ライフサイエンスコーパス: VEGFR-1

1 VEGFR-1 activation led to an increase in expression of t

2 VEGFR-1 and soluble VEGFR-1 expression increased in both

3 VEGFR-1 and VEGFR-2 mRNAs were detected in normal monkey

4 VEGFR-1 blockade and genetic deletion of the tyrosine ki

5 VEGFR-1 blocking antibodies had a marginal inhibitory ef

6 VEGFR-1 contributes to tumor growth and metastasis, but

7 VEGFR-1 deficiency promoted tip cell formation and endot

8 VEGFR-1 expression was detected in the cytoplasm and the

9 VEGFR-1 is a kinase-defective receptor tyrosine kinase (

10 VEGFR-1 is devoid of ligand-dependent tyrosine autophosp

11 VEGFR-1 knockout led to abundant accumulation of VEGFR-2

12 VEGFR-1 mRNA was also detectable in purified CD4+ T cell

13 VEGFR-1 mRNA was also reduced in FGR fetal cotyledon (P<

14 VEGFR-1 or VEGFR-2 inhibition decreased tumor burden not

15 VEGFR-1 siRNA had no effect on the stability of VEGFR-2

16 VEGFR-1 was expressed in all CRC cell lines studied as d

17 VEGFR-1, and not VEGFR-2, signaling is responsible for t

18 r A (VEGF-A) and its receptors, Flt-1/FLT-1 (VEGFR-1) and Flk-1/KDR (VEGFR-2), are key regulators of

19 vating two receptor tyrosine kinases, Flt-1 (VEGFR-1) and KDR (VEGFR-2), both of which are selectivel

20 vating two receptor tyrosine kinases, Flt-1 (VEGFR-1) and KDR (VEGFR-2), both of which are selectivel

21 vating two receptor tyrosine kinases, Flt-1 (VEGFR-1) and KDR (VEGFR-2).

22 homologous tyrosine kinase receptors: Flt-1 (VEGFR-1) and KDR (VEGFR-2).

23 thelial growth factor (VEGF) receptor flt-1 (VEGFR-1) die from vascular overgrowth, caused primarily

24 or receptor-1/fms-related tyrosine kinase 1 (VEGFR-1/FLT1) is expressed as a membrane-bound receptor

25 h factor (VEGF) and express VEGF receptor 1 (VEGFR-1) and VEGFR-2.

26 TGF-beta1 potently induces VEGF receptor 1 (VEGFR-1) expression in endothelial cells and thereby pre

27 scular endothelial growth factor receptor 1 (VEGFR-1/Flt1) promoter that merges human VEGF and p53 pa

28 VEGF receptor-1 (VEGFR-1 or Flt-1) is a high-affinity receptor for VEGF a

29 mined mice heterozygous for VEGF receptor-1 (VEGFR-1(+/-)), VEGF receptor-2 (VEGFR-2(+/-)), and overe

30 Although VEGF receptor-1 (VEGFR-1) and VEGFR-2 are known to be high affinity recep

31 blocking antibodies against VEGF receptor-1 (VEGFR-1) and VEGFR-2 potently inhibited inflammation and

32 scular endothelial growth factor receptor-1 (VEGFR-1) expression on human pancreatic cancer cell line

33 scular endothelial growth factor receptor-1 (VEGFR-1) is a member of the VEGFR family, and binds to V

34 Selective activation of VEGF receptor-1 (VEGFR-1) stimulated hepatocyte but not endothelial proli

35 scular endothelial growth factor receptor-1 (VEGFR-1) was upregulated in macrophages in response to L

36 ain reaction, expression of VEGF receptor-1 (VEGFR-1), but not VEGFR-2, was detected in murine kerati

37 rized two VEGF-A receptors, VEGF receptor-1 (VEGFR-1, also known as Flt-1) and VEGF receptor-2 (VEGFR

38 on of VEGF(121), VEGF(165), VEGF receptor-1 (VEGFR-1, or Flt-1), and VEGFR-2 (or KDR/Flk-1) was deter

39 scular endothelial growth factor receptor-1 (VEGFR-1/Flt-1) is a potential therapeutic target for car

40 scular endothelial growth factor receptor-1 (VEGFR-1/sFlt-1), which serves to antagonize VEGF-mediate

41 ion of heterodimers between VEGF receptor-1 (VEGFR-1; Flt-1) and VEGFR-2 (KDR; Flk-1) (VEGFR(1-2)) in

42 scular endothelial growth factor receptor-1 [VEGFR-1]) and soluble endoglin (sEng) are elevated in pr

43 f neuropilin-1, and VEGF receptors-1 and -2 (VEGFR-1 and VEGFR-2).

