-6, stem cell factor (SCF), Flt3

108 d in the presence of stem cell factor (SCF), interleukin 3 (IL-3), IL-7, granulocyte-macrophage colon

109 Stable expression of C/EBPepsilonT75A in interleukin 3 (IL-3)-dependent 32Dcl3 did not result in

110 When stably expressed in an interleukin 3 (IL-3)-dependent cell line, ATFx suppresse

111 Stable transfection of the Mer chimera into interleukin 3 (IL-3)-dependent murine 32D cells resulted

112 sfected EGFRvIII cDNA into a nontumorigenic, interleukin 3 (IL-3)-dependent murine hematopoietic cell

113 of IRS-1 signaling that inhibit apoptosis of interleukin 3 (IL-3)-deprived 32D myeloid progenitor cel

114 th factor receptor-beta (PDGFbetaR), confers interleukin 3 (IL-3)-independent growth on Ba/F3 hematop

115 Ten of 14 c-KIT mutations conferred interleukin 3 (IL-3)-independent growth.

116 These compounds inhibited interleukin 3 (IL-3)-independent proliferation of BaF3/N

117 ignal transduction pathways that mediate the interleukin 3 (IL-3)-induced enhancement of retinoic aci

118 ed on blood IPCs after in vitro culture with interleukin 3 (IL-3).

119 gated the effect of proteasome inhibition on interleukin-3 (IL-3) activation of the JAK/STAT pathway

120 32D cl3 cells proliferate in interleukin-3 (IL-3) and differentiate to neutrophils in

121 and induces hyperproliferative responses to interleukin-3 (IL-3) and Epo.

122 CSFs granulocyte-macrophage (GM)-CSF, G-CSF, interleukin-3 (IL-3) and erythropoietin and decreased th

123 etins (MPOs) are a family of engineered dual interleukin-3 (IL-3) and granulocyte colony-stimulating

124 e C (PKC) in the suppression of apoptosis in interleukin-3 (IL-3) and granulocyte-macrophage (GM)-CSF

125 und that the leukemic cells expressed excess interleukin-3 (IL-3) and granulocyte-macrophage colony-s

126 lated by T-cell-derived cytokines, including interleukin-3 (IL-3) and IL-9, and by stem cell factor (

127 liferate if the culture is supplemented with interleukin-3 (IL-3) and macrophage inflammatory protein

128 cells undergoing self-renewal in response to interleukin-3 (IL-3) and multilineage differentiation in

129 immortalized using Hoxb8 in the presence of interleukin-3 (IL-3) and outgrowing cell lines selected

130 d toward the myeloid lineage by culture with interleukin-3 (IL-3) and retinoic acid.

131 Interleukin-3 (IL-3) and stem cell factor (SCF) are impo

132 FL5.12 cells are interleukin-3 (IL-3) dependent for growth, proliferation

133 poptosis of 32D myeloid cells in response to interleukin-3 (IL-3) deprivation and exposure to chemoth

134 ogical processes, including apoptosis due to interleukin-3 (IL-3) deprivation and iron transport.

135 member of lipocalin family, is induced upon interleukin-3 (IL-3) deprivation and plays a pivotal rol

136 We show here that, during interleukin-3 (IL-3) deprivation-induced apoptosis of 32

137 BCR) are susceptible to apoptosis induced by interleukin-3 (IL-3) deprivation.

138 In cells that are dependent on interleukin-3 (IL-3) for survival, pharmacological inhib

139 that undergoes apoptosis upon withdrawal of interleukin-3 (IL-3) from the medium.

140 The antiapoptotic action of interleukin-3 (IL-3) has been linked to a signaling path

141 ophage colony-stimulating factor (GM-CSF) or interleukin-3 (IL-3) have established unique roles for t

142 ose metabolism are coordinately regulated by interleukin-3 (IL-3) in cytokine-dependent cells.

