ライフサイエンスコーパス: Fms-like tyrosine kinase

1 by two homologous tyrosine kinase receptors, fms-like tyrosine kinase 1 (Flt-1) and kinase domain rec

2 Furthermore, VEGF receptor fms-like tyrosine kinase 1 (Flt-1) was elevated, whereas

3 r endothelial growth factor and its receptor fms-like tyrosine kinase 1 (Flt1) were up-regulated, and

4 enhanced expression of PGF and its receptor, FMS-like tyrosine kinase 1 (Flt1).

5 GF-induced phosphorylation of KDR but not of FMS-like tyrosine kinase 1 (FLT1)/VEGF receptor 1.

6 Here we show that FMS-like tyrosine kinase 1 (Flt1, also known as VEGFR1)

7 e placental growth factor (PlGF) and soluble Fms-like tyrosine kinase 1 (sFlt-1) as clinical biomarke

8 or limits angiogenesis by increasing soluble fms-like tyrosine kinase 1 (sFlt-1) gene expression.

9 Excess soluble fms-like tyrosine kinase 1 (sFlt-1) of vascular endothel

10 The ratio of soluble fms-like tyrosine kinase 1 (sFlt-1) to placental growth

11 Excess soluble fms-like tyrosine kinase 1 (sFlt-1), a soluble inhibitor

12 Soluble fms-like tyrosine kinase 1 (sFlt-1), an alternatively sp

13 s of placental growth factor (PlGF), soluble fms-like tyrosine kinase 1 (sFlt-1), and soluble endogli

14 ns of VEGF and its soluble receptor, soluble fms-like tyrosine kinase 1 (sFlt-1), were measured by en

15 data suggest that excess circulating soluble fms-like tyrosine kinase 1 (sFlt-1), which binds placent

16 the disease pathophysiology, such as soluble fms-like tyrosine kinase 1 (sFlt-1).

17 levels of other angiogenic proteins [soluble fms-like tyrosine kinase 1 (sFlt1) and placental growth

18 ured plasma levels of antiangiogenic soluble fms-like tyrosine kinase 1 (sFlt1) and proangiogenic pla

19 Up-regulation of placental soluble fms-like tyrosine kinase 1 (sFlt1) contributes to the pa

20 rictor sensitivity and elevations in soluble fms-like tyrosine kinase 1 (sFLT1), a circulating antian

21 Soluble fms-like tyrosine kinase 1 (sFlt1), a circulating antian

22 g PM, placental trophoblasts produce soluble fms-like tyrosine kinase 1 (sFlt1), also known as solubl

23 Here, we confirm that placental soluble fms-like tyrosine kinase 1 (sFlt1), an antagonist of VEG

24 Alterations in circulating soluble fms-like tyrosine kinase 1 (sFlt1), an antiangiogenic pr

25 , and excess placental production of soluble fms-like tyrosine kinase 1 (sFLT1), an antiangiogenic pr

26 scription of antiangiogenic factors, soluble fms-like tyrosine kinase 1 (sFLT1), and soluble endoglin

27 receptor potential channels (TRPCs), soluble fms-like tyrosine kinase 1 (sFLT1; also known as soluble

28 The angiogenic factors soluble fms-like tyrosine kinase 1 and placental growth factor,

29 uteroplacental tissues, and elevated soluble fms-like tyrosine kinase 1 and soluble endoglin, markers

30 giogenic ligand PlGF and its target receptor fms-like tyrosine kinase 1 modulate vascular growth and

31 The antepartum ratio of soluble fms-like tyrosine kinase 1 to placental growth factor po

32 t tertile of the antepartum ratio of soluble fms-like tyrosine kinase 1 to placental growth factor wa

33 as the antiangiogenic factor, sFLT1 (soluble fms-like tyrosine kinase 1) in the pathogenesis of the m

34 posure to endotoxin (ETX) or sFlt-1 (soluble fms-like tyrosine kinase 1), and in a postnatal model du

35 I, maternal factors, and the sFlt-1 (soluble fms-like tyrosine kinase 1)/PlGF (placental growth facto

36 ted blood pressure, increased plasma soluble fms-like tyrosine kinase 1, and renal dysfunction.