44 one VEGFR-2-specific monomer (VEGF-E) and a VEGFR-1-specific monomer (PlGF-1).

45 In contrast, administration of a VEGFR-1/Fc fusion protein, which blocks all VEGF isoform

46 Pretreatment of tumor cells with a VEGFR-1 blocking antibody inhibited the VEGFR-1-induced

47 Vessel survival is further stimulated with a VEGFR-1-specific ligand, placental growth factor 1.

48 al-dependent paracrine and intracrine VEGF-A/VEGFR-1 signaling contributes to human primary multiple

49 and placental growth factor (PlGF) activate VEGFR-1 selectively, however, mice lacking either ligand

50 s, we show that once sufficiently activated, VEGFR-1 signals in a similar manner to VEGFR-2 in endoth

51 ands selective for VEGF and VEGFR-2 but also VEGFR-1 agonists rescued survival and repopulation of VE

52 spite reductions in both soluble VEGFR-1 and VEGFR-1, VEGF ligand signaling is lower in DM compared w

53 vascular prosurvival genes via both NP-1 and VEGFR-1.

54 regulation of the VEGF receptors VEGFR-2 and VEGFR-1 (Flt-1) in vivo compared with benign hemangiomas

55 Further, we show that VEGFR-2 and VEGFR-1 blocking antibodies displayed opposing effects o

56 mor-derived VEGF is mediated by VEGFR-2, and VEGFR-1 alone has very limited independent effects but c

57 tions showed that cytotrophoblast VEGF-A and VEGFR-1 staining decreased; staining for PlGF was unaffe

58 VEGF-A and VEGFR-1 were prominent in adjacent parenchyma in the SS-

59 This confirms the importance of PEDF and VEGFR-1 in the negative regulation of angiogenesis.

60 and VEGFR-3 and, at term, VEGF-A, PlGF, and VEGFR-1.

61 Our findings indicate VEGF and VEGFR-1 are determinants of arteriogenesis.

62 The VEGF and VEGFR-1 promoters both contain a hypoxia regulatory elem

63 Treatment with anti-VEGFR-1 antibodies also reduced the number of proliferat

64 PEDF on VEGF-induced angiogenesis as well as VEGFR-1 cleavage.

65 tively, supporting the presence of autocrine VEGFR-1- and paracrine VEGFR-2-mediated pathways in lymp

66 s VEGF-A increased CNV before injury because VEGFR-1 activation was silenced by secreted protein, aci

67 h factor-1 (PlGF-1), which exclusively binds VEGFR-1, decreased hyperoxia-induced retinal vaso-oblite

68 Both VEGFR-1 and VEGFR-2 signal pathways converged on Akt, as

69 of pan-receptor scV/Zr was mediated by both VEGFR-1 and VEGFR-2 at an approximately 2:1 ratio.

70 RPE cells expressed both VEGFR-1 and -2 in vitro; however, the expression of VEGF

71 -29 and SW480 with VEGF-A (a ligand for both VEGFR-1 and -2) or VEGF-B (a ligand specific for VEGFR-1

72 rcinoma liver metastases, inhibition of both VEGFR-1 and VEGFR-2 was required to induce growth delay.

73 <0.05), decreased soluble and membrane-bound VEGFR-1 (NC versus DM: 1.44+/-0.30 versus 0.85+/-0.08 an

74 d by the addition of VEGF and was blocked by VEGFR-1- and VEGFR-2-specific antibodies.

75 ion of VEGFR-2 promoter activity elicited by VEGFR-1 siRNA.

76 Activation of eNOS by VEGFR-1 was dependent on Tyr794 and was mediated via pho

77 The changes mediated by VEGFR-1 in this pancreatic carcinoma cell line are highl

78 y VEGFR-2 inhibition for lung EC and more by VEGFR-1 inhibition for liver EC.

