ライフサイエンスコーパス: VEGFR-3

1 l form, which showed preferential binding to VEGFR-3.

2 sions and affected colocalization of FAK and VEGFR-3.

3 ve shown the physical association of FAK and VEGFR-3.

4 rg(108)) is critical for binding VEGFR-2 and VEGFR-3.

5 VEGF receptor (VEGFR)-1, but not VEGFR-2 or VEGFR-3.

6 t Src family kinases are upstream of PKC and VEGFR-3.

7 ired for H(2)O(2)-induced phosphorylation of VEGFR-3.

8 PI3K activator prevented the effects of anti-VEGFR-3.

9 healthy adult blood donors are positive for VEGFR-3.

10 imilar degree of tyrosine phosphorylation of VEGFR-3.

11 helial receptor tyrosine kinases VEGFR-2 and VEGFR-3.

12 othelial hyaluronan receptor 1 (LYVE-1), and VEGFR-3.

13 nism involving signaling of both VEGFR-2 and VEGFR-3.

14 ermal macrophages themselves did not express VEGFR-3.

15 different growth factor receptors, including VEGFR-3.

16 EC-expressed growth factor receptors such as VEGFR-3.

17 inase 1/2 (ERK1/2), a downstream effector of VEGFR-3.

18 ynthesis and promoted protein degradation of VEGFR-3.

19 Anti-VEGFR-3 abolished CCL21 gradients around lymphatics, alt

20 cells resulted in the formation of adherent VEGFR-3(+)Ac-LDL(+) (Ac-LDL = acetylated low-density lip

21 Normally, VEGFR-3 activates Akt signaling in lymphatic endothelial

22 provide direct evidence for the key role of VEGFR-3 activation in metastasis.

23 Inhibition of VEGFR-3 activation more potently suppressed regional and

24 eraction (Arg737) compromised VEGF-C induced VEGFR-3 activation.

25 scular endothelial growth factor receptor 3 (VEGFR-3) ameliorated aGVHD and improved survival in muri

26 re ECs do not express CD133, coexpression of VEGFR-3 and CD133 on CD34(+) cells identifies a unique p

27 f (1) inhibiting the biochemical function of VEGFR-3 and FAK, (2) inhibiting proliferation of a diver

28 he protein-protein interface between FAK and VEGFR-3 and identified compound C4 (chloropyramine hydro

29 O(2) induced the tyrosine phosphorylation of VEGFR-3 and its association with the signaling adaptor p

30 een beta(1) integrin and VEGFR-3 in both 293/VEGFR-3 and primary DMEC cells.

31 Here, we identified VEGFR-3 and Prox1 as downstream targets of the NF-kappaB

32 ssion of lymphatic specific genes, including VEGFR-3 and Prox1.

33 s VEGF-C, thereby blocking signaling through VEGFR-3 and suppressing lymphangiogenesis induced by VEG

34 was down-regulated around lymphatics by anti-VEGFR-3 and this was dependent on heparanase-mediated de

35 The VEGF-C/VEGFR-3 and VEGF-A/VEGF-R2 signaling pathways are two of

36 This nuanced understanding of VEGFR-3 and VEGF-C in stroke pathology advises caution r

37 trate, for the first time, the expression of VEGFR-3 and VEGF-C on tissue DC, which implicate a novel

38 Both VEGFR-3 and VEGFR-2 were involved in corneal suture-indu

39 zed to receive intraperitoneal injections of VEGFR-3 and VLA-1-neutralizing antibodies or their contr

40 placental growth factor (PlGF), VEGFR-1, and VEGFR-3 and, at term, VEGF-A, PlGF, and VEGFR-1.

41 Neutralizing antibodies against VEGFR-3 and/or VEGFR-2 were administrated systemically w

42 scular endothelial growth factor receptor 3 (VEGFR-3) and podoplanin.

43 scular endothelial growth factor receptor-3 (VEGFR-3) and Prox1.

44 ced 68% by blocking VEGFR-2, 83% by blocking VEGFR-3, and 99% by blocking both receptors.

45 growth factor receptor (VEGFR) -1, VEGFR-2, VEGFR-3, and c-kit.