37 This locus is near the FLT1 gene encoding Fms-like tyrosine kinase 1, providing biological support

38 neonatal and maternal outcomes, and soluble fms-like tyrosine kinase 1/placental growth factor ratio

39 difference in neonatal outcomes nor soluble fms-like tyrosine kinase 1/placental growth factor ratio

40 veloped angiogenic biomarker(7), the soluble fms-like tyrosine kinase 1:placental growth factor (sFLT

41 -scavenging soluble VEGF receptor 1 (soluble fms-like tyrosine kinase 1; sFlt-1).

42 lating soluble VEGF receptor (sFlt1 [soluble Fms-like tyrosine kinase 1]).

43 Both LP plasma and soluble FMS-like tyrosine-kinase 1 (sFlt1) in NP plasma abolishe

44 dothelial growth factor (VEGF) receptor-1 or Fms-like tyrosine kinase-1 (Flt-1) but not VEGF receptor

45 receptors, fetal liver kinase-1 (flk-1) and fms-like tyrosine kinase-1 (flt-1), was examined in rat

46 nase (p85) is constitutively associated with FMS-like tyrosine kinase-1 (Flt-1).

47 tein (AGP), soluble endoglin (sEng), soluble fms-like tyrosine kinase-1 (sFlt-1) and placental growth

48 ed higher levels of soluble proteins such as fms-like tyrosine kinase-1 (sFlt-1) and placental growth

49 genic markers, mediated primarily by soluble fms-like tyrosine kinase-1 (sFlt-1) and soluble endoglin

50 s, placental-like growth factor, and soluble Fms-like tyrosine kinase-1 (sFlt-1) are associated with

51 inetics of the antiangiogenic factor soluble Fms-like tyrosine kinase-1 (sFlt-1) in 136 consecutive R

52 regulation of expression of VEGF or soluble fms-like tyrosine kinase-1 (sFlt-1) in both an aortic ri

53 with increased circulating levels of soluble fms-like tyrosine kinase-1 (sFlt-1) in the third trimest

54 Soluble Fms-like tyrosine kinase-1 (sFlt-1) is an antiangiogenic

55 Soluble fms-like tyrosine kinase-1 (sFlt-1) seems to interfere w

56 lampsia is associated with increased soluble fms-like tyrosine kinase-1 (sFlt-1), a circulating antag

57 terised by hypertension and elevated soluble Fms-Like Tyrosine Kinase-1 (sFlt-1).

58 vents, are due to excess circulating soluble fms-like tyrosine kinase-1 (sFlt-1, also referred to as

59 nta-derived growth factor (PLGF) and soluble Fms-like tyrosine kinase-1 (sFLT-1, the soluble form of

60 y to suppress the pathogenic protein soluble FMS-like tyrosine kinase-1 (sFLT1) in a baboon model of

61 However, elevated levels of soluble fms-like tyrosine kinase-1 (sFLT1) in the placenta and i

62 rong evidence that overproduction of soluble fms-like tyrosine kinase-1 (sFLT1) in the placenta is a

63 giogenic factor and preeclampsia risk marker fms-like tyrosine kinase-1 (sFLT1) in the placenta tissu

64 ound, GYY4137, inhibited circulating soluble fms-like tyrosine kinase-1 and soluble endoglin levels a

65 rfering RNA increased the release of soluble fms-like tyrosine kinase-1 and soluble endoglin, as asse

66 m placental growth factor, and serum soluble fms-like tyrosine kinase-1 at 35 to 37 weeks of gestatio

67 on serum placental growth factor and soluble fms-like tyrosine kinase-1 concentrations 1 and 3 weeks

68 nd hemin by abolishing both sEng and soluble fms-like tyrosine kinase-1 induction.

69 giogenesis by inducing both sEng and soluble fms-like tyrosine kinase-1 secretion from human villous

70 nd serum placental growth factor and soluble fms-like tyrosine kinase-1 were measured.