143 We reported that interleukin-3 (IL-3) levels are increased in bone marrow

144 phage colony-stimulating factor (GM-CSF) and interleukin-3 (IL-3) manifest insulitis, destruction of

145 P and colony-stimulating factor-1 (CSF-1) or interleukin-3 (IL-3) modulates MAPK in the myeloid proge

146 granulocyte (G)-CSF, macrophage (M)-CSF, and interleukin-3 (IL-3) mRNA expression and cytokine secret

147 se quiescent BCR-ABL+ cells contained either interleukin-3 (IL-3) or granulocyte colony-stimulating f

148 The addition of SDF-1 to interleukin-3 (IL-3) or stem cell factor (SCF) had no ef

149 Here we report that the cytokine interleukin-3 (IL-3) potentiates inflammation in sepsis.

150 Cytokines such as interleukin-3 (IL-3) promote the survival of hematopoiet

151 s of TEL-AML1 mutants on the AML1-responsive interleukin-3 (IL-3) promoter, a potentially relevant ge

152 recombinant chimeric proteins that are both interleukin-3 (IL-3) receptor and granulocyte colony-sti

153 he p85 subunit of PI-3K, others, such as the interleukin-3 (IL-3) receptor beta common chain (betac)

154 Interleukin-3 (IL-3) regulates cell growth by affecting

155 Interestingly, the addition of interleukin-3 (IL-3) rescued BCR/ABL-transformed cells f

156 Whereas treatment of control animals with interleukin-3 (IL-3) resulted in expanded myelopoiesis w

157 rapidly undergo apoptosis upon withdrawal of interleukin-3 (IL-3) supplement in culture.

158 We found that interleukin-3 (IL-3) was also induced by the imbalanced

159 Expression of interleukin-3 (IL-3) was increased in the lungs of Op/Op

160 The in vivo functions of interleukin-3 (IL-3) were investigated by generating IL-

161 n pre-B hematopoietic cells FL5.12 following interleukin-3 (IL-3) withdrawal.

162 cytic cells that undergo apoptosis following interleukin-3 (IL-3) withdrawal.

163 The contribution of interleukin-3 (IL-3), a hematopoietic growth factor and

164 a/F3 cell apoptosis induced by withdrawal of interleukin-3 (IL-3), a survival factor for this cell, a

165 sive cell lines with stem cell factor (SCF), interleukin-3 (IL-3), and granulocyte-macrophage colony-

166 crophage colony-stimulating factor (GM-CSF), interleukin-3 (IL-3), and IL-5 (GMRbetaC) with a truncat

167 ed levels, proliferation in response to Epo, interleukin-3 (IL-3), and stem cell factor was attenuate

168 resulted in primed PLA(2) activity, whereas interleukin-3 (IL-3), GM-CSF, and tumor necrosis factor

169 The receptors for interleukin-3 (IL-3), granulocyte-macrophage colony-stim

170 ir characteristic proliferative responses to interleukin-3 (IL-3), IL-4, and IL-9 in combination with

171 In contrast, cultures containing interleukin-3 (IL-3), IL-6, and leukemia inhibitory fact

172 ent CH-296 in the presence of growth factors interleukin-3 (IL-3), IL-6, and stem cell factor.

173 then expanded for 12 days in the presence of interleukin-3 (IL-3), IL-6, and stem cell factor.

174 crophage colony-stimulating factor (GM-CSF), interleukin-3 (IL-3), IL-6, erythropoietin (Epo) +/- SLF

175 Addition of other cytokines, including interleukin-3 (IL-3), IL-6, granulocyte-macrophage colon

176 crophage colony-stimulating factor (GM-CSF), interleukin-3 (IL-3), IL-6, thrombopoietin (TPO), and tu

177 Although hematopoietic cytokines such as interleukin-3 (IL-3), IL-7, stem cell factor (SCF), macr

178 o respond to erythropoietin, thrombopoietin, interleukin-3 (IL-3), or granulocyte/macrophage colony-s

179 ulture containing stem cell factor (SCF) and interleukin-3 (IL-3), produced immortalized immature mye

180 crophage colony-stimulating factor (GM-CSF), interleukin-3 (IL-3), steel factor (SF), and thrombopoie

181 y isolated G0CD34(+) cells were activated by interleukin-3 (IL-3), stem cell factor (SCF), and flt3-l

182 phage colony-stimulating factor (GM-CSF) and interleukin-3 (IL-3), was expressed in yeast under the c

183 IH3T3 fibroblasts or cytokine deprivation in interleukin-3 (IL-3)-dependent 32D murine myeloid cells.

184 nd-mediated ALK signaling is investigated in interleukin-3 (IL-3)-dependent 32D murine myeloid cells.