46 nase receptor proteins-VEGFR-1, VEGFR-2, and VEGFR-3, and identify novel inhibitors for Vascular Endo

47 elial growth factor C (VEGF-C), its receptor VEGFR-3, and lymphangiogenesis during development of exp

48 a VEGF-C/-D/VEGFR-3-independent pathway as a VEGFR-3 antagonist selectively inhibited VEGF-C-induced,

49 Systemic treatment with either VEGFR-2 or VEGFR-3 antagonistic antibodies suppressed tumor lymphan

50 The administration of anti-VEGFR-3 antibodies did not interfere with hematopoietic

51 ion treatment with the anti-VEGFR-2 and anti-VEGFR-3 antibodies more potently decreased lymph node an

52 scular endothelial growth factor receptor 3 (VEGFR-3) antibody to block lymphangiogenesis in mice.

53 that signals from both beta(1) integrin and VEGFR-3 are required for this cell function.

54 scular endothelial growth factor receptor-3 (VEGFR-3) are protein tyrosine kinases that are overexpre

55 scular endothelial growth factor receptor 3 (VEGFR-3) are the major lymphatic growth factor and recep

56 genic growth factor VEGF-C and its receptor, VEGFR-3, are essential for SC development.

57 ke phenotype of the SC, implicate VEGF-C and VEGFR-3 as critical regulators of SC lymphangiogenesis,

58 ox 1-enhanced green fluorescence protein and VEGFR-3 as markers.

59 Overexpression of VEGFR-3 attenuated CPX inhibition of ERK1/2 phosphorylat

60 ness of preexisting lymphatic endothelium to VEGFR-3 binding factors, VEGF-C and VEGF-D, ultimately r

61 156S, a mutant form of VEGF-C with selective VEGFR-3 binding, alleviates an established rejection res

62 In addition, in the VEGFR-3 blockade group, the percent reduction of HA is s

63 plantation of an 80-ng bFGF micropellet with VEGFR-3 blockade.

64 Phe(93) to Thr(98), is required for binding VEGFR-3 but not VEGFR-2.

65 xpression of podoplanin and VEGF receptor 3 (VEGFR-3) but not of LYVE-1 and prospero homeobox protein

66 During contact hypersensitivity, VEGFR-3, CCL21, and HS expression were all attenuated, a

67 By comparison, VEGFR-3, CD31, and CD105 had decreases in the range of 2

68 Analysis of the human VEGFR-3 cDNA and genomic sequence reveals that these two

69 CD34(+)VEGFR-3(+) cells from fetal liver coexpress the stem/pre

70 Incubation of isolated CD34(+)VEGFR-3(+) cells in EC growth medium resulted in a stron

71 racterized the phenotype and distribution of VEGFR-3(+) cells.

72 feration (40-fold in 2 weeks) of nonadherent VEGFR-3(+) cells.

73 let-derived growth factor receptor beta, and VEGFR-3 cellular receptor autophosphorylation was also o

74 3 (VEGFR-3) expression, as overexpression of VEGFR-3 conferred partial resistance to CPX inhibitory e

75 that human CD34(+)CD133(+) cells expressing VEGFR-3 constitute a phenotypically and functionally dis

76 he association between the NH(2) terminus of VEGFR-3, containing the peptide identified by phage disp

77 interventions that inhibit gB activation of VEGFR-3 could be useful in the treatment of this neoplas

78 A structural model of the VEGF-C/VEGFR-3 D1-7 complex derived from small-angle X-ray scat

79 complex with VEGFR-3 domains D1-2 and of the VEGFR-3 D4-5 homodimer.

80 VEGFR-3(+) DC are CD11c(+)CD45(+)CD11b(+), and are mostl

81 VEGFR-3(+) DC in normal corneas are VEGF-C(-)neuropilin-

82 on, there is rapid increase in the number of VEGFR-3(+) DC in the cornea associated with heightened m

83 A thermodynamic analysis of VEGFR-3 deletion mutants showed that D3, D4-5, and D6-7

84 In vivo, long-term activation or blockade of VEGFR-3 did not affect steady-state murine megakaryopoie

85 Inhibition of VEGFR-2/VEGFR-3 did not prevent the formation of BALT.

86 Interestingly, knockdown of VEGFR-3 does not affect galectin-8-mediated lymphatic en

87 crystal structures of VEGF-C in complex with VEGFR-3 domains D1-2 and of the VEGFR-3 D4-5 homodimer.