79 Cardiac VEGFR-1 expression was reduced 4-fold in all paced dogs,

80 REC-I), but not levels of NRP2, gp130, CD31, VEGFR-1, or VEGFR-2.

81 cine aortic endothelial cells, both chimeric VEGFR-1 and -2 autophosphorylate in response to addition

82 de, suggesting a minor role for compensatory VEGFR-1 signaling during postnatal development and vascu

83 The absence of compensatory VEGFR-1 signaling by VEGF-B and PlGF may have important

84 By contrast, VEGFR-1-specific siRNA markedly not only downregulated t

85 In contrast, VEGFR-1(+/-) showed impaired: perfusion recovery, perico

86 Conversely, VEGFR-1-specific blockade produced virtually no obvious

87 carboxyl terminus of another receptor, i.e., VEGFR-1, restored the ligand-dependent activation of the

88 lular adhesion molecule-2), but not all (eg, VEGFR-1 and VEGFR-2), EC-enriched genes.

89 known about the precise role of endothelial VEGFR-1 and its downstream effectors in this process.

90 cess provides direct evidence of endothelial VEGFR-1 in NO-driven in vitro angiogenesis.

91 subpopulations that constitutively expressed VEGFR-1 but not in ABCB5(-) bulk populations that were p

92 levels of NRP1, NRP2, and to a lesser extent VEGFR-1 and VEGFR-2, and block the binding and in vitro

93 In both monkey and rat eyes, VEGFR-1 and VEGFR-2 mRNAs were localized to the inner nu

94 er square millimeter and mRNA expression for VEGFR-1 were, respectively, 89% and 37% lower from 3 to

95 EGF-deficient HSCs, revealing a function for VEGFR-1 signalling during haematopoiesis.

96 PlGF, one of the ligands for VEGFR-1, has been implicated in tumor angiogenesis.

97 we have constructed a chimeric receptor for VEGFR-1 (CTR) and VEGFR-2 (CKR) in which the extracellul

98 gether, these data describe a novel role for VEGFR-1 in keratinocytes and suggest that VEGF may play

99 A role for VEGFR-1 in keratinocytes was also shown in vivo because

100 Thus, our study reveals a critical role for VEGFR-1 in the HemSC-to-EC differentiation that underpin

101 Here we identify a critical role for VEGFR-1 signaling in ABCB5(+) MMIC-dependent VM and tumo

102 R-1 and -2) or VEGF-B (a ligand specific for VEGFR-1) led to activation of Erk-1/2, SAPK/JNK, and tra

103 rowth of tumor cells expressing a functional VEGFR-1 rather than stimulation of angiogenesis.

104 11 or MF-1 (targeting tumor VEGFR-1 and host VEGFR-1) had no effect.

105 However, VEGFR-1 siRNA significantly inhibited VEGFR-2 promoter a

106 th species-specific antibodies against human VEGFR-1 (6.12), human VEGFR-2 (IMC-1C11), murine VEGFR-1

107 t-in-class selective PET tracers for imaging VEGFR-1 and VEGFR-2 were constructed and successfully va

108 The same trend was found in VEGFR 1 and 2 which were significantly reduced in WT gro

109 ributes in part to increased angiogenesis in VEGFR-1-deficient mice.

110 TKs and corresponds to aspartic acid, but in VEGFR-1 it is substituted to asparagine.

111 (VEGF) receptor tyrosine kinases, including VEGFR-1/Flt-1, VEGFR-2/KDR, VEGFR-3/Flt-4, the platelet-

112 a consequence of poor growth factor-induced VEGFR-1 autophosphorylation however, observations from t

113 In addition, PlGF induced VEGFR-1 signaling and biological responses in tumor cell

114 We report here that VEGF-A or VEGF-B induces VEGFR-1-mediated ERK1/2 phosphorylation in HemSCs and pr

115 which binds to two receptor tyrosine kinases VEGFR-1 (Flt-1) and VEGFR-2 (Flk-1/KDR), VEGF-B and PlGF

116 VEGFs activate 3 receptor tyrosine kinases, VEGFR-1, VEGFR-2, and VEGFR-3, promoting angiogenic and

117 kout to abrogate the expression of all known VEGFR-1 functional domains in neonatal and adult mice an

118 e postinfarct ischemic cardiomyopathy model, VEGFR-1 deficiency supported robust angiogenesis and pro

119 R-1 (6.12), human VEGFR-2 (IMC-1C11), murine VEGFR-1 (MF-1), or murine VEGFR-2 (DC101).

120 EGFR-2, whereas mAbs against human or murine VEGFR-1 had no effect on mice survival.

121 The mutant VEGFR-1 (Asp(1050)) promoted endothelial cell proliferat

122 tment of excisional wounds with neutralizing VEGFR-1 antibodies delayed re-epithelialization.

