ライフサイエンスコーパス: growth factor

1 se activity upon stimulation with fibroblast growth factor.

2 of the graft bed by agarose-basic fibroblast growth factor.

3 talloproteinases 1, and vascular endothelial growth factor.

4 omain, apply force, and release the TGF-beta growth factor.

5 original secretion mechanism of a particular growth factor.

6 cancer progression, such as the insulin-like growth factors.

7 mediator downstream of various cytokines and growth factors.

8 ins multiple anti-inflammatory cytokines and growth factors.

9 C1 by amino acid stimulation, rather than by growth factors.

10 t state partially in response to profibrotic growth factors.

11 s to use naturally occurring combinations of growth factors.

12 cient for Akt phosphorylation in response to growth factors.

13 any exogenous material such as scaffolds or growth factors.

14 nvironmental inputs, including nutrients and growth factors.

15 Human insulin-like growth factor 1 (IGF-1) is a 70 amino acid protein hormo

16 rculating levels of insulin and insulin-like growth factor 1 (IGF-1).

17 munoassay for quantification of insulin-like growth factor 1 (IGF1) in human plasma.

18 t and are diagnosed by elevated insulin-like growth factor 1 levels and growth hormone levels; initia

19 s lineage and was stimulated by insulin-like growth factor 1 receptor (IGF1R) activation.

20 roRNA levels regulate SIRT1 and insulin-like growth factor 1 signalling.

21 ment of insulin resistance, and insulin-like growth factor 1.

22 metabolites in combination with insulin-like growth factor-1 are shown to promote the corneal epithel

23 mical positivity for p4E-BP1 or insulin-like growth factor-1 receptor was statistically significantly

24 Impaired insulin/insulin-like growth factor-1 signalling (IGF-1) and insulin resistanc

25 Fibroblast Growth Factor 19 (FGF19) is one of the most frequently a

26 GR5, the BA-induced gut hormones, fibroblast growth factor 19 and glucagon-like peptide 1, and the BA

27 Fibroblast growth factor 2 (FGF2) has previously been implicated in

28 Fibroblast growth factor 2 (FGF2) is crucial for the development an

29 Drosophila imaginal disc growth factor 2 (IDGF2) is a member of chitinase-like pr

30 Insulin-like growth factor 2 (IGF2) is the major fetal growth hormone

31 actor alpha and lower levels of insulin-like growth factor 2.

32 VAT activity was associated with fibroblast growth factor-2 (FGF2) levels.

33 ed increased expression levels of fibroblast growth factor-2, transforming growth factor-beta1, and p

34 of inflammation, serum levels of fibroblast growth factor 21 (FGF21), and activation of signaling pa

35 stance with increased circulating fibroblast growth factor 21 (FGF21), elevated Fgf21 mRNA and protei

36 terestingly, fasting induction of fibroblast growth factor 21 in liver was attenuated.

37 irculating levels of bone-derived fibroblast growth factor 23 (FGF23) increase early during acute and

38 and dynamic expression pattern of fibroblast growth factor 8 (Fgf8) in the HAA anlage, which was regu

39 (PDGFRalpha) and its ligand platelet-derived growth factor A (PDGF-A) are co-expressed in migrating c

40 lacental growth factor; vascular endothelial growth factor A and D; vascular endothelial growth facto

41 ; hepatocyte growth factor; platelet-derived growth factor AA and BB; placental growth factor; vascul

42 othelial growth factor, and platelet-derived growth factor AB) before and after completing 2 therapy

43 e migration and proliferation in response to growth factor activation to form new vessel branches.

44 antibodies or small molecules that mitigate growth factor activity.

45 p66shc is a growth factor adaptor protein that contributes to mitoch

46 ffect of switching anti-vascular endothelial growth factor agents for treatment of neovascular age-re

47 nduced by the overexpression of transforming growth factor-alpha (TGF-alpha), established by the pres

48 a- and extravascular transport of nutrients, growth factors and drugs; and cell proliferation in comp

49 organogenesis and are primarily regulated by growth factors and extracellular matrix.