71 immune landscape and serum levels of soluble Fms-like tyrosine kinase-1, a clinical biomarker of pre-

72 ers of endothelial (angiopoetin-1/2, soluble fms-like tyrosine kinase-1, soluble vascular cell adhesi

73 a commonly used standard, the plasma soluble fms-like tyrosine kinase-1/placental growth factor (sFlt

74 'FMS'-like tyrosine kinase 3 (FLT3) mutations in acute my

75 ophage colony stimulating factor I receptor (Fms)-like tyrosine kinase 3 (Flt-3) ligand supported fur

76 re, treatment with Feline McDonough sarcoma (FMS)-like tyrosine kinase 3 ligand (Flt3L) plus ICB ther

77 Mutations of Fms-like tyrosine kinase 3 (FLT3) are among the most fre

78 Activating mutations in FMS-like tyrosine kinase 3 (FLT3) are common in acute my

79 Activating mutations of FMS-like tyrosine kinase 3 (FLT3) are present in approxi

80 Constitutive activation of FMS-like tyrosine kinase 3 (FLT3) by internal tandem dup

81 Mutations in the FMS-like tyrosine kinase 3 (FLT3) gene in 13q12.2 are am

82 Internal tandem duplication (ITD) of fms-like tyrosine kinase 3 (FLT3) in acute myeloid leuke

83 goal of this study was to define the role of FMS-like tyrosine kinase 3 (FLT3) in the heart.

84 nd the ensuing expansion of T(reg) cells are Fms-like tyrosine kinase 3 (Flt3) independent, occur in

85 Fms-like tyrosine kinase 3 (FLT3) inhibition has elicite

86 he efficacy of B-cell lymphoma 2 (BCL-2) and FMS-like tyrosine kinase 3 (FLT3) inhibition with veneto

87 seen to emerge as resistant mutations after FMS-like tyrosine kinase 3 (FLT3) inhibitor therapy.

88 oral, selective, second-generation, type-II FMS-like tyrosine kinase 3 (FLT3) inhibitor with high bi

89 Combining FMS-like tyrosine kinase 3 (FLT3) inhibitors with intens

90 teosome inhibitors, antiangiogenesis agents, Fms-like tyrosine kinase 3 (FLT3) inhibitors, and apopto

91 the discovery of irreversible inhibitors of FMS-like tyrosine kinase 3 (FLT3) involved in the pathog

92 Oncogenic addiction to the Fms-like tyrosine kinase 3 (FLT3) is a hallmark of acute

93 Fms-like tyrosine kinase 3 (FLT3) is a receptor tyrosine

94 FMS-like tyrosine kinase 3 (FLT3) is a receptor tyrosine

95 Fms-like tyrosine kinase 3 (Flt3) is a type III receptor

96 FMS-like tyrosine kinase 3 (FLT3) is almost universally

97 FMS-like tyrosine kinase 3 (FLT3) is considered an impor

98 FMS-like tyrosine kinase 3 (FLT3) is expressed in human

99 FMS-like tyrosine kinase 3 (FLT3) is mutated in approxim

100 Fms-like tyrosine kinase 3 (FLT3) is often overexpressed

101 Signal transduction of FMS-like tyrosine kinase 3 (FLT3) is regulated by protei

102 e myeloid leukemia (AML) and determined that FMS-like tyrosine kinase 3 (FLT3) is transactivated by S

103 xclusively from pre-DCs under the control of fms-like tyrosine kinase 3 (Flt3) ligand, inhibitor of D

104 Fms-like tyrosine kinase 3 (FLT3) mutations are associat

105 Ever since the recognition that FMS-like tyrosine kinase 3 (FLT3) mutations exert a prof

106 Activating FMS-like tyrosine kinase 3 (FLT3) mutations have been id

107 Constitutively activating mutations of FMS-like tyrosine kinase 3 (FLT3) occur in approximately

108 Mutations that activate the fms-like tyrosine kinase 3 (FLT3) receptor are among the

109 rnal tandem duplication (ITD) mutants of the Fms-like tyrosine kinase 3 (Flt3) receptor in leukemogen

110 Internal tandem duplications (ITDs) of the FMS-like tyrosine kinase 3 (FLT3) receptor tyrosine kina

111 The fms-like tyrosine kinase 3 (FLT3) receptor tyrosine kina

112 mia (AML) harbor activating mutations in the FMS-like tyrosine kinase 3 (FLT3) receptor tyrosine kina