88 d whether a combined blockade of VEGFR-2 and VEGFR-3 effectively suppresses early-, middle-, or late-

89 Consequently, higher levels of VEGFR-3 enable stimulation of LECs with VEGF-C which is

90 However, the origin of VEGFR-3(+) endothelial cells (ECs) and the mechanisms by

91 inhibited VEGF-C-induced phosphorylation of VEGFR-3, ERK1/2, and AKT.

92 Furthermore, we observed that VEGFR-3 expression and activation enhance KSHV infection

93 blots and immunostaining revealed VEGF-C and VEGFR-3 expression in CNV lesions, mainly in macrophages

94 inflammatory stimuli also elevated Prox1 and VEGFR-3 expression in cultured lymphatic endothelial cel

95 Here we define VEGFR-3 expression in GEnC and investigate the effects o

96 We report that Notch induces VEGFR-3 expression in vitro in human endothelial cells a

97 ity decreased more than 70%, and VEGFR-2 and VEGFR-3 expression was reduced in surviving endothelial

98 del, following local phVEGF-C gene transfer, VEGFR-3 expression was significantly increased.

99 ergizes with the p50 of NF-kappaB to control VEGFR-3 expression.

100 rized by blood vessels that are positive for VEGFR-3 expression.

101 scular endothelial growth factor receptor-3 (VEGFR-3) expression, as overexpression of VEGFR-3 confer

102 VEGF-C and VEGFR-3 expressions were examined with immunohistochemis

103 rol several lineage-specific genes including VEGFR-3, FGFR-3, and neuropilin-1 and is required along

104 urn, interaction of VEGF-C with its receptor VEGFR-3 (FLT-4) promotes leukemia survival and prolifera

105 nases, including VEGFR-1/Flt-1, VEGFR-2/KDR, VEGFR-3/Flt-4, the platelet-derived growth factor recept

106 opment of these vessels depends on Vegfc and VEGFR-3/Flt4 signaling.

107 scular endothelial growth factor receptor 3 (VEGFR-3/FLT4) is a receptor tyrosine kinase that regulat

108 rozygous for null alleles of both Notch1 and VEGFR-3 had significantly reduced viability and displaye

109 Although VEGFR-3 has been linked primarily to the regulation of l

110 Mutations in VEGFR-3 have been identified in patients with primary ly

111 VEGFR-2/VEGFR-3 heterodimers were more abundant in the dilated l

112 red for VEGF-D to drive formation of VEGFR-2/VEGFR-3 heterodimers which have recently been shown to p

113 ), and by inhibition of VEGF-C activity with VEGFR-3-Ig (AdVEGFR-3-Ig).

114 contrast, inhibition of VEGF-C activity with VEGFR-3-Ig inhibited lymphangiogenesis and angiogenesis

115 In response to dermal immunization, K14-VEGFR-3-Ig mice produced lower Ab titers.

116 ll-mediated CHS responses were strong in K14-VEGFR-3-Ig mice, but importantly, their ability to induc

117 tact hypersensitivity (CHS) challenge in K14-VEGFR-3-Ig mice, which lack dermal lymphatic capillaries

118 Functionally, specific activation of VEGFR-3 impaired the transition to polyploidy of CD41+ c

119 act genetically, that Notch directly induces VEGFR-3 in blood endothelial cells to regulate vascular

120 an association between beta(1) integrin and VEGFR-3 in both 293/VEGFR-3 and primary DMEC cells.

121 CLEC14A formed a complex with VEGFR-3 in endothelial cells (ECs), and CLEC14A KO resul

122 tics to target the signaling between FAK and VEGFR-3 in human tumors.

123 the present study, we demonstrate a role for VEGFR-3 in megakaryopoiesis.

124 s strongly, suggesting a regulatory role for VEGFR-3 in megakaryopoiesis.

125 ut not the lymphoedema-linked mutant form of VEGFR-3 in porcine artery endothelial cells significantl

126 However, activation of VEGFR-3 in sublethally irradiated mice resulted in signi

127 in the increased tyrosine phosphorylation of VEGFR-3 in the absence of a cognate ligand.

128 GEnC expressed VEGFR-3 in tissue sections and culture, and VEGF-C incre

129 the lymphangiogenic receptor tyrosine kinase VEGFR-3 in venous endothelial cells in postnatal mice.