50 Genetic assays revealed that Abl allows growth factors and Semaphorin/Plexin repellents to combi

51 factor receptor (PDGFR) senses extracellular growth factors and transfer the signals inside the cells

52 ciated tyrosine kinase, vascular endothelial growth factor, and cell cycle pathways, whereas esophage

53 broblast growth factor, vascular endothelial growth factor, and platelet-derived growth factor AB) be

54 RNAs encoding various chemokines, cytokines, growth factors, and angiogenesis mediators, with CXCL12

55 h angiocrine factors, which include secreted growth factors (angiokines), extracellular matrix molecu

56 Anti-vascular endothelial growth factor (anti-VEGF) drugs can cause phenotypic alt

57 y driven by use of anti-vascular endothelial growth factor (anti-VEGF) injections from 2012 to 2013.

58 ate tumor uptake of the vascular endothelial growth factor antibody bevacizumab could explain lack of

59 Many angiogenic growth factors are regulated by hypoxia-inducible factor

60 Circulating cytokines and growth factors are regulators of inflammation and have b

61 Growth factors are signaling molecules which orchestrate

62 f fat with ROS or PGZ on i) platelet-derived growth factor-BB (PDGF-BB)-stimulated proliferation of h

63 ng growth factor-beta1, and platelet-derived growth factor-BB at 2 weeks compared with baseline, foll

64 cal prosclerotic growth factor, transforming growth factor beta (TGF-beta), is thought to play a pivo

65 ignal transduction molecules in transforming growth factor beta (TGFbeta) ligand pathways that have b

66 ing, or A83-01, an inhibitor of transforming growth factor beta (TGFbeta) signaling.

67 a2SP(+/-) LSCs was activated by transforming growth factor beta (TGFbeta)-activated kinase 1 (TAK1; M

68 pressed many genes regulated by transforming growth factor beta 1 that mediate immunosuppression.

69 e colony-stimulating factor and transforming growth factor beta alone, whereas CD14(+) classical mono

70 pic chondrogenic induction with transforming growth factor beta to set up a dual-compartment culture.

71 ation-progenitor, proliferation-transforming growth factor beta, and Wnt-catenin beta1.

72 CV-infected hepatocytes express transforming growth factor beta, which activates stromal fibroblast m

73 Transforming growth factor beta-activated kinase 1 (TAK1) is a key me

74 ea with decreased periostin and transforming growth factor beta-positive cells within Asm bundles, in

75 , but surprisingly, more active transforming growth factor beta.

76 In the transforming growth factor-beta (Tgf-beta) pathway, exposure to ligan

77 We have shown a vital role for transforming growth factor-beta (TGF-beta) signals in safe-guarding s

78 mming was similarly enhanced on transforming growth factor-beta and WNT inhibition and was achieved m

79 found that a combination of the transforming growth factor-beta inhibitor SB431542 and the WNT inhibi

80 1C (ACVR1C), a component of the transforming growth factor-beta receptor superfamily.

81 rkers of fibrosis (collagen and transforming growth factor-beta) and immunostaining for beta catenin.

82 myeloid deficiency of TGF-beta (transforming growth factor-beta) signaling.

83 used by a point mutation in the transforming growth factor-beta-induced (TGFBI) gene, located on chro

84 ically, sphingosine ameliorates transforming growth factor-beta-induced collagen accumulation, CTGF,

85 suppressed the IL10 effects on transforming growth factor-beta-induced fibrotic signaling in BM-FPCs

86 reparative cytokines, including transforming growth factor-beta.

87 Increased transforming growth factor beta1 (TGF-beta1) in mammary adipose tissu

88 Transforming growth factor beta1 (TGFbeta1) is the principal pro-fibr

89 eptor 1, 2, and 3; osteopontin; transforming growth factor beta1 and beta2; thrombospondin 2; interce

90 Because the signaling of transforming growth factor-beta1 (TGF-beta1) and tumor necrosis facto

91 y increased accumulation of the transforming growth factor-beta1 (TGF-beta1) in skeletal muscles and

92 ations (versus normal aorta) of transforming growth factor-beta1 (TGF-beta1), connective tissue growt

93 p9, which could activate latent transforming growth factor-beta1 (TGF-beta1).

