ライフサイエンスコーパス: VEGF-A

1 VEGF-A and EGFR expression was determined by immunohisto

2 VEGF-A and ID1 expression was examined in peritoneal bio

3 VEGF-A and p-Ser166-Mdm2 protein levels were measured in

4 VEGF-A antagonists have revolutionized wet AMD treatment

5 VEGF-A blockade in tumors was associated with HIF1alpha

6 VEGF-A is a promising target for molecular fluorescence

7 VEGF-A mRNA may have therapeutic potential for regenerat

8 VEGF-A pre-mRNA is alternatively spliced at the terminal

9 VEGF-A protein expression was determined by enzyme-linke

10 VEGF-A regulation through ID1 was confirmed by siRNA in

11 VEGF-A showed high in-cell expression, but VEGF-C had lo

12 VEGF-A stimulated proliferation of MM cells in monolayer

13 VEGF-A was a potent inducer of glycolysis in tubulogenic

14 VEGF-A was immunolocalized to peritoneal mesothelium and

15 VEGF-A was increased in peritoneal fluid from women with

16 VEGF-A was measured in peritoneal fluid by ELISA (n = 16

17 VEGF-A, an angiogenic factor, is increased in the perito

18 VEGF-A-dependent Mdm2 phosphorylation was demonstrated i

19 Levels of ADAMTS-1, VEGF-A, and HIF-1alpha in GCF and serum were quantified

20 a significant correlation between ADAMTS-1, VEGF-A, and HIF-1alpha levels in the GCF and clinical pe

21 ctivity and is modulated by endogenous IGF-1/VEGF-A signaling.

22 microRNA-125b/TGF-beta1/TGF-beta receptor 1/VEGF-A signaling.

23 F, IL-6, MCP-1, MIP-1alpha, IL-12p70, IL-18, VEGF-A, PDGF-BB and IL-1RA significantly correlated with

24 as a central mediator of STAT3, HIF-1alpha, VEGF-A and angiogenesis via multiple signalling mechanis

25 These data demonstrate that the HIF-1alpha/VEGF-A axis is an essential aspect of tumor immunity.

26 newly identified TR4/lincRNA-p21/HIF-1alpha/VEGF-A signaling with Bex, an FDA-approved drug, may inc

27 ia modulating the TR4/lincRNA-p21/HIF-1alpha/VEGF-A signaling.

28 sult of the increased expression of VEGFR-2, VEGF-A, VEGF-C, and VEGF-D.

29 on mRCC patients with (89)Zr-bevacizumab, a VEGF-A-binding antibody tracer.

30 rmined tumor uptake of (89)Zr-bevacizumab, a VEGF-A-binding PET tracer, in mRCC patients before and d

31 was only improved with the adjuvant use of a VEGF-A/Ang2-bispecific CovX-body (CVX-241) but not when

32 lidate vascular endothelial growth factor A (VEGF-A) and epidermal growth factor receptor (EGFR)-targ

33 Vascular endothelial growth factor A (VEGF-A) and its binding to VEGFRs is an important angiog

34 rn, by vascular endothelial growth factor A (VEGF-A) and platelet-derived growth factor-BB (PDGF-BB).

35 lowing vascular endothelial growth factor A (VEGF-A) exposure.

36 hibits vascular endothelial growth factor A (VEGF-A) expression.

37 2) and vascular endothelial growth factor A (VEGF-A) expression.

38 ), and vascular endothelial growth factor A (VEGF-A) genes.

39 factor vascular endothelial growth factor A (VEGF-A) is subject to a multitude of stimulus-dependent,

40 Tumor vascular endothelial growth factor A (VEGF-A) level may be useful.

41 coding vascular endothelial growth factor A (VEGF-A) or buffered saline placebo (ethical obligations

42 Vascular endothelial growth factor A (VEGF-A) produced locally is supposed to play an importan

43 of all vascular endothelial growth factor A (VEGF-A) splice isoforms from the kidney results in prote

44 ion in vascular endothelial growth factor A (VEGF-A) stimulated HREC cultures.

45 ), and vascular endothelial growth factor A (VEGF-A) were analyzed by means of Western blotting.

46 nesis, vascular endothelial growth factor A (VEGF-A), and platelet-derived growth factor B chain (PDG

47 ctors, vascular endothelial growth factor A (VEGF-A), and VEGF-C.