185 ng factor (G-CSF)-induced differentiation of interleukin-3 (IL-3)-dependent 32Dcl3 hematopoietic prec

186 ng to Bim phosphorylation in Ba/F3 cells, an interleukin-3 (IL-3)-dependent B-cell line.

187 TEL/PDGF beta R transforms interleukin-3 (IL-3)-dependent Ba/F3 and 32D cells to IL

188 or in lymphoid cells, we expressed in murine interleukin-3 (IL-3)-dependent Ba/F3 pro-B-lymphocyte ce

189 (R988C and T1010I), when introduced into the interleukin-3 (IL-3)-dependent BaF3 cell line, regulated

190 p55 confers growth factor independence on an interleukin-3 (IL-3)-dependent cell line (Ba/F3) when th

191 f c-Cbl (Cbl-DeltaY371) was expressed in the interleukin-3 (IL-3)-dependent cell line 32Dcl3 to deter

192 these three processes was examined using an interleukin-3 (IL-3)-dependent cell line.

193 t induce PKR activation or inhibit growth of interleukin-3 (IL-3)-dependent cells in the presence of

194 abundant supply of extracellular glutamine, interleukin-3 (IL-3)-dependent cells were unable to main

195 The interleukin-3 (IL-3)-dependent expression of the Id-1 ge

196 By utilizing an interleukin-3 (IL-3)-dependent hematopoietic cell line,

197 Using DNA microarrays to analyze interleukin-3 (IL-3)-dependent murine FL5.12 pro-B cells

198 c hTEL/mJAK2(JH1) fusion gene, transform the interleukin-3 (IL-3)-dependent murine hematopoietic cell

199 c acid (MPA), a specific IMPDH inhibitor, in interleukin-3 (IL-3)-dependent murine hematopoietic cell

200 Expression of this deletion mutant in the interleukin-3 (IL-3)-dependent murine myeloid cell line

201 ion of cell lines derived from 32D cells, an interleukin-3 (IL-3)-dependent murine myeloid cell line.

202 bility of E2A-HLF to prolong the survival of interleukin-3 (IL-3)-dependent murine pro-B cells after

203 h factor deprivation or gamma-irradiation in interleukin-3 (IL-3)-dependent murine pro-B cells.

204 respectively) were expressed in parental H7 interleukin-3 (IL-3)-dependent myeloid cells.

205 nc finger (ZF) protein by screening a murine interleukin-3 (IL-3)-dependent NFS/N1.H7 myeloid cell cD

206 regulation of the promoter in nontransformed interleukin-3 (IL-3)-dependent parental cells.

207 Insulin strongly inhibited apoptosis of interleukin-3 (IL-3)-deprived 32D(IR) cells expressing I

208 Each factor maintained complete survival of interleukin-3 (IL-3)-deprived FDCP-Mix cells but, unexpe

209 n of the RBM6-CSF1R fusion protein conferred interleukin-3 (IL-3)-independent growth in BaF3 cells, a

210 constitutive activation of FLT3, and confers interleukin-3 (IL-3)-independent growth to Ba/F3 and 32D

211 d EGFR-L858R, could transform Ba/F3 cells to interleukin-3 (IL-3)-independent growth, in a ligand-ind

212 n of FLT3-N841I cDNA into Ba/F3 cells led to interleukin-3 (IL-3)-independent proliferation, receptor

213 of the MPRO promyelocytes while potentiating interleukin-3 (IL-3)-induced commitment of EML cells to

214 H-Ras in the inside-out signaling pathway of interleukin-3 (IL-3)-induced integrin activation in the

215 from ATF3-deficient mice are unresponsive to interleukin-3 (IL-3)-induced maturation signals, and thi

216 wth factors, such as erythropoietin (EPO) or interleukin-3 (IL-3).

217 lated in vitro by stem cell factor (SCF) and interleukin-3 (IL-3).

218 in IC.DP premast cells by the withdrawal of interleukin-3 (IL-3).

219 ce both to chemotherapy and to withdrawal of interleukin-3 (IL-3).