130 Moreover, activation of VEGFR-3 increased platelet counts in thrombopoietin-trea

131 ulated lymphangiogenesis through a VEGF-C/-D/VEGFR-3-independent pathway as a VEGFR-3 antagonist sele

132 d not influence binding to either VEGFR-2 or VEGFR-3, indicating distinct determinants of receptor bi

133 Thus, the VEGFR-3-induced lymphatic endothelial cell tip cell form

134 2 phosphorylation, whereas downregulation of VEGFR-3 inhibited ERK1/2 phosphorylation in LECs.

135 of the wild-type but not the mutant form of VEGFR-3 inhibited H(2)O(2)-induced apoptosis.

136 However, the blockade of VEGFR-3 inhibited only LV (P=0.0002) without concurrent

137 acological blockade of lymphangiogenesis via VEGFR-3 inhibition results in increased corneal thicknes

138 The use of a VEGFR-3 inhibitor prevented lymphangiogenesis and led to

139 These results demonstrate that Notch1 and VEGFR-3 interact genetically, that Notch directly induce

140 Our data demonstrate that the FAK-VEGFR-3 interaction can be targeted by small druglike mo

141 Thus, the FAK/VEGFR-3 interaction may have a potential use to develop

142 ition to its involvement with cell survival, VEGFR-3 is a primary factor in lymphatic angiogenesis.

143 VEGFR-3 is a transmembrane receptor tyrosine kinase that

144 ne and primary murine BM cells, we show that VEGFR-3 is expressed on megakaryocytic progenitor cells

145 We have also shown that VEGFR-3 is overexpressed in human breast tumors and canc

146 scular endothelial growth factor receptor-3 (VEGFR-3) is a primary modulator of lymphatic endothelial

147 We have studied the expression of VEGFR-3, its ligand VEGF-C and the co-receptor neuropili

148 trophils, and epithelial cells expressed the VEGFR-3 ligands VEGF-C or VEGF-D.

149 ndent on VEGF-A/VEGFR-2 signaling but not on VEGFR-3 ligands.

150 lymphangiogenesis, showing its dependence on VEGFR-3 ligands.

151 are not known, and the possible existence of VEGFR-3(+) lymphatic or vascular EC progenitors has not

152 l analysis using lymphatic-specific markers: VEGFR-3, lymphatic endothelial hyaluronan receptor-1, to

153 not co-express any lymphatic markers such as VEGFR-3, LYVE-1 or SLC.

154 Regulating the function of VEGFR-3 may therefore be a mechanism for modulating adap

155 mation at least, in part, through inhibiting VEGFR-3-mediated ERK signaling pathway.

156 VEGFR-3-mediated lymphangiogenesis thus appears to modul

157 Intriguingly, the VEGFR-3-mediated signaling was required for the lymphati

158 rap (sVEGFR-3) and antibody directed against VEGFR-3 (mF4-31C1) significantly reduced tumor lymphangi

159 lial cells (LECs), whereas downregulation of VEGFR-3 mimicked the effect of CPX, blocking the tube fo

160 VEGF-C phosphorylated VEGFR-2 but not VEGFR-3, myosin light chain-2, or VE-cadherin.

161 VEGFR-3 neutralization for 2 weeks before mating blocked

162 lymphatic imaging to determine the effect of VEGFR-3 neutralization on lymph transport from paws to d

163 erine blood or lymphatic vascular densities, VEGFR-3 neutralization reduced serum and ovarian estradi

164 Embryos from VEGFR-3-neutralized dams developed normally when transfe

165 Compared with IgG treatment, VEGFR-3 neutralizing antibody treatment significantly de

166 scular endothelial growth factor receptor 3 (VEGFR-3) neutralizing antibody, VEGFR-2 neutralizing ant

167 Through induction of VEGFR-3, Notch increased endothelial cell responsiveness

168 trate, for the first time, the expression of VEGFR-3 on corneal dendritic cells (DC) and its up-regul

169 Recent evidence also suggests expression of VEGFR-3 on some tumor-associated macrophages.

170 scular endothelial growth factor receptor 3 (VEGFR-3) on the surface of microvascular endothelial cel

171 atment with blocking antibody against either VEGFR-3 or beta(1) integrin inhibited cell migration ind

172 r FN was able to induce the migration of 293/VEGFR-3 or DMEC cells to a limited extent.