123 ld be blocked by treatment with neutralizing VEGFR-1 antibodies.

124 VEGFR-2 receptors and neuropilin-1, but not VEGFR-1 receptors.

125 VEGFR-2- but not VEGFR-1-specific blockade led to the same results.

126 in tumor endothelium after treatment but not VEGFR-1.

127 ious reports which show a limited ability of VEGFR-1 to mediate signalling cascades, we show that onc

128 Also, genetic ablation of VEGFR-1 signaling in the host did not affect the efficac

129 edly not only downregulated the abundance of VEGFR-1 but also significantly reduced VEGFR-2 protein a

130 ific siRNA had no effect on the abundance of VEGFR-1 protein.

131 ted HIF-1alpha levels, whereas activation of VEGFR-1 alone upregulated HIF-2alpha.

132 esults implicate induction and activation of VEGFR-1 as critical targets to prevent vessel loss.

133 the neonatal retina, and that activation of VEGFR-1 by PlGF-1 is a selective strategy for preventing

134 However, activation of VEGFR-1 did not increase CRC cell proliferation.

135 In contrast, activation of VEGFR-1 plays a stationary role in angiogenesis by antag

136 ers of the caspase family, via activation of VEGFR-1.

137 hosphorylation of VEGFR-2 in lung ECs and of VEGFR-1 in liver ECs.

138 ignaling proceeds via autophosphorylation of VEGFR-1 and activation of the phosphatidylinositol 3-kin

139 for the poor tyrosine autophosphorylation of VEGFR-1, we have either deleted the carboxyl terminus of

140 nisms underlying the decoy characteristic of VEGFR-1 is linked to the replacement of a highly conserv

141 anism responsible for this characteristic of VEGFR-1 is not known.

142 The decoy characteristic of VEGFR-1 is required for normal development and angiogene

143 planation for this unusual characteristic of VEGFR-1.

144 Analysis of the subcellular distribution of VEGFR-1 revealed the appearance of an 80-kDa C-terminal

145 ic ablation of the tyrosine kinase domain of VEGFR-1 in the host did not result in growth inhibition

146 ic deletion of the tyrosine kinase domain of VEGFR-1 resulted in enhanced tumor angiogenesis.

147 dent kinase activation and downregulation of VEGFR-1 and its ability to convey the angiogenic respons

148 Notch1(+/-) mice had decreased expression of VEGFR-1 compared with macrophages from wild-type mice, w

149 nations, revealed preferential expression of VEGFR-1 on ABCB5(+) tumor cells purified from clinical m

150 and -2 in vitro; however, the expression of VEGFR-1 was very low.

151 ines were heterogeneous in the expression of VEGFR-1, -3, c-Kit and RET, most cells expressed PDGFR-a

152 anscriptionally repressing the expression of VEGFR-1, thereby curtailing a central angiogenic driver

153 Given our previous finding of VEGFR-1-mediated tumor cell invasion and migration in pa

154 trophoblast secretion of the soluble form of VEGFR-1 in vitro also increased.

155 ere we report the expression and function of VEGFR-1 in CRC cell lines.

156 rylation, demonstrating the functionality of VEGFR-1 in human T cells.

157 tracers that enable the selective imaging of VEGFR-1 and VEGFR-2.

158 TGF-beta1 induction of VEGFR-1 in endothelial cells explains pericyte protectio

159 ime RT-PCR identified a 60-fold induction of VEGFR-1 mRNA in retina from P3 (early vascularization) t

160 Inhibition of VEGFR-1 abrogated multiple myeloma cell proliferation an

161 The inhibition of VEGFR-1 results in a dramatic decrease in the number of

162 elanoma-specific shRNA-mediated knockdown of VEGFR-1 blocked the development of ABCB5(+) VM morpholog

163 GF-A both induce tyrosine phosphorylation of VEGFR-1 and render it susceptible to ectodomain shedding

164 e to inhibit VEGF-induced phosphorylation of VEGFR-1.