113 l-3-kinase (PI3K)/protein kinase B (AKT) and Fms-like tyrosine kinase 3 (FLT3) signaling are aberrant

114 on of HoxA9 and Meis1a and with mutations in FMS-like tyrosine kinase 3 (FLT3) to drive acute leukemi

115 Secondary point mutations in the Fms-like tyrosine kinase 3 (FLT3) tyrosine kinase domain

116 FMS-like tyrosine kinase 3 (FLT3), a class III receptor

117 aled that normal villus epithelium expresses Fms-like tyrosine kinase 3 (Flt3), a known regulator of

118 ation and discovered that ADP transactivates Fms-like tyrosine kinase 3 (Flt3), a receptor tyrosine k

119 cation (ITD) in the juxtamembrane portion of Fms-like tyrosine kinase 3 (FLT3), a type III receptor t

120 The ligand for the receptor tyrosine kinase fms-like tyrosine kinase 3 (flt3), also referred to as f

121 r of the type III receptor tyrosine kinases: FMS-like tyrosine kinase 3 (FLT3), platelet-derived grow

122 iated by HSC-specific genes such as CD34 and Fms-like tyrosine kinase 3 (FLT3), respectively.

123 Small molecule inhibitors that target fms-like tyrosine kinase 3 (FLT3)-activating mutations h

124 Multiple FMS-like tyrosine kinase 3 (FLT3)-inhibitors have been s

125 thal partners with gilteritinib treatment in fms-like tyrosine kinase 3 (FLT3)-internal tandem duplic

126 Signaling pathways regulated by mutant Fms-like tyrosine kinase 3 (FLT3)-internal tandem duplic

127 Rhesus macaques were injected with Fms-like tyrosine kinase 3 (Flt3)-ligand (FL) to expand

128 FMS-like tyrosine kinase 3 (FLT3)-mutant acute myeloid l

129 tion was identified in the gene encoding the Fms-like tyrosine kinase 3 (Flt3).

130 the IL-7 receptor (IL-7R), Janus kinase, and Fms-like tyrosine kinase 3 (FLT3).

131 A 46-year-old white woman with a history of Fms-like tyrosine kinase 3 acute myeloid leukemia presen

132 and primary patient specimens independent of Fms-like tyrosine kinase 3 expression and stromal-mediat

133 expansion, cooperated with mutations in the FMS-like tyrosine kinase 3 gene (Flt3(ITD)) and the nucl

134 internal tandem duplication mutation in the FMS-like tyrosine kinase 3 gene (FLT3-ITD) have a poor p

135 An internal tandem duplication in the fms-like tyrosine kinase 3 gene (FLT3/ITD) is associated

136 is a Janus kinase 2 (JAK2), JAK2(V617F), and Fms-like tyrosine kinase 3 inhibitor that does not inhib

137 isocitrate dehydrogenase 1 and 2 inhibitors, FMS-like tyrosine kinase 3 inhibitors, and menin inhibit

138 In Fms-like tyrosine kinase 3 internal tandem duplication (

139 In Fms-like tyrosine kinase 3 internal tandem duplication (

140 treated with the hematopoietic growth factor fms-like tyrosine kinase 3 ligand (FL), which dramatical

141 C precursors that can be expanded in vivo by Fms-like tyrosine kinase 3 ligand (FL).

142 Fms-like tyrosine kinase 3 ligand (Flt3L) administration

143 and activation of cDC1s by administration of FMS-like tyrosine kinase 3 ligand (Flt3L) and TLR/CD40 a

144 egies to increase the numbers of cDC1s using FMS-like tyrosine kinase 3 ligand (FLT3L) and/or their a

145 observation that Langerin-CD11b- migDCs are Fms-like tyrosine kinase 3 ligand (Flt3L) dependent and

146 Here, we observe subcutaneous immunity is Fms-like tyrosine kinase 3 ligand (Flt3L) dependent.

147 In contrast, injection of FMS-like tyrosine kinase 3 ligand (Flt3L) DNA, which exp

148 und that immunization of wild-type mice with FMS-like tyrosine kinase 3 ligand (Flt3L) DNA, which inc