48 -myc), vascular endothelial growth factor A (VEGF-A), and Wnt family member 1 (WNT1)] by targeting th

49 evated vascular endothelial growth factor A (VEGF-A), which was induced in vivo by infection with Tcd

50 ion of vascular endothelial growth factor A (VEGF-A).

51 9) and vascular endothelial growth factor A (VEGF-A).

52 lly by vascular endothelial growth factor A (VEGF-A).

53 s, the vascular endothelial growth factor A (VEGF-A)/VEGF receptor 2 (VEGFR-2) signaling pathway medi

54 Vascular endothelial growth factor-A (VEGF-A) acts via 2 vascular endothelial growth factor re

55 w that vascular endothelial growth factor-A (VEGF-A) and platelet-derived growth factor-BB (PDGF-BB)

56 campal vascular endothelial growth factor-A (VEGF-A) in both male and female mice, as well as increas

57 Vascular endothelial growth factor-A (VEGF-A) is thought to be a critical mediator of vascular

58 luding vascular endothelial growth factor-A (VEGF-A) isoforms and platelet-derived growth factor-BB (

59 erived vascular endothelial growth factor-A (VEGF-A) promotes tumor progression and angiogenesis.

60 gands, vascular endothelial growth factor-A (VEGF-A), contributing to neurodegeneration.

61 BDNF), vascular endothelial growth factor-A (VEGF-A), insulin-like growth factor-1 (IGF-1) and Klotho

62 nodes, vascular endothelial growth factor-A (VEGF-A), vascular endothelial growth factor-C (VEGF-C) w

63 -2 and vascular endothelial growth factor-A (VEGF-A), with ranibizumab in patients with diabetic macu

64 ia the vascular endothelial growth factor-A (VEGF-A)/VEGF receptor 2 (VEGFR2) pathway.

65 cts of vascular endothelial growth factor-A (VEGF-A/VEGF) and its receptors on endothelial cells func

66 ascular endothelial growth factor isoform A (VEGF-A) and islet vascularization on beta-cell function

67 ctor-A vascular endothelial growth factor A [VEGF-A], and terminal deoxynucleotidyl transferase dUTP

68 coding vascular endothelial growth factor-A [VEGF-A] or thymosin beta 4 [Tbeta4]) was applied regiona

69 s revealed increased CD8+ T cell activation, VEGF-A, and PI3K/Akt/mTOR pathway activity.

70 An adenovirus expressing VEGF-A (Ad-VEGF-A(164)) replicates the tumor vasculature in mice wi

71 c vessel type to form in tumors and after Ad-VEGF-A(164).

72 As in tumors, Ad-VEGF-A(164) strikingly increased endothelial nitric oxid

73 spectively, and validated the known affinity VEGF-A(121):VEGFR2 as K(D) = 0.66 nM.

74 the context of progressive depletion of all VEGF-A isoforms from the podocytes.

75 change in the NOD2-responsive NO, TNF-alpha, VEGF-A, and IL-12 levels was observed.

76 p was found among GCF endocan and TNF-alpha, VEGF-A, CAL, and GI for all groups (P <0.05).

77 Although VEGF-A failed to support an enduring vascular response,

78 HIF1A and VEGF A (VEGFA) mRNA, a transcriptional target of HIF-1,

79 measured binding kinetics for VEGFA(165) and VEGF-A(121), but binding kinetics of the other two pro-

80 and its downstream effectors HIF-1alpha and VEGF-A in cell lines, xenografts, and transgenic murine

81 imultaneous inhibition of angiopoietin-2 and VEGF-A with faricimab for patients with DME.

82 s and binds to the AP-1 site at the IL-6 and VEGF-A promoters.

83 RC cells contained higher levels of IL-6 and VEGF-A than that from vector control cells and significa

84 Fos to enhance the transcription of IL-6 and VEGF-A, which promotes angiogenesis in CRC.

85 ionally activated the expression of IL-6 and VEGF-A.

86 Ang2 and VEGF-A treatment rescued angiogenesis in Nox2-silenced c

87 nib also inhibited chronic PDGF-A and -B and VEGF-A and -B expressions.

88 if treated simultaneously with TGF-beta and VEGF-A.

89 d state in the presence of both TGF-beta and VEGF-A.