94 In activation of the transforming growth factor-beta1 precursor (pro-TGF-beta1), integrins

95 t enrichment analysis uncovered transforming growth factor-beta1 signaling activation in vastus later

96 of fibroblast growth factor-2, transforming growth factor-beta1, and platelet-derived growth factor-

97 ibers secrete and concentrate the fibroblast growth factor binding protein 1 (FGFBP1) at NMJs.

98 unx1-dependent transcription of insulin-like growth factor binding protein 3 (IGFBP3), and that this

99 ker of cell cycle arrest (urine insulin-like growth factor-binding protein 7) and, finally, by functi

100 and Wnt pathway genes, and connective tissue growth factor by Pofut1 in skeletal muscle, with additio

101 manipulation of the in vitro environment and growth factors can direct differentiation of human pluri

102 cle regulator cyclin A and connective tissue growth factor (CTGF).

103 the transplant setting include keratinocyte growth factor, cytokines (IL-7 and IL-22), and hormonal

104 maximal thrombospondin and platelet-derived growth factor D expression.

105 Furthermore, decreased nerve growth factor, decreased c-fos and increased sympathetic

106 hin cells, and suggest that platelet-derived growth factor-dependent "redoxosomes," contribute to pro

107 )CD235a(-) mesoderm in a WNT- and fibroblast growth factor-dependent manner.

108 cell adhesion, migration, proliferation and growth factor-dependent signaling.

109 hat miR-874 inhibits CCNE1 expression during growth factor deprivation and that miR-874 down-regulati

110 Soluble klotho down-regulates growth factor-driven PI3K signaling, contributing to ext

111 molecular pathways, including the epidermal growth factor (EGF) pathway.

112 Epidermal growth factor (EGF) was found to stimulate CAR homodimer

113 as membrane localization, inhibits epidermal growth factor (EGF)-stimulated Ras signaling and diminis

114 chemotherapeutic agent doxorubicin (DXR) and growth factors (EGF and IGF-1).

115 Up-regulation of vascular endothelial growth factor enhances the therapeutic effect of human a

116 We find that platelet-derived growth factor evokes transient oxidation on or close to

117 Activating mutations in fibroblast growth factor (FGF) receptor 3 and inactivating mutation

118 atments lead to activation of the fibroblast growth factor (FGF) receptor, phospholipase C (PLC), pro

119 Fibroblast growth factor (Fgf) receptors have a recognized role in

120 Fibroblast Growth Factor (FGF) signaling promotes self-renewal in p

121 glycolytic enzymes downstream of fibroblast growth factor (FGF) signaling.

122 Fibroblast growth factor (FGF) signalling in the distal limb primes

123 that the loss of an intracellular fibroblast growth factor (FGF), FGF13, in the mouse DRG neurons sel

124 terning, identifying a network of fibroblast growth factor (FGF), wingless-related integration site (

125 XR were given daily injections of fibroblast growth factor (FGF)19.

126 the N-terminal prodomain from the C-terminal growth factor (GF) domain in each monomer, pro-TGF-beta

127 ins, matrix-bound chemokines, cytokines, and growth factors (GFs) influence functional properties of

128 Several growth factors (GFs) that together promote quiescent hum

129 Vascular endothelial growth factor has emerged as a significant contributor t

130 Hepatocyte growth factor (HGF) induces cell migration and scatterin

131 hese endothelial cells supply the hepatocyte growth factor (HGF) required for the chemotactic gradien

132 es could be MET, the receptor for hepatocyte growth factor (HGF).