220 Expression of bcr-abl in interleukin-3 (IL-3)/granulocyte-macrophage colony-stimu

221 y of Tregs to inhibit the differentiation of interleukin-3 (IL-3)/stem cell factor (colony-forming un

222 grew significantly slower in the presence of interleukin-3 (IL-3); they underwent apoptotic cell deat

223 (HDAC) to silence RUNX1 target genes [e.g., interleukin-3 (IL-3)].We previously reported that expres

224 72 hours of stimulation with growth factors (interleukin-3 [IL-3] 12 ng/mL, stem cell factor 10 ng/mL

225 crophage-colony stimulating factor [GM-CSF], interleukin-3 [IL-3], and granulocyte-CSF [G-CSF]) withi

226 s that promote myeloid cell differentiation (interleukin-3 [IL-3], stem cell factor [SCF], and all-tr

227 rforming representative biomarker assays for interleukin 3 (IL3) and Tumor Necrosis Factor (TNF-alpha

228 Five related cytokine genes, interleukin 3 (Il3), interleukin 4 (Il4), interleukin 5

229 ence of supraphysiological concentrations of interleukin-3 (IL3) and stem cell factor (SCF).

230 cyte and monocyte colony-stimulating factor, interleukin-3 (IL3), and IL5.

231 FLAP disappeared 4 h after withdrawal of interleukin-3 in bcl-xL cells but not in control cells,

232 st cells stimulated with stem cell factor or interleukin-3, in serum-stimulated fibroblasts, or in an

233 pression by the PI3K pathway correlated with interleukin-3 independence and inhibition of differentia

234 Prolonged exposure to Bcr-Abl PTK results in interleukin-3 independent growth and decreased p53 prote

235 Both A1 and pim-1 were required to induce interleukin 3-independent cell growth, inhibit activatio

236 ion are necessary for neuregulin-stimulated, interleukin 3-independent cell proliferation in the 32D/

237 pendent kinase activation, transformation to interleukin 3-independent growth, and relocalization of

238 RKL is required for p210(BCR-ABL) to support interleukin-3-independent growth of myeloid progenitor c

239 the Ba/F3 murine hematopoietic cell line to interleukin-3-independent growth.

240 he murine hematopoietic cell line, Ba/F3, to interleukin-3-independent growth.

241 HIP1/PDGFbetaR transforms the Ba/F3 cells to interleukin-3-independent growth.

242 In addition, ORMDL3 regulates interleukin-3-induced expression of CD48 and CD48-mediat

243 Interleukin-3-induced nuclear translocation of the M2 is

244 soform of pyruvate kinase was sufficient for interleukin-3-induced nuclear translocation.

245 vitronectin, cortisol, AXL receptor kinase, interleukin-3, interleukin-13, matrix metalloproteinase-

246 presence of multiple cytokines (kit ligand, interleukin-3, interleukin-6, and granulocyte colony-sti

247 l factor, Fms-like tyrosine kinase 3 ligand, interleukin-3, interleukin-6, and granulocyte colony-sti

248 of 6 known early-acting cytokines, including interleukin-3, interleukin-6, granulocyte macrophage col

249 um containing a cytokine cocktail (with SCF, interleukin-3, interleukin-6, granulocyte-macrophage col

250 ced production of proinflammatory cytokines (interleukin-3, interleukin-6, interleukin-13, interleuki

251 The monocyte differentiation factors interleukin-3, macrophage colony-stimulating factor (M-C

252 te-macrophage colony-stimulating factor, and interleukin-3 mRNAs.

253 ynergized with stem cell factor but not with interleukin-3 or granulocyte-macrophage colony-stimulati

254 showed normal colony formation stimulated by interleukin-3 or granulocyte-macrophage CSF, and expansi

255 Withdrawal of interleukin-3 or incubation with staurosporine (STS) or

256 e that in lymphocyte cell lines dependent on interleukin-3 or interleukin-7, or primary lymphocytes d

257 The combination of BAH-1 plus interleukin-3 or of BAH-1 plus human TPO significantly i

258 mRNA levels increased rapidly in response to interleukin-3 over the first 24 h of EML cell differenti

259 mobilized from miniature swine with porcine interleukin 3 (pIL-3), porcine stem cell factor (pSCF),

260 (pSCF, 100 microg/kg) and swine recombinant interleukin 3 (pIL-3, 100 microg/kg), administered intra