90 GF-beta signaling molecules, Tenascin-C, and VEGF-A, while pro-fibrotic molecules, including several

91 -thirds were downregulated including CA9 and VEGF-A.

92 EGF-R2 expression in corneal CD31 cells, and VEGF-A and IFNgamma expression in corneal CD4 T cells.

93 a, and the downstream genes GLUT-1, EPO, and VEGF-A (p < 0.05), in the absence of a significant decre

94 le microvasculature to insulin, exercise and VEGF-A and reduce microvascular density.

95 on and proliferation whereas both GW0742 and VEGF-A promoted tubulogenesis.

96 )-dependent signaling event, m-SCF/c-Kit and VEGF-A/vascular endothelial growth factor receptor 2 (VE

97 onnect between HIF-1alpha protein levels and VEGF-A expression.

98 fect on the bone marrow microenvironment and VEGF-A/VEGFR targeting restores bone marrow function.

99 EC coculture increased VEC proliferation and VEGF-A protein expression, whereas blocking VEGF-A signi

100 ced superoxide formation and Ang2, Tie2, and VEGF-A expression.

101 In HPMEC, LPS-induced Ang2, Tie2, and VEGF-A protein expression was preceded by increased supe

102 C mesothelial-to-mesenchymal transition, and VEGF-A production.

103 n affinities between VEGF-A(165a):VEGFR1 and VEGF-A(165a):VEGFR2, 1.0 pM and 10 pM respectively, and

104 so reduced the number of CD31(+) vessels and VEGF-A-positive cells in fibrotic peritoneum.

105 L25, IL-2RB, IL-15RA, CD6) and angiogenesis (VEGF-A) were significantly increased only in AD.

106 Outside the breeding season (BS), angiogenic VEGF-A stimulates vessel growth in the infundibulum, aid

107 ificant upregulation of pro(lymph)angiogenic VEGF-A, VEGF-C, VEGF-D and infiltration of macrophages.

108 -A knockout and overexpression of angiogenic VEGF-A isoforms each worsen diabetic nephropathy.

109 Concentrations of angiogenic (VEGF-A, Ang1, Ang2), anti-angiogenic (VEGF-A165b ) and l

110 n = 25) or previously were treated with anti-VEGF A therapy (n = 26).

111 received intravenous bevacizumab-800CW (anti-VEGF-A), cetuximab-800CW (anti-EGFR), control tracer IgG

112 y, 7 of 13 (54%) did not require rescue anti-VEGF-A therapy and the mean change in BCVA from baseline

113 s comparable to aflibercept (an FDA-approved VEGF-A antagonist).

114 Although astrocytic VEGF-A was also increased, anti-VEGF failed to rescue va

115 by reproducing the known affinities between VEGF-A(165a):VEGFR1 and VEGF-A(165a):VEGFR2, 1.0 pM and

116 t cancer showed inverse correlations between VEGF-A expression and CD8(+) T cell infiltration, and a

117 Mice lacking NRP1 or NRP1-binding VEGF-A isoforms have defective RGC axon organisation alo

118 VEGF-A protein expression, whereas blocking VEGF-A significantly reduced VEC proliferation (P = 0.04

119 e have recently shown that VEGF(165)b blocks VEGF-A-induced endothelial vascular endothelial growth f

120 y by preventing Cdc42 and Pak2 activation by VEGF-A and Slit2.

121 Tumor growth and angiogenesis induced by VEGF-A, histamine, and serotonin are almost completely i

122 compared these effects with those induced by VEGF-A.

123 in sub-podocyte space coverage, produced by VEGF-A depletion.

124 proliferation and survival are triggered by VEGF-A activation of VEGFR2.

125 ery) and vascular permeability (triggered by VEGF-A).

126 ized monoclonal antibody against circulating VEGF-A, when added to CCNU chemotherapy in patients with

127 However, their role in controlling VEGF A and FGF 2 signaling in the CL of water buffalo is

128 preclinical models, the angiogenic cytokine VEGF-A has been identified as a critical regulator of NM

129 Increased concentrations of the cytokine VEGF-A in the cornea are associated with HSK severity.

130 pregulated the secretion levels of cytokines VEGF-A, PGE2, and TGF-beta1 in hybrid spheroid system.