133 Inhibition of the insulin-like growth factor I receptor (IGF-IR) is a new therapeutic s

134 es, including glucose, insulin, insulin-like growth factor I, triglycerides, cholesterol, cortisol, a

135 ive checkpoint role of TEC-expressed insulin growth factor (IGF) binding protein-7 (IGFBP7/angiomodul

136 eversible mechanisms identified Insulin-like growth factor (IGF1) deficiency with inadequate compensa

137 s of systemic administration of insulin-like growth factor II (IGF-II), a polypeptide that crosses th

138 enchymal cells, but not vascular endothelial growth factor in Hyal2(-/-) embryonic hearts, suggest th

139 ere persistent at skin sites and had similar growth factors in nonimmune blood.

140 ganoids, PPAR agonism is sufficient to drive growth-factor-independent growth in the context of concu

141 ry factors (e.g. inhibin alpha and VGF nerve growth factor-inducible), 2) activation of a signaling c

142 egimens that included a vascular endothelial growth factor inhibitor.

143 s specific to receiving vascular endothelial growth factor inhibitors (anti-VEGF) for wet age-related

144 intravitreal dosing of vascular endothelial growth factor inhibitors in DME could be associated with

145 Subsequently, anti-vascular endothelial growth factor injections and panretinal photocoagulation

146 n requiring 1 or 2 anti-vascular endothelial growth factor injections only.

147 erate when challenged with stressors such as growth factor insufficiency.

148 Progranulin (PGRN), a secreted growth factor, is a key regulator of inflammation and is

149 old increase in the expression of hepatocyte growth factor, known to be involved in myogenesis, cell

150 Epidermal growth factor-like (EGF) repeats are also small cysteine

151 factor-beta1 (TGF-beta1), connective tissue growth factor, matrix metalloproteinase-2 (MMP-2), MMP-1

152 Nerve growth factor (NGF) antagonism is on the verge of becomi

153 derived neurotrophic factor (BDNF) and nerve growth factor (NGF) are crucial modulators in the neurod

154 The neurotrophin nerve growth factor (NGF) has been implicated as a key mediato

155 nel subfamily M, member 8 (TRPM8); and nerve growth factor (NGF) in nasal biopsy specimens.

156 covered that KIF1Bbeta is required for nerve growth factor (NGF)-dependent neuronal differentiation t

157 mutants of ATL1 in PC-12 cells inhibit nerve growth factor (NGF)-induced neurite outgrowth.

158 patients with high expression of hepatocyte growth factor or unmethylated O(6)-methylguanine-DNA met

159 real injections of anti-vascular endothelial growth factor or verteporfin photodynamic therapy in com

160 x interactions between different cell types, growth factors, or cytokines and their receptors.

161 a multiplicity of cell types, cytokines, and growth factors participate.

162 chymal cell activation in a platelet-derived growth factor (PDGF)-dependent manner.

163 n CTS SSCT and that the presence of fibrotic growth factor, PDGF-AA, results in increased proliferati

164 ogenesis factors (angiopoietin 2; hepatocyte growth factor; platelet-derived growth factor AA and BB;

165 ore chondrogenic phenotype in the absence of growth factors, potentially providing an eventual therap

166 Plasma rich in growth factors (PRGF) is a concentrated suspension of gr

167 dies indicates that these treatments enhance growth factor production that in turn facilitates hair f

168 lls required the expression of the epidermal growth factor receptor (EGFR) and of its ligand, amphire

169 r bound 2 (GRB2) to phosphorylated epidermal growth factor receptor (EGFR) as a model system.

170 The role of epidermal growth factor receptor (EGFR) inhibition in chemoradiati

171 Epidermal growth factor receptor (EGFR) interacts with integrins d

172 concurrent administration of anti-epidermal growth factor receptor (EGFR) monoclonal antibodies with

173 Here, using a beta-cell specific epidermal growth factor receptor (EGFR) null mouse, we show that e

174 xpression of amplified and mutated epidermal growth factor receptor (EGFR) presents a substantial cha

175 helial growth factor (VEGFR)-2 and epidermal growth factor receptor (EGFR) signaling by enhancing the