149 Fms-like tyrosine kinase 3 ligand (Flt3L) expands dendri

150 n the presence of stem cell factor (SCF) and FMS-like tyrosine kinase 3 ligand (FLT3L) give rise to n

151 Fms-like tyrosine kinase 3 ligand (Flt3L) is a hematopoi

152 ested this hypothesis by using DC-deficient, fms-like tyrosine kinase 3 ligand (Flt3L) knockout (KO)

153 Daily treatment of mice with fms-like tyrosine kinase 3 ligand (Flt3L) leads to a sig

154 Fms-like tyrosine kinase 3 ligand (Flt3L) mobilizes stem

155 , leading to the identification of Notch and Fms-like tyrosine kinase 3 ligand (FLT3L) pathways, toge

156 Conversely, endogenous DC expansion using FMS-like tyrosine kinase 3 ligand (Flt3L) protected mice

157 In this study we demonstrate that Fms-like tyrosine kinase 3 ligand (Flt3L) recruits plasm

158 Fms-like tyrosine kinase 3 ligand (Flt3L) reverses the f

159 d deficiency (DCML deficiency) with elevated Fms-like tyrosine kinase 3 ligand (Flt3L) was observed i

160 ge inflammatory protein-1alpha (MIP-1alpha), fms-like tyrosine kinase 3 ligand (Flt3L), and the DNA v

161 regimen with intratumoral administration of Fms-like tyrosine kinase 3 ligand (Flt3L), local irradia

162 ed this by acutely treating intact mice with FMS-like tyrosine kinase 3 ligand (Flt3l), which promote

163 Multiple subsets of FMS-like tyrosine kinase 3 ligand (FLT3L)-dependent dend

164 ne liver pDCs, we expanded them in vivo with fms-like tyrosine kinase 3 ligand (Flt3L).

165 ministration of the potent DC growth factor, fms-like tyrosine kinase 3 ligand (Flt3L).

166 ained in secondary lymphoid organs (SLOs) by Fms-like tyrosine kinase 3 ligand (FLT3L).

167 Mice lacking fms-like tyrosine kinase 3 ligand (Flt3L-/-) as the resu

168 rotein 3alpha (hCCL20/hMIP-3alpha), or human fms-like tyrosine kinase 3 ligand (hFlt3-L), factors pre

169 ce of SphK2 increased the differentiation of FMS-like tyrosine kinase 3 ligand dendritic cells as wel

170 was activated by stem cell factor (SCF) and FMS-like tyrosine kinase 3 ligand in HSCs but SCF, inter

171 Furthermore, we proposed a strategy with Fms-like tyrosine kinase 3 ligand to specifically induce

172 IP-1alpha) and the DC-specific growth factor fms-like tyrosine kinase 3 ligand with the DNA vaccine r

173 ivo was achieved by overexpression of FLT3L (Fms-like tyrosine kinase 3 ligand), while the effect of

174 SCs in normal mice in response to SCF, IL-7, fms-like tyrosine kinase 3 ligand, and IL-15.

175 nes, including caveolin-1, semaphorin E, and FMS-like tyrosine kinase 3 ligand, have putative roles i

176 ter their stimulation with stem cell factor, Fms-like tyrosine kinase 3 ligand, interleukin-3, interl

177 DC progenitors and accumulate in response to Fms-like tyrosine kinase 3 ligand, yet appear divergent

178 lls were defective in generating pDCs in the fms-like tyrosine kinase 3 ligand-based culture system a

179 DC differentiation depends on IRF-4, whereas Fms-like tyrosine kinase 3 ligand-mediated differentiati

180 freshly isolated, immunobead-purified (>90%) fms-like tyrosine kinase 3 ligand-mobilized C57BL/10 (B1

181 DNA that encoded the secreted form of human fms-like tyrosine kinase 3 ligand.

182 The protein kinase fms-like tyrosine kinase 3 receptor (Flt3) has an import

183 ns leading to constitutive activation of the FMS-like tyrosine kinase 3 receptor (FLT3) occur in blas

184 The ligand for the FMS-like tyrosine kinase 3 receptor (Flt3L) is necessary

185 ndritic cells (cDCs) requires the ligand for FMS-like tyrosine kinase 3 receptor (flt3L), but little

186 transcriptional and epigenetic landscape of fms-like tyrosine kinase 3(+) (Flt3(+)) DC progenitors a

187 tion activating gene 1(+) lymphomyeloid, and Fms-like tyrosine kinase 3(+) fetal monocyte lineages.