131 E-1, soluble VEGFR1, VEGF-A, VEGF-C, VEGF-D, VEGF-A isoform 121, bone morphogenetic protein 7, macrop

132 enuated CD8+ T cell activation and decreased VEGF-A levels.

133 defects are caused exclusively by defective VEGF-A signalling in RGCs or are exacerbated by abnormal

134 red, both epidermal and myeloid cell-derived VEGF-A contributed to regeneration-induced tumorigenesis

135 ons of epidermal versus myeloid cell-derived VEGF-A during HPV-mediated tumorigenesis, with possible

136 ion of epidermal versus myeloid cell-derived VEGF-A in HPV-mediated skin cancer by interbreeding an H

137 Although only epidermal-derived VEGF-A was essential for initiation of skin tumor develo

138 Tumor-derived VEGF-A, PLGF-2, and VEGF-B augment pain sensitivity thro

139 ciliary genes in endothelial cells disrupts VEGF-A/VEGFR2 internalization and downstream signaling.

140 pha) and this transcription factor can drive VEGF-A expression, we analyzed the expression of HIF-1al

141 mediated miR-150 transfer and miR-150-driven VEGF-A/VEGFR/PI3K/Akt pathway activation, thereby modula

142 Skin microdialysis revealed elevated VEGF-A protein levels at mRNA-treated sites versus place

143 Serum and GCF endocan, VEGF-A, and TNF-alpha levels were significantly higher i

144 However, AnxA1 treatment enhanced VEGF-A release from cardiac macrophages, and its deliver

145 To establish VEGF-A isoform expression and functional effects in IPF.

146 An adenovirus expressing VEGF-A (Ad-VEGF-A(164)) replicates the tumor vasculature

147 ges are the predominant cell type expressing VEGF-A during Leishmania major infection.

148 alpha protein levels, and to a lesser extent VEGF-A levels, in renal cystadenoma cells in a Tsc2+/- m

149 ation of Akt by the potent angiogenic factor VEGF-A does not strongly stabilize microtubules or suffi

150 reduced expression of the angiogenic factor VEGF-A.

151 ted with vascular endothelial growth factor (VEGF-A) and tumor necrosis factor (TNF)-alpha levels.

152 1alpha), vascular endothelial growth factor (VEGF-A), and clinical parameters of periodontitis.

153 downstream of the angiogenic growth factors VEGF-A and Slit2.

154 We measured the binding kinetics for VEGF-A(165), -A(165b), and -A(121) with VEGFR1 and VEGF-

155 were 0.10 fg/mL for DSG3, and 0.20 fg/mL for VEGF-A, VEGF-C and beta-Tub.

156 s have previously revealed a requirement for VEGF-A, the class 3 semaphorin SEMA3C, and their shared

157 s well tolerated and led to local functional VEGF-A protein expression and transient skin blood flow

158 rentiating the splice variants in all future VEGF-A studies.

159 The combination inhibited orthotopic growth, VEGF-A expression, and tumor vasculature of both TNBC an

160 ze HUVEC heterogeneity and observe that 24 h VEGF-A(165) treatment induces a ~15% decrease in VEGFR2

161 nregulation of VEGFR2 concentration via 24 h VEGF-A(165) treatment.

162 -enhanced miR-185-5p also promotes HIF2alpha/VEGF-A expression via binding to the promoter region of

163 Immunohistochemistry showed high VEGF-A expression in 79%-96% and high EGFR expression in

164 at TP53 mutations are associated with higher VEGF-A expression (P = 0.006).

165 in response to acute exercise and identified VEGF-A as a key stimulator of Mdm2 phosphorylation on Se

166 a transcription factor highly implicated in VEGF-A and VEGF-C gene regulation.

167 of TGF-beta1 and ID1 has been implicated in VEGF-A regulation during tumor angiogenesis.

168 cellular and molecular mediators involved in VEGF-A/VEGFR-2 signaling using a murine model of infecti

169 in health and in vascular disease, including VEGF-A(121) and an anti-angiogenic variant, VEGF-A(165b)

170 sion of HIF2alpha-dependent genes, including VEGF-A, PAI-1, and cyclin D1 in ccRCC cell lines and tum

171 Clinical trials including VEGF-A administration for therapeutic angiogenesis have

172 nificantly increased tumor burden, increased VEGF-A, reduced IL-33, and enhanced vascularity.