261 tor (CVF), pig hematopoietic growth factors (interleukin-3 (pIL3) and stem cell factor (pSCF))--or wi

262 and AML1B synergistically transactivated an interleukin 3 promoter reporter gene construct, yet the

263 apoptotic protein, Mcl-1, and the neutrophil interleukin 3 receptor alpha subunit (IL-3Ralpha), sugge

264 Because BPDCN blasts overexpress the interleukin-3 receptor (IL3R), the activity of SL-401, d

265 The interleukin-3 receptor alpha chain (CD123) has been iden

266 5, and were contiguous to DCs expressing the interleukin-3 receptor CD123 or DC-SIGN.

267 ulocyte-macrophage colony-stimulating factor/interleukin-3 receptor driving glycolytic substrate util

268 In addition, expression of components of the interleukin-3 receptor, IL3Ra and the common beta chain,

269 CD123, the transmembrane alpha chain of the interleukin-3 receptor, is expressed in the majority of

270 interleukin (IL)-27 induces nuclear factor, interleukin 3 regulated (NFIL3), which promotes permissi

271 nscriptional repressor NFIL3 (nuclear factor interleukin 3-regulated) hindered FOXO transcription fac

272 IL-10 and is bound by NFIL3 (nuclear factor, interleukin 3-regulated), a B-ZIP transcription factor.

273 cells prevented their apoptotic death after interleukin-3 removal, but Fes(act)-expressing cells rem

274 steel factor (KIT ligand) without affecting interleukin-3 response, whereas a DNA-binding mutant ant

275 nant human (rh) stem cell factor (rhSCF), rh interleukin-3 (rhIL-3; first week only), and rhIL-6.

276 nced the growth of myeloid progenitors in an interleukin 3/stem cell factor (IL-3/SCF)-dependent mann

277 Both basal and interleukin 3-stimulated phosphorylation of Akt on serin

278 In this study, we demonstrate that interleukin-3 stimulation induces a wortmannin-sensitive

279 not affect cell proliferation in response to interleukin-3, suggesting that the effect is specific fo

280 nhanced cell proliferation in the absence of interleukin-3, suggesting that the nuclear pyruvate kina

281 trast, Bcl-x(L)-expressing cells deprived of interleukin-3 survive in a more vegetative state, in whi

282 te-macrophage colony-stimulating factor, and interleukin-3, termed NSG-SGM3.

283 ne growth factors, such as erythropoietin or interleukin-3, through activation of a phosphatidylinosi

284 er, recognized AU-rich sequences from c-fos, interleukin-3, tumor necrosis factor-alpha, and granuloc

285 g Ba/f3 cells in which STAT5 is activated by interleukin-3, we have identified novel STAT5 binding si

286 essed the induction of STAT5 target genes by interleukin-3, whereas the histone deacetylase inhibitor

287 t decrease in translation rate compared with interleukin-3, which is a mitogen for these cells.

288 totic death after Sindbis virus infection or interleukin 3 withdrawal.

289 tants of Bcl-2 had increased protection from interleukin-3 withdrawal and Sindbis virus-induced apopt

290 uced by amino acid starvation, etoposide, or interleukin-3 withdrawal did not affect cell death in th

291 n of the phosphomimetic Bcl2 mutants, either interleukin-3 withdrawal or treatment of cells with the

292 n murine pre-B hematopoietic cells FL5.12 by interleukin-3 withdrawal results in increased associatio

293 death following diverse stress stimuli (e.g. interleukin-3 withdrawal, sodium arsenite treatment, and

294 JNK can suppress interleukin-3 withdrawal-induced apoptosis via phosphory

295 rference renders 32D cells more sensitive to interleukin-3 withdrawal-induced apoptosis, suggesting t

296 vent regulating the activation of BAD during interleukin-3 withdrawal-induced apoptosis.

297 tein family, interacts with Bax and promotes interleukin-3 withdrawal-induced Bax conformational chan

298 3 cells resulted in protection of cells from interleukin-3 withdrawal-induced cell death similar to t

299 gen-activated protein kinase JNK1 suppresses interleukin-3 withdrawal-induced cell death through phos

300 d during cell death following growth factor (interleukin-3) withdrawal is conserved between human and