173 scular endothelial growth factor receptor-3 (VEGFR-3 or Flt4) that appeared to be required for cell m

174 The tyrosine phosphorylation of VEGFR-3 or isoforms of PKC was completely inhibited by t

175 troducing a mutation at the kinase domain of VEGFR-3 or treatment with blocking antibody against eith

176 By using VEGFR-3-transfected 293 cells (293/VEGFR-3) or primary dermal microvascular endothelial cel

177 We then coupled a 12-amino-acid VEGFR-3 peptide, AV3, to a TAT cellular penetration sequ

178 FLT4 rs307826 increased VEGFR-3 phosphorylation, membrane trafficking, and recep

179 ndothelial growth factor receptor (VEGFR)-2, VEGFR-3, platelet-derived growth factor receptor beta, F

180 Vascular endothelial growth factor-3 (VEGFR-3) plays a critical role in embryonic cardiovascul

181 The proportion of neointestinal VEGFR-3-positive cells increased and ultimately, tubular

182 The 10.1.1 antibody recognizes VEGFR-2- and VEGFR-3-positive lymphatic sinuses and vessels within ly

183 Anti-VEGFR-3 prevented migration of CD4 T cells into lymphati

184 Blockade of VEGFR-3 promoted endoreplication consistently.

185 /suppressor of hairless/Lag1 (CSL) bound the VEGFR-3 promoter and transactivated VEGFR-3 specifically

186 1, and both NF-kappaB and Prox1 activate the VEGFR-3 promoter leading to increased receptor expressio

187 VEGF-C signaling through VEGFR-3 promotes lymphangiogenesis, which is a clinicall

188 ptor tyrosine kinases, VEGFR-1, VEGFR-2, and VEGFR-3, promoting angiogenic and lymphangiogenic signal

189 These studies suggest that VEGFR-3 protects against oxidative damage in endothelial

190 and D mediate lymphangiogenesis through the VEGFR-3 receptor on lymphatic endothelia.

191 blished inhibitors for VEGFR-1, VEGFR-2, and VEGFR-3 receptor proteins.

192 F-C-mediated Erk1/2 activation and abrogated VEGFR-3 receptor-dependent binding of VEGF-C to the lymp

193 Both VEGFR-2 and VEGFR-3 receptors were shown to be expressed in human sa

194 structural homology and activate VEGFR-2 and VEGFR-3, receptors on endothelial cells that signal for

195 scular endothelial growth factor receptor 3 (VEGFR-3) regulates cardiovascular development and physio

196 gh signaling via VEGF receptor (VEGFR)-2 and VEGFR-3, respectively.

197 sessed after antibody blockade of VEGFR-2 or VEGFR-3 RESULTS: Although high-dose bFGF stimulation ind

198 the results here show that the expression of VEGFR-3(S) is up-regulated in >75% of HBxAg positive hep

199 In conclusion, HBxAg may short circuit VEGFR-3(S) signaling in liver cancer.

200 Blocking VEGFR-3(S) signaling may be effective in preventing tumo

201 VEGFR-3(S) siRNA partially blocked the ability of HBxAg

202 VEGFR-3(S) up-regulation correlates with the expression

203 factor receptor-3 short form splice variant (VEGFR-3(S)) expression in HBxAg positive compared to neg

204 sed tumor lymphangiogenesis, indicating that VEGFR-3 signaling affects the rate of tumor cell entry i

205 n Adipo-VD mice during stress in vivo and if VEGFR-3 signaling afforded neuroprotection to challenged

206 VEGF-C/VEGFR-3 signaling and genotoxic stress-induced IL6 drive

207 20 genes that encode proteins acting around VEGFR-3 signaling but also downstream of other tyrosine

208 Inhibition of VEGFR-3 signaling completely prevented the growth of lym

209 iogenesis and vascular permeability and that VEGFR-3 signaling does not compensate for VEGFR-2 blocka

210 Chronic VEGFR-3 signaling in Adipo-VD subcutaneous adipose tissu

211 In vitro, we found that chronic elevation of VEGFR-3 signaling in developing mVC neurons changes the

212 cular homeostasis by fine-tuning VEGFR-2 and VEGFR-3 signaling in ECs, suggesting its relevance in th

213 Overall, chronically increasing VEGFR-3 signaling in neurons has a synergistic impact on

214 Here, we provide evidence that activation of VEGFR-3 signaling in response to hydrogen peroxide (H(2)

215 es during the development of OAD, and VEGF-C/VEGFR-3 signaling modulated innate and adaptive immune r

216 endothelial growth factor receptor (VEGFR)-2/VEGFR-3 signaling of lung lymphatics in sustained inflam

217 VEGFR-3 signaling plays an important role in development

218 Blockade of either VEGFR-2 or VEGFR-3 signaling reduces both HA and LA; however, the p

219 Vascular endothelial growth factor C/VEGFR-3 signaling through PI3Kalpha regulates the activi

220 Blockade of VEGFR-3 signaling using a small-molecule inhibitor inhib

221 vical lymph nodes and is regulated by VEGF-C/VEGFR-3 signaling.