173 Exercise increased VEGF-A and p-Ser166-Mdm2 protein levels respectively by

174 sitive regulation on the HIF2alpha-increased VEGF-A expression that resulted in increasing VEGF-A in

175 EGF-A expression that resulted in increasing VEGF-A in the VHL-wt RCC cells.

176 +/-)LoxP-VEGF-A(+/+) to conditionally induce VEGF-A isoform deletion specifically in the alveolar typ

177 during infection and that infection-induced VEGF-A production is mediated by ARNT/HIF activation.

178 gs indicate critical roles for toxin-induced VEGF-A and colonic vascular permeability in CDI pathogen

179 Brolucizumab directly inhibits VEGF-A function, providing visual outcomes comparable to

180 r mass of approximately 26 kDa that inhibits VEGF-A.

181 Instead, VEGF-A acts via the neuropilin-1 (NRP-1) co-receptor.

182 Intradermal VEGF-A mRNA was well tolerated and led to local function

183 ator, especially the earliest-known isoform, VEGF-A(165a).

184 displayed reduced expression of KLF2, KLF4, VEGF-A, VEGF-C, and FGFR3 and elevated expression of p57

185 uate correlation between GCF endocan levels, VEGF-A, and TNF-alpha levels with periodontal probing de

186 zumab (an antibody to the angiogenic ligand, VEGF-A) in breast cancer have found improved responses i

187 ansgenic mouse SPC-rtTA(+/-)TetoCre(+/-)LoxP-VEGF-A(+/+) to conditionally induce VEGF-A isoform delet

188 w that L. major infection induces macrophage VEGF-A production in an ARNT/HIF-dependent manner and su

189 These results suggest that c-Kit-mediated VEGF-A action in beta-cells plays a pivotal role in main

190 expression, suggesting that mTORC1 mediates VEGF-A expression via both HIF-1alpha-dependent and -ind

191 , we and others showed that P130CAS mediates VEGF-A and PDGF signalling in vitro, but its cardiovascu

192 VEGFR) 2 as well as VEGF signaling molecules VEGF-A, VEGF-C, and VEGF-D.

193 tes from HD mice and patients contained more VEGF-A, which triggers proliferation of endothelial cell

194 r defects through modulation of the Akt/mTOR/VEGF-A pathway, indicating that c-Kit signaling in beta-

195 splicing leads to the generation of multiple VEGF-A isoforms, including VEGF165.

196 had a significant increase in HMGA1, c-MYC, VEGF-A, and WNT1, potentially due to regulation by the A

197 g to a significant decrease in HMGA1, c-MYC, VEGF-A, and WNT1.

198 binds the promoter regions of HMGA1, c-MYC, VEGF-A, and WNT1.

199 Aflibercept ('VEGF Trap', which neutralizes VEGF-A, VEGF-B and PlGF) showed greater efficacy than ne

200 Neutralizing VEGF-A in vivo using bevacizumab inhibited sympathetic i

201 S6K1 inhibition reduces HIF-1alpha but not VEGF-A expression, suggesting that mTORC1 mediates VEGF-

202 The PlGF and PlGF/VEGF dimers (but not VEGF-A) down-regulated the protein expression of glucose

203 at the tubulogenic effect of GW0742, but not VEGF-A, was PPARbeta/delta- and sirtuin-1-dependent.

204 hat mutant GlyRS-mediated disruption of Nrp1/VEGF-A signalling is permissive to maturation and mainte

205 stand the role of EGR mediated regulation of VEGF A and FGF 2 signaling in buffalo luteal cells.

206 Alternate splicing in the exon-8 of VEGF-A results in the formation of VEGFxxxa (VEGF(165)a)

207 ted culture system reinforced by addition of VEGF-A, VEGF-C, and EGF most efficiently generated LECs,

208 rdiac macrophages to release high amounts of VEGF-A, thus inducing neovascularization and cardiac rep

209 However, reduced extracellular binding of VEGF-A to Nrp1 is known to disrupt post-natal blood vess

210 icate that changes in the bioavailability of VEGF-A sourced from ATII cells, namely the ratio of VEGF

211 Concentration of VEGF-A was further increased in patients with lower C1-I

212 Plasma concentrations of VEGF-A, VEGF-C, Ang1, and Ang2 were higher in patients w

213 r, little is known about the contribution of VEGF-A splice isoforms to kidney physiology and patholog

214 monary fibrosis, ATII-specific deficiency of VEGF-A or constitutive overexpression of VEGF-A165b inhi

215 mice harboring myofiber-specific deletion of VEGF-A (mVEGF(-/-)) and in vitro in primary human and ro

216 Deletion of VEGF-A, an HIF target gene, in CD8(+) T cells accelerate

217 mouse model with a conditional disruption of VEGF-A restricted to either epidermal or myeloid cells.