176 Epidermal growth factor receptor (EGFR) signaling is a known media

177 In addition, epidermal growth factor receptor (EGFR) signaling is regulated by

178 d solid tumor targets, such as the epidermal growth factor receptor (EGFR) that effectively induces c

179 Current anti-epidermal growth factor receptor (EGFR) therapy for oral cancer do

180 repair pathway, controlled by the epidermal growth factor receptor (EGFR), is critical to recovery f

181 ported to regulate the function of epidermal growth factor receptor (EGFR), the effect of protein met

182 , a well-characterized paradigm of epidermal growth factor receptor (EGFR)-Ras-ERK signaling, has ide

183 ole-brain radiotherapy (WBRT), and epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors

184 ated that RCN2 interacted with the epidermal growth factor receptor (EGFR).

185 lls resulted in a higher level of fibroblast growth factor receptor (FGFR) activation and ERK1/2 phos

186 Platelet-derived growth factor receptor (PDGFR) senses extracellular grow

187 ed ALL proliferation in ABL/platelet-derived growth factor receptor (PDGFR)-mutant models with mean 6

188 ctor receptor alpha (PDGFRA), and fibroblast growth factor receptor 1 (FGFR1) to cell proliferation a

189 denced by a decrease in vascular endothelial growth factor receptor 1 positive (VEGFR1(+)) myeloid ce

190 growth factor A and D; vascular endothelial growth factor receptor 1, 2, and 3; osteopontin; transfo

191 latory mechanism of one such RTK, fibroblast growth factor receptor 2 (FGFR2) kinase, is still unknow

192 ologists recommendations for human epidermal growth factor receptor 2 (HER2) testing in breast cancer

193 detection and estimation of human epidermal growth factor receptor 2 (HER2), a biomarker for breast

194 ors, 70.5% of luminal B-like human epidermal growth factor receptor 2 (HER2)-negative tumors, 82.8% o

195 efficacy of chemotherapy and human epidermal growth factor receptor 2 (HER2, encoded by the gene ERBB

196 Vascular endothelial growth factor receptor 2 (VEGFR2) localized on the surfa

197 types: luminal A, luminal B, human epidermal growth factor receptor 2 enriched, and basal like.

198 tric oxide synthase/Akt/vascular endothelial growth factor receptor 2 signaling, and a reduction in o

199 sed on estrogen receptor and human epidermal growth factor receptor 2 status was also assessed.

200 on of anti-TLR2 and antivascular endothelial growth factor receptor 2 yielded an additive therapeutic

201 S in patients with high-risk human epidermal growth factor receptor 2-negative breast cancer compared

202 For 145 human epidermal growth factor receptor 2-negative patients younger than

203 v 6%; P = .08), but not for human epidermal growth factor receptor 2-positive (luminal and nonlumina

204 treatment of node-positive, human epidermal growth factor receptor 2-positive early-stage breast can

205 by a gain-of function mutation in fibroblast growth factor receptor 3 (FGFR3).

206 homeobox protein 1 and vascular endothelial growth factor receptor 3) as well as blood endothelial m

207 MAN2A1-FER in 4 cell lines led to epidermal growth factor receptor activation of BRAF, MEK, and AKT;

208 r tyrosine kinase (KIT) and platelet-derived growth factor receptor alpha (PDGFRA) mutations.

209 , tyrosine kinase 2 (TYK2), platelet-derived growth factor receptor alpha (PDGFRA), and fibroblast gr

210 Here, we show that platelet-derived growth factor receptor alpha (PDGFRalpha) and its ligand

211 Here we report that platelet-derived growth factor receptor alpha (PDGFRalpha) positive ( + )

212 gnaling pathways, including platelet-derived growth factor receptor alpha (PDGFRalpha) signaling, whi

213 Platelet-derived growth factor receptor alpha (PDGFRalpha), a tyrosine ki

214 asis suppressor interacts with the epidermal growth factor receptor and mediates its downstream signa

215 ized SHP2 co-localizes with platelet-derived growth factor receptor and NOX1/4.