165 Furthermore, the down-regulation of VEGFR-1 in the HemSCs results in decreased formation of

166 he removal of the ectodomain, the remnant of VEGFR-1 remains attached to the membrane, and the activi

167 phorylation or shRNA-mediated suppression of VEGFR-1 prevents HemSC-to-EC differentiation.

168 Thus, the carboxyl tail of VEGFR-1 restrains the ligand-dependent kinase activation

169 The deletion of carboxyl terminus of VEGFR-1 did not reverse its defective ligand-dependent a

170 have either deleted the carboxyl terminus of VEGFR-1 or exchanged it with the carboxyl terminus of VE

171 factor receptor was substituted for that of VEGFR-1 (EGLT) or VEGFR-2 (EGDR) and transduced into pri

172 The identification Tyr794 of VEGFR-1 as a key residue in this process provides direct

173 GF-Trap, a composite decoy receptor based on VEGFR-1 and VEGFR-2 fused to an Fc segment of IgG1.

174 te that liver metastases are more reliant on VEGFR-1 than lung metastases to mediate angiogenesis due

175 ion of the VEGF and PlGF receptor, Flt-1 (or VEGFR-1), consists of seven immunoglobulin-like domains.

176 R-2) and Flt-1 (fms-like tyrosine kinase, or VEGFR-1).

177 At 5 days postpartum (P5), VEGFR-1 protein was colocalized with retinal vessels, wh

178 F-A, VEGF-C, placental growth factor (PlGF), VEGFR-1, and VEGFR-3 and, at term, VEGF-A, PlGF, and VEG

179 (-) bulk populations that were predominantly VEGFR-1(-).

180 engineered to overexpress the PlGF receptor (VEGFR-1), neutralization of PlGF using four novel blocki

181 VEGF-receptor (VEGFR-1 and -2) expression was determined using reverse

182 d exclusively by the corresponding receptor, VEGFR-1 or VEGFR-2, respectively.

183 GF-B with the second domain of its receptor, VEGFR-1.

184 actor (VEGF) and its high-affinity receptors VEGFR-1 and VEGFR-2 was investigated in normal eyes.

185 tiates signaling by dimerizing the receptors VEGFR-1 and VEGFR-2.

186 ascular endothelial growth factor receptors (VEGFR-1 and VEGFR-2) that bind VEGF, the Tie-1 and Tie-2

187 tumor cells and that acts through receptors (VEGFR-1, VEGFR-2, and neuropilin) that are expressed on

188 (VEGF188, VEGF164, VEGF120), VEGF receptors (VEGFR-1, VEGFR-2, Npn-1, Npn-2), and pigment epithelium-

189 1 Hz), whereas expression of VEGF receptors (VEGFR-1, VEGFR-2, or NRP1) is unaffected.

190 ascular endothelial growth factor receptors, VEGFR-1 and VEGFR-2, that play important and distinct ro

191 s 2 transmembrane tyrosine-kinase receptors, VEGFR-1 and VEGFR-2, constitute a ligand-receptor signal

192 rough interactions with its major receptors, VEGFR-1 and VEGFR-2.

193 levels of the high affinity VEGF receptors, VEGFR-1 and VEGFR-2, most prominently during the neonata

194 c analysis demonstrate that Notch1 regulates VEGFR-1 and cytokine expression in macrophages.

195 VR2 with enhanced affinity to, respectively, VEGFR-1 and VEGFR-2, were constructed.

196 ted by two receptor tyrosine kinases (RTKs), VEGFR-1 and VEGFR-2, which differ considerably in signal

197 Soluble VEGFR-1 and soluble VEGFR-2 modified the formation of co

198 full-length VEGF receptor (VEGFR)-1, soluble VEGFR-1, and markers of downstream VEGF signaling (n=20

199 -23-IgG) blocking murine VEGF-A or a soluble VEGFR-1 receptor IgG chimeric construct [mFlt(1-3)-IgG],

200 er, blocking VEGF by administering a soluble VEGFR-1, which acts extracellularly, induced only minor

201 VEGFR-1 and soluble VEGFR-1 expression increased in both groups, but the fol

202 ischemia, despite reductions in both soluble VEGFR-1 and VEGFR-1, VEGF ligand signaling is lower in D

203 VEGF-Trap and to a lesser extent by soluble VEGFR-1.

204 Injection of soluble VEGFR-1 results in malformed vascular networks and the a

205 These data demonstrate that soluble VEGFR-1, an angiogenesis inhibitor, is regulated in skel

206 Moreover, melanoma-specific VEGFR-1 knockdown markedly inhibited tumor growth (by >

207 topoiesis in vivo, we selectively stimulated VEGFR-1 and VEGFR-2 by continuous infusion of receptor-s

208 common tumor of infancy, as a means to study VEGFR-1 activation in pathological vasculogenesis.