218 then result in increasing the expression of VEGF-A and VEGF-C via targeting the 3'UTR of mRNAs at a

219 TcdA or TcdB also induced the expression of VEGF-A in human colonic mucosal biopsies.

220 determined whether peritoneal expression of VEGF-A is regulated by TGF-beta1 through the ID1 pathway

221 melatonin-induced differential expression of VEGF-A isoforms culminates in alterations in gonadotroph

222 We demonstrate that half of VEGF-A-regulated gene promoters are characterized by a t

223 Here, we examined the impact of VEGF-A on neurologic changes that underly HSK using a mo

224 We found a significant increase of VEGF-A, VEGF-C, and Ang1 levels in U-HAE patients compar

225 and that it functions largely independent of VEGF-A (vascular endothelial growth factor-A).

226 are phenocopied by intraocular injection of VEGF-A or pericyte-specific inactivation of the murine g

227 VEGF antagonist that blocks all isoforms of VEGF-A in patients with neovascular age-related macular

228 intenance of this phenotype, as knockdown of VEGF-A gene expression or treatment with VEGF-A-inactiva

229 EC-Glrx TG mice showed higher levels of VEGF-A in the tumors, indicating hypoxia, which may stim

230 myeloid cells produced pathogenic levels of VEGF-A within HSV-1-infected corneas, and CD4(+) cell de

231 ere characterized by higher plasma levels of VEGF-A, VEGF-C, and Ang2 compared with the other patient

232 present study indicate that manipulation of VEGF-A splice isoforms could be a novel therapeutic aven

233 Surprisingly, the classical mechanism of VEGF-A action via interaction with VEGF receptors does n

234 Both neutralization of VEGF-A and inhibition of its signalling pathway attenuat

235 The differential regulation of VEGF-A vs VEGF-C by AR may then result in differential i

236 there is no clear information on the role of VEGF-A in IPF.

237 Previous studies of VEGF-A:VEGFR binding have measured binding kinetics for

238 fector of TGFbeta1 dependent upregulation of VEGF-A, and highlights a novel potential therapeutic tar

239 -C expression, yet this miR-185-5p effect on VEGF-A was reversed via AR's positive regulation on the

240 Only VEGF-A stimulated HUVEC migration and proliferation wher

241 SUV(max) was not related to plasma VEGF-A at all scan moments.

242 ized uptake values were compared with plasma VEGF-A and time to disease progression.

243 ignaling may limit inflammation by promoting VEGF-A production and, thus, lymphangiogenesis during in

244 rAAV.VEGF-A, though stimulating angiogenesis, induced neither

245 As a result, rAAV.Tbeta4 but not rAAV.VEGF-A improved EF in db hearts (34.5 +/- 1.4%), but les

246 We quantified the kinetics of the recent VEGF-A:PDGFRbeta interaction for the first time with KD

247 ineered single-chain version of pan-receptor VEGF-A with an N-terminal cysteine-containing tag for si

248 Recombinant VEGF-A elevated p-Ser166-Mdm2 by 50-125% and stimulated

249 and the 2 KLF proteins cooperate to regulate VEGF-A, VEGF-C, FGFR3, and p57 by binding to the regulat

250 -1 cells and primary islets, c-Kit regulates VEGF-A expression via the Akt/mammalian target of rapamy

251 3776 and rs114254831 (C2/CFB), and rs943080 (VEGF-A)-and the genetic risk score (GRS) were assessed f

252 CDI patients had significantly higher serum VEGF-A that subsequently decreased after treatment.

253 ts as a result of their expression of single VEGF-A isoforms.