222 eling and improved resistance to stress with VEGFR-3 signaling.

223 scular endothelial growth factor receptor-3 (VEGFR-3) signaling significantly suppresses corneal anti

224 ocampus of adult mice through VEGF receptor (VEGFR-3) signaling.

225 Our results thus suggest VEGFR-3-signaling as a novel strategy to regulate T-cell

226 Here, we investigated the effect of chronic VEGFR-3-specific activation on adipose arbor morphometry

227 The effects of VEGF-C156S, a VEGFR-3-specific agonist, and VEGF-A were also studied.

228 rate that implantation of pellets containing VEGFR-3-specific ligands (VEGF-C156S and recombinant mur

229 The implantation of pellets containing VEGFR-3-specific ligands also leads to the recruitment o

230 eduction of HA is significantly greater with VEGFR-3-specific ligands than that by VEGF-A or VEGF-C.

231 Consequently, a VEGFR-3-specific neutralizing antibody markedly inhibite

232 Collectively, our data suggest that VEGFR-3-specific signaling can induce new blood vessels,

233 ound the VEGFR-3 promoter and transactivated VEGFR-3 specifically in endothelial cells.

234 stimulator of hemangiogenesis (HA), whereas VEGFR-3 stimulates lymphangiogenesis (LA).

235 argeting domain of FAK and was homologous to VEGFR-3, suggesting these two tyrosine kinases physicall

236 truncated isoform of this molecule, soluble VEGFR-3 (sVEGFR-3), which is critical for corneal alymph

237 million compounds for VEGFR-1, VEGFR-2, and VEGFR-3 targets.

238 wed by sequential up-regulation of Prox1 and VEGFR-3 that preceded lymphangiogenesis by 4 and 2 days,

239 CLEC14A KO resulted in a marked reduction in VEGFR-3 that was concomitant with increases in VEGFR-2 e

240 ependence of lymphangiectasia on VEGFR-2 and VEGFR-3, the condition was not reversed by blocking both

241 Anti-VEGFR-3 therapy had no significant impact on growth of m

242 t whilst in the mouse there is only a single Vegfr-3 transcript, in humans there are two transcripts

243 By using VEGFR-3-transfected 293 cells (293/VEGFR-3) or primary d

244 Our data show that anti-VEGFR-3 treatment ameliorates lethal aGVHD and identifie

245 phosphorylation of the major VEGF-C receptor VEGFR-3 upon VEGF-C stimulation.

246 to investigate whether combined blockade of VEGFR-3 (vascular endothelial growth factor receptor-3)

247 eno-associated viral vector-mediated soluble VEGFR-3 (VEGF-C/D Trap) completely blocked lymphangiogen

248 Tammela et al. in Nature show that VEGFR-3, via Notch regulation, is present on endothelial

249 This increased tyrosine phosphorylation of VEGFR-3 was diminished by pretreatment with a blocking a

250 en or FN-induced tyrosine phosphorylation of VEGFR-3 was inhibited by treatment with cytochalasin D,

251 e, a hereditary lymphoedema-linked mutant of VEGFR-3 was not phosphorylated by H(2)O(2) treatment.

252 Blockade of VEGFR-3 was sufficient to inhibit the development of lym

253 In vivo, VEGFR-3 was upregulated in endothelial cells with active

254 mation of coronary arteries, whereas soluble VEGFR-3 was without effect.

255 A, exhibited enhanced potency for activating VEGFR-3, was able to promote increased COX-2 mRNA levels

256 al antibodies to the extracellular domain of VEGFR-3, we show that 11% +/- 1% of CD34(+) cells isolat

257 c growth in adult mice, but both VEGFR-2 and VEGFR-3 were required for the development of lymphangiec

258 cated by staining with laminin, VEGFR-2, and VEGFR-3, whereas Ad-VEGF-A(165) stimulated the selective

259 scular endothelial growth factor receptor 3 (VEGFR-3), with its cognate ligand vascular endothelial g