209 The carboxyl terminus-swapped VEGFR-1, however, displayed ligand-dependent autophospho

210 We conclude that VEGFR-1 is critical in maintaining the vasculature of th

211 or cells of epithelial origin, we found that VEGFR-1 is present and functional on CRC cells, and acti

212 creatic carcinoma cells, we hypothesize that VEGFR-1 plays a role in tumor progression in pancreatic

213 enotype and morphology, we hypothesized that VEGFR-1 activation induces molecular alterations that me

214 These findings indicate that VEGFR-1 subunits modulate VEGF activity predominantly by

215 er of capillary connections, indicating that VEGFR-1 ligands promote branching angiogenesis.

216 Our results show that VEGFR-1 function in MMIC regulates VM and associated lam

217 In this study, we show that VEGFR-1 is devoid of ligand-dependent downregulation and

218 Western blotting showed that VEGFR-1 activation led to decreased expression of the ep

219 s to E-cadherin and beta-catenin showed that VEGFR-1 activation led to translocation of E-cadherin an

220 Taken together, our data suggest that VEGFR-1 receptor is a critical determinant of VEGFR-2 ab

221 The VEGFR-1-specific ligand placental growth factor-1 (PlGF-

222 Consistent with these findings, the VEGFR-1-specific ligand placenta growth factor-1 activat

223 th a VEGFR-1 blocking antibody inhibited the VEGFR-1-induced immunohistochemical and molecular change

224 ultured mouse podocytes possess at least the VEGFR-1 receptor, confirmed by RT-PCR, immunoblotting, a

225 associated with increased expression of the VEGFR-1 in RPE cells and increased receptor affinity for

226 slocation of the transmembrane domain of the VEGFR-1.

227 l angiogenesis through interactions with the VEGFR-1 and VEGFR-2 receptors.

228 pancreatic cancer cell line L3.6pl with the VEGFR-1 ligands VEGF-A and VEGF-B led to morphologic cha

229 multiple myeloma cell growth and therefore, VEGFR-1 blockade is a potential therapeutic strategy for

230 perates in an autocrine loop, likely through VEGFR-1 and PI3K, to stimulate alpha3(IV) collagen produ

231 F-A signaling was routed principally through VEGFR-1.

232 Thus, VEGFR-1 agonists may have therapeutic potential for pres

233 VEGFR-2 (Flk-1/KDR), VEGF-B and PlGF bind to VEGFR-1 and not VEGFR-2.

234 relative contributions of VEGF-B and PlGF to VEGFR-1 signaling may be masked in the presence of VEGF-

235 tment with IMC-1C11 or MF-1 (targeting tumor VEGFR-1 and host VEGFR-1) had no effect.

236 reatment with 6.12 or DC101 (targeting tumor VEGFR-1 and host VEGFR-2) reduced established DLBCL xeno

237 , vascular endothelial growth factor (VEGF), VEGFR-1, VEGFR-2, phospho-VEGFR-2, cyclooxygenase (COX)-

238 VEGF, VEGFR-1, and VEGFR-2 are constitutively expressed in the

239 Ocular VEGF, VEGFR-1, and VEGFR-2 expression was studied using a comb

240 An alternate VEGFR, VEGFR-1 or neuropilin-1, may modulate adhesion of leukoc

241 hodox antiangiogenic effect was mediated via VEGFR-1 activation and VEGFR-2 deactivation, the latter

242 ibit T-cell development via VEGFR-2, whereas VEGFR-1 signaling decreases this inhibition.

243 ll carcinoma lung metastases by 26%, whereas VEGFR-1 antibody (MF-1) had no effect.

244 no effect on RenCa liver metastases, whereas VEGFR-1 neutralization decreased RenCa liver metastases

245 ith macrophages from wild-type mice, whereas VEGFR-1 expression in Notch4(-/-) macrophages was normal

246 anti-PlGF treatment strongly correlates with VEGFR-1 expression in tumor cells, but not with antiangi

247 were observed for VEGFR-2 co-expressed with VEGFR-1.