188 ion with the receptor tyrosine kinases FLT3 (Fms-like tyrosine kinase 3) or KIT-induced ligand indepe

189 ations of the receptor tyrosine kinase FLT3 (Fms-like tyrosine kinase 3) play an important role in le

190 Recently, Flt3 (Fms-like tyrosine kinase 3)-ligand has been identified a

191 DC), the majority of which were derived from fms-like tyrosine kinase 3-dependent pre-DC, and CD11b(+

192 enic tyrosine kinases, including BCR-ABL and FMS-like tyrosine kinase 3-internal tandem duplication (

193 discuss their discovery that methylation of fms-like tyrosine kinase 3-internal tandem duplication (

194 a network of regulatory loops driven by the FMS-like tyrosine kinase 3-internal tandem duplication (

195 efractory acute myeloid leukaemia (AML) with FMS-like tyrosine kinase 3-internal tandem duplication (

196 etic cell transplant (HCT) for patients with FMS-like tyrosine kinase 3-internal tandem duplication (

197 In FMS-like tyrosine kinase 3-internal tandem duplication (

198 FMS-like tyrosine kinase 3-internal tandem duplication (

199 f a juxtamembrane mutation in the FLT3 gene (FMS-like tyrosine kinase 3-internal tandem duplication [

200 Distinct expression patterns for FMS-like tyrosine kinase 3-internal tandem duplication w

201 Increases in fms-like tyrosine kinase-3 (FLT-3) ligand, reflecting FL

202 in or point mutation in the kinase domain of FMS-like tyrosine kinase-3 (FLT-3) mediates ligand-indep

203 yrosine kinase domain (TKD) mutations of the fms-like tyrosine kinase-3 (FLT3) gene in acute myeloid

204 We examined 6 different FMS-like tyrosine kinase-3 (FLT3) inhibitors (lestaurtin

205 Fms-like tyrosine kinase-3 (FLT3) inhibitors have been u

206 Fms-like tyrosine kinase-3 (Flt3) ligand (FL) and Interl

207 viously demonstrated that pretreatments with fms-like tyrosine kinase-3 (Flt3) ligand (Flt3L), a dend

208 In a randomized trial of therapy for FMS-like tyrosine kinase-3 (FLT3) mutant acute myeloid l

209 al tandem duplication (ITD) mutations of the FMS-like tyrosine kinase-3 (FLT3) receptor found in acut

210 Activating mutations of the FMS-like tyrosine kinase-3 (FLT3) receptor occur in appr

211 andem duplication (ITD) mutations within the FMS-like tyrosine kinase-3 (FLT3) render the receptor co

212 FMS-like tyrosine kinase-3 (FLT3) tyrosine kinase inhibi

213 r of clinical trials testing the efficacy of FMS-like tyrosine kinase-3 (FLT3) tyrosine kinase inhibi

214 Mutant Fms-Like Tyrosine kinase-3 (FLT3), which is expressed in

215 The clinical benefit of adding FMS-like tyrosine kinase-3 (FLT3)-directed small molecul

216 FMS-like tyrosine kinase-3 (FLT3)-internal tandem duplic

217 rbor a constitutively activating mutation in FMS-like tyrosine kinase-3 (FLT3).

218 cluding 14 (93%) of 15 patients with mutated FMS-like tyrosine kinase-3 (FLT3; the 15th patient had c

219 verexpression have been identified including FMS-like tyrosine kinase-3 and nucleophosmin, which will

220 Fms-like tyrosine kinase-3 ligand (Flt3L) is a hemopoiet

221 mon DC progenitor with conventional DCs, and Fms-like tyrosine kinase-3 ligand is essential for their

222 rsely, DC expansion induced either by Flt3L (fms-like tyrosine kinase-3 ligand) or adoptive transfer

223 kin-7, interleukin-15, stem cell factor, and fms-like tyrosine kinase-3 ligand).