216 The molecular adapter growth factor receptor binding protein 14 (Grb14) is an

217 this occurs in vivo, we used the binding of growth factor receptor bound 2 (GRB2) to phosphorylated

218 specific protein 6, oncostatin M, hepatocyte growth factor receptor etc.

219 Members of the epidermal growth factor receptor family (ErbB family) possess a wi

220 Activation of the fibroblast growth factor receptor FGFR4 by FGF19 drives hepatocellu

221 Purpuric drug eruptions caused by epidermal growth factor receptor inhibitors are uncommon and have

222 purpuric skin eruptions caused by epidermal growth factor receptor inhibitors.

223 inase inhibitor crizotinib and the epidermal growth factor receptor kinase inhibitor canertinib; thes

224 Eps15 (epidermal growth factor receptor pathway substrate 15)-homology do

225 and incorporation into glutathione, linking growth factor receptor signaling with amino acid uptake

226 te acetate, Gq/11-coupled GPCR, or epidermal growth factor receptor stimulation promotes beta-arresti

227 iate the increase independently of epidermal growth factor receptor transactivation.

228 The epidermal growth factor receptor tyrosine kinase inhibitor erlotin

229 sease progression after first-line epidermal growth factor receptor tyrosine kinase inhibitor therapy

230 Epidermal growth factor receptor tyrosine kinase inhibitors, inclu

231 agments F(ab')2 and Fab) targeting epidermal growth factor receptor were labeled with Alexa750 or (64

232 criptional regulation of the human epidermal growth factor receptor-2 (HER2) contributes to an enhanc

233 luding estrogen receptor and human epidermal growth factor receptor-2.

234 ve tissue progenitor cells, platelet-derived growth factor receptor-alpha-positive cells, and alpha-s

235 binding of the isolated SH2 domain of Grb2 (growth factor receptor-bound protein 2) and the isolated

236 tokine TNFalpha and ligands of the epidermal growth factor receptor.

237 ns, are barriers to effective anti-epidermal-growth-factor-receptor (EGFR) therapy.

238 horylation (on S2159) in response to certain growth factor receptors (i.e., EGF-receptor but not insu

239 CAM-1, VE-cadherin, and vascular endothelial growth factor receptors (VEGFRs) that resides at endothe

240 ctivity associated with vascular endothelial growth factor receptors 1, 2, and 3, currently in phase

241 Many receptor systems, notably including growth factor receptors and G protein-coupled receptors,

242 uired for efficient internalization of major growth factor receptors involved in liver regeneration a

243 p positive correlated gene, while hepatocyte growth factor-regulated tyrosine kinase substrate as the

244 Tr (also known as delta/notch-like epidermal growth factor-related receptor [DNER]; 0.006%).

245 The growth and motility factor Hepatocyte Growth Factor/Scatter Factor (HGF/SF) and its receptor,

246 mportance of posttranslational regulation of growth factor signaling in this process.

247 Regulation of growth factor signaling involves reversible inactivation

248 ecialized processes such as neurogenesis and growth factor signaling.

249 ) blocks AngII-induced genes associated with growth-factor signaling and atherosclerosis.

250 Here we report that oncogenic kinase and growth-factor signaling converge to induce the expressio

251 primary regulator of stimulated cytokine and growth factor signalling.

252 Nutrients and growth factor stimuli converge on the conserved protein

253 if the up-regulation of vascular endothelial growth factor strengthens the protective effect of amnio

254 anges in vascular permeability are driven by growth factors such as VEGF and pro-inflammatory cytokin

255 Cs by utilizing hypoxia and basic fibroblast growth factor supplementation.

256 r cells focus on long-term maintenance under growth factor supplements into cell lines, which usually

257 ding the use of soluble vascular endothelial growth factor (sVEGF)-VEGF165, have been developed in th

258 ed with increased production of transforming growth factor (TGF) beta and interleukin (IL)-8.