254 promoting in vivo HIF-1alpha stabilization, VEGF-A production, and revascularization in the ischemic

255 UB cells synthesize VEGF-A and PDGF-BB proteins and RNA, whereas the MM cell

256 Therapeutic intervention by targeting VEGF-A, VEGFR2, and VEGFR3 inhibited tumor growth, consi

257 ease in expression of the HIF-1alpha targets VEGF-A, glucose transporter-1, and lactate dehydrogenase

258 It was observed that VEGF A and FGF 2 induced angiogenesis, cell proliferatio

259 We found that VEGF-A stimulation can induce a tyrosine phosphorylation

260 We found that VEGF-A(121) also binds VEGFR1 with an affinity K(D) = 3.

261 Here we report that VEGF-A and IGF-1 differ in their ability to stabilize ne

262 UVEC monolayers, flux analysis revealed that VEGF-A promoted glycolysis at the expense of fatty acid

263 These studies suggest that VEGF-A acts via interaction with NRP-1 to trigger intrac

264 The VEGF-A isoforms play a crucial role in vascular developm

265 Differential splicing of the VEGF-A gene produces multiple functional isoforms includ

266 xamined the vasculoprotective effects of the VEGF-A isoform VEGF-A165b in diabetic nephropathy.

267 therapies, specifically those targeting the VEGF-A/VEGFR2 pathway, have been approved for subsets of

268 zation and vascular barrier function via the VEGF-A/VEGFR2 signaling pathway.

269 , but the overall beneficial effects of this VEGF-A targeting agent are relatively modest, in part du

270 Thus, VEGF-A can shape the sensory and sympathetic nerve lands

271 VWF also binds to VEGF-A and fibroblast growth factor-2 (FGF-2) in human p

272 sel formation in animal models comparable to VEGF-A.

273 fferent functional behavior when compared to VEGF-A or TGF-beta treatment alone.

274 longs to the VEGF family, but in contrast to VEGF-A, VEGF-B does not regulate blood vessel growth.

275 retinal vascular endothelial cells (ECs) to VEGF-A, leading to upregulation of angiopoietin-2 (Ang2)

276 therapy may overcome an escape mechanism to VEGF-A suppression in the management of nAMD.

277 lations that were intrinsically resistant to VEGF-A blockade did not exhibit any of these features, c

278 elanomas that are intrinsically resistant to VEGF-A blockade do not show any evidence of compensatory

279 Tumor xenografts that initially responded to VEGF-A inhibition underwent an adaptation in vivo, leadi

280 study, we examined the adaptive response to VEGF-A inhibition by a loss-of-function analysis using p

281 s, melanomas that are initially sensitive to VEGF-A blockade acquire adaptive resistance by adopting

282 GCF total VEGF-A content was significantly higher in the GAgP grou

283 and 4E-BP1 regulate HIF-1alpha translation, VEGF-A is primarily under the control of 4E-BP1/eIF4E.

284 eries offer a new paradigm for understanding VEGF-A, while further stressing the need to take care in

285 monstrated that the anti-angiogenic variant, VEGF-A(165b) selectively prefers VEGFR2 binding at an af

286 VEGF-A(121) and an anti-angiogenic variant, VEGF-A(165b).

287 rowth factor, soluble TIE-1, soluble VEGFR1, VEGF-A, VEGF-C, VEGF-D, VEGF-A isoform 121, bone morphog

288 revascularization and relapse, in part, via VEGF-A release.

289 osts promote VEC proliferation, probably via VEGF-A signaling, whereas IFNgamma shows an antiangiogen

290 by macrophages within the bridge, which via VEGF-A secretion induce a polarized vasculature that rel

291 In vitro, VEGF-A from infected corneas repressed sensory nerve gro

292 sub-podocyte space coverage is reduced when VEGF-A is depleted, all of which are rescued in VEGF-A16

293 cells were then cultured and stimulated with VEGF A and FGF 2.

294 luteal cells were cultured and treated with VEGF A and FGF 2 and the mRNA expression pattern of EGR

295 (FGF-2) in human plasma and colocalizes with VEGF-A in ECs.

296 ic disease-particularly, in combination with VEGF-A blockers (but not VEGFR2 TKIs) in resected breast

297 conditions, but also highly correlated with VEGF-A and Klotho.

298 current findings linking TP53 mutation with VEGF-A upregulation offered a mechanistic explanation fo

299 of VEGF-A gene expression or treatment with VEGF-A-inactivating antibody reduces these responses.

300 lar dysfunction in diabetic nephropathy, yet VEGF-A knockout and overexpression of angiogenic VEGF-A