224 endothelial cells were identified: endoglin, Fms-like tyrosine kinase-3 ligand, EGF-like repeats and

225 Internal tandem duplication of the Fms-like tyrosine kinase-3 receptor (FLT3) internal tand

226 ecreased in Mysm1(-/-) mice and defective in Fms-like tyrosine kinase-3(Flt3) ligand-induced, but not

227 Based on fms-like tyrosine kinase-3-internal tandem duplication m

228 l cell line-derived neurotrophic factor, and FMS-like tyrosine kinase-3.

229 e myeloid leukaemia (AML) have a mutation in FMS-like-tyrosine-kinase-3 (FLT3).

230 acute respiratory distress syndrome, soluble fms-like tyrosine kinase decreased more quickly and von

231 ert domain-containing receptor (KDR) and the fms-like tyrosine kinase (Flt).

232 eraction with two receptor tyrosine kinases, fms-like tyrosine kinase (Flt-1) or VEGF receptor 1 and

233 ty for soluble kinase domain region (KDR) or Fms-like tyrosine kinase (FLT-1) receptors.

234 ain-containing receptor [KDR]), and VEGF-R1 (fms-like tyrosine kinase [Flt]) in bovine retinal endoth

235 Internal tandem duplication of the FMS-like tyrosine kinase (FLT3-ITD) receptor is present

236 ML) have an activating mutation in the FLT3 (fms-like tyrosine kinase) gene, which represents a targe

237 ated levels of hemopoietic cytokines such as fms-like tyrosine kinase ligand (FLT3-L, a dendritic cel

238 We tested the prediction that expression of fms-like tyrosine kinase ligand 3 (Flt3L) in the brain w

239 mpartment was associated with elevated serum fms-like tyrosine kinase ligand and reduced circulating

240 containing receptor, or VEGFR-2) and Flt-1 (fms-like tyrosine kinase, or VEGFR-1).

241 inding to the kinase domain receptor and the Fms-like tyrosine kinase receptor (Flt-1), the extracell

242 rosine kinase receptors, VEGF receptor 1 [or fms-like tyrosine kinase receptor (Flt-1)] and VEGF rece

243 PO), placental growth factor (PlGF), soluble fms-like tyrosine kinase receptor (sFlt)-1, and galectin

244 mediated by soluble VEGF receptor 1/soluble Fms-like tyrosine kinase receptor 1 and soluble endoglin

245 We studied the effects of fms-like tyrosine kinase receptor 3 ligand (Flt3-L) or G

246 Fms-like tyrosine kinase receptor 3-ligand (Flt3-L) and

247 tion of specific DC subsets-using GM-CSF and fms-like tyrosine kinase receptor 3-ligand (Flt3-L)-on t

248 ie2 (sTie2) and VEGF signalling with soluble Fms-like tyrosine kinase receptor-1 (sFlt1).

249 levels of brain natriuretic factor, soluble fms-like tyrosine kinase receptor-1, troponin I, and cre

250 oxidase, B-type natriuretic peptide, soluble fms-like tyrosine kinase receptor-1, troponin I, soluble

251 Activating mutations in FMS-like tyrosine kinase receptor-3 (FLT3) and Nucleopho

252 ically linked to the extracellular domain of Fms-like tyrosine kinase receptor-3 ligand (FLex; a DC g

253 We conclude that fms-like tyrosine kinase receptor-3 signaling is require

254 ethymic signal through the cytokine receptor fms-like tyrosine kinase receptor-3 was required for the

255 controlled in part by regulatory T cells and fms-like tyrosine kinase receptor-3.

256 asma angiogenic factor expression of soluble fms-like tyrosine kinase (sFlt)-1.

257 Soluble Fms-like tyrosine kinase (sFlt-1/sVEGFR1) is a naturally

258 vascular endothelial growth factor, soluble fms-like tyrosine kinase, von Willebrand factor, E-selec