259 Herein, we analyzed the role of transforming growth factor (TGF)-beta signaling for CNV formation by

260 nted protein known to stimulate transforming growth factor (TGF)-beta1 to -beta3 translation in vitro

261 AM10 expression is increased by transforming growth factor (TGF)-beta1, and ADAM10-mediated sEphrin-B

262 ential of this platform for: i) transforming growth factor (TGF)-beta1-induced spatial differentiatio

263 Angiopoietins are a family of growth factors that are ligands for the tyrosine kinase

264 ctors (PRGF) is a concentrated suspension of growth factors that promotes restoration of lost periodo

265 ipants who received antivascular endothelial growth factor therapies for neovascular AMD had decrease

266 n on the effect of anti-vascular endothelial growth factor therapy in eyes with diabetic macular edem

267 t of intravitreous anti-vascular endothelial growth factor therapy.

268 ression of a broad spectrum of cytokines and growth factors to allow virus replication and spread in

269 brosis whereby the prototypical prosclerotic growth factor, transforming growth factor beta (TGF-beta

270 Atomic force microscopy analysis of PRP and growth factor treated cartilage gave a 5-fold increase i

271 ding the highly cancer relevant insulin-like growth factor type 1 receptor (IGF-1R).

272 Insulin-like growth factor type 2 (IGF2) receptor (IGF2R) recognizes

273 to quantify angiogenesis factors (fibroblast growth factor, vascular endothelial growth factor, and p

274 t-derived growth factor AA and BB; placental growth factor; vascular endothelial growth factor A and

275 ular density (MVD), and vascular endothelial growth factor (VEGF) expression) from 9 patients with pr

276 Vascular endothelial growth factor (VEGF) is implicated in the peritoneal mem

277 e feedback regulator of vascular endothelial growth factor (VEGF) receptor activation.

278 We also show how vascular endothelial growth factor (VEGF) regulates PRKCB promoter function i

279 Because deficiency of vascular endothelial growth factor (VEGF) results in thrombotic microangiopat

280 trate the importance of Vascular Endothelial Growth Factor (VEGF) secretion for this pathway of hypox

281 cers and isoforms along vascular endothelial growth factor (VEGF) signaling pathways at concentration

282 Here, we showed that vascular endothelial growth factor (VEGF) signaling within the glomeruli of A

283 Anti-vascular endothelial growth factor (VEGF) therapy has demonstrated efficacy i

284 tion (nAMD) during anti-vascular endothelial growth factor (VEGF) treatment.

285 factor 1 (SDF-1alpha), vascular endothelial growth factor (VEGF), hypoxia-inducible factor 1-alpha (

286 terleukin (IL)-6, IL-8, vascular endothelial growth factor (VEGF), monocyte chemoattractive protein 1

287 Vascular endothelial growth factor (VEGF)-A has been implicated in this conte

288 licing in the exon-8 of vascular endothelial growth factor (VEGF)-A results in production of proangio

289 ation by regulating the vascular endothelial growth factor (VEGF)-A, VEGF-C, FGFR3, and p57/CDKN1C ge

290 ebrand factor (vWF) and vascular endothelial growth factor (VEGF)-C expression were measured.

291 Vascular endothelial growth factor (VEGF)-D is capable of inducing angiogenes

292 For example, vascular endothelial growth factor (VEGF)-mediated angiogenesis is inhibited

293 angiogenesis induced by vascular endothelial growth factor (VEGF).

294 iseases, supported with vascular endothelial growth factor (VEGF-A) and tumor necrosis factor (TNF)-a

295 t was shown to modulate vascular endothelial growth factor (VEGFR)-2 and epidermal growth factor rece

296 The sensitivity of cells to DXR and to growth factors was evaluated using an MTT assay.

297 weight gain (GWG), birth size, and childhood growth factors with adult BMI in daughters at midlife us

298 chanism that protects tumor cells from serum growth factor withdrawal.

299 mphiphiles (PAs) that encapsulates cells and growth factors within a muscle-like unidirectionally ord

300 It incorporates leukocytes, platelets, and growth factors within the dense fibrin matrix and can be