ライフサイエンスコーパス: growth factor

1 rkA) is the high-affinity receptor for nerve growth factor.

2 PDAC cells induced by CAF-derived hepatocyte growth factor.

3 ated relevant pathways associated with these growth factors.

4 ility, and decreases dependence on exogenous growth factors.

5 vivo, in part via secretion of a cocktail of growth factors.

6 differentiation, cytoskeleton components and growth factors.

7 nts and adhesion molecules to chemokines and growth factors.

8 Third, we uncovered that insulin-like growth factor 1 (IGF1) is produced by tumor-associated m

9 T activation can be promoted by insulin-like growth factor 1 (IGF1) or insulin via a pathway includin

10 Evidence suggests Insulin-like growth factor 1 (IGF1) signaling is involved in the init

11 ncluding significantly elevated insulin-like growth factor 1 levels, larger weight and body length, h

12 dema) involves the synergism of insulin-like growth factor 1 receptor (IGF1R) with TSHR autoantibodie

13 (2) from the alpha-chain of the insulin-like growth factor 1 receptor that is critical for receptor a

14 l hypertrophy induced by IGF-1 (insulin-like growth factor 1).

15 of-function mutations affecting insulin-like growth factor 1, fibroblast growth factor receptor and W

16 rowth Factor Beta (TGFbeta) and insulin-like growth factor-1 (IGF-1) are known to promote fibrosis; h

17 , milk contains calcium and the insulin-like growth factor-1 that are of major relevance for children

18 IGF-1 (insulin-like growth factor-1) is markedly decreased in normal preterm

19 eptor), the growth factor IGF1 (insulin-like growth factor-1), and the splenic red pulp macrophage ge

20 urite markers betaIII tubulin and fibroblast growth factor 12, with differential effects in patients

21 dafermin, an engineered analog of fibroblast growth factor 19, inhibits bile acid synthesis and regul

22 Using fibroblast growth factor 2 (FGF2) as a model system, we addressed t

23 and IL-18, growth factors such as fibroblast growth factor 2 (FGF2), redox enzymes such as thioredoxi

24 rain-derived neurotrophic factor, fibroblast growth factor-2, and ciliary neurotrophic factor (CNTF),

25 actor, platelet concentrates, and fibroblast-growth factor-2.

26 ession of the metabolic regulator fibroblast growth factor 21 (FGF21) was blunted by TCS.

27 a coactivator 1-alpha) and FGF21 (fibroblast growth factor 21).

28 te systemic and direct effects of Fibroblast growth factor 23 (FGF23) and Klotho, which normally regu

29 ho functions as a co-receptor for fibroblast growth factor 23 (FGF23) signaling, whereas its shed ext

30 The discovery of fibroblast growth factor 23 (FGF23), which revolutionized the diagn

31 lar reabsorption of phosphate and fibroblast growth factor-23 (FGF23) at all CKD stages, and lower bl

32 wn-regulation of adenosine deaminase-related growth factor A (Adgf-A) from enterocytes is necessary f

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

34 proangiogenic factors, vascular endothelial growth factor A (VEGFA) and angiopoietin 2 (Ang2/ANGPT2)

35 Blockade of vascular endothelial growth factor A (VEGFA) and angiopoietin-2 (ANGPT2) comb

36 ntified four immune signatures, representing growth factors (A), type-2/3 cytokines (B), mixed type-1

37 ith reduced hippocampal vascular endothelial growth factor-A (VEGF-A) in both male and female mice, a

38 ther macrophage-derived vascular endothelial growth factor-A (Vegf-A) is crucial to establishing NMJ

39 owth factor-beta(1) and vascular endothelial growth factor-A secretion was measured in serum and/or c

40 deno-associated virus 1-vascular endothelial growth factor-A165 under control of a hypoxia-response e

41 Anti-vascular endothelial growth factor acts faster than laser therapy, which may

42 ential efficacy of anti-vascular endothelial growth factor agents in the treatment of DME as well as

43 Treatment with anti-vascular endothelial growth factor agents.

44 rine release of the EGFR ligand transforming growth factor alpha in a TACE-dependent manner.

45 and the expressions of vascular endothelial growth factor and core-binding factor subunit alpha-1 we

46 -stimulating factor (GM-CSF), a myelopoietic growth factor and pro-inflammatory cytokine, plays a cri

47 ate a fibrotic micro-environment and produce growth factors and cytokines that enhance tumor cell pro

48 e second characterised by high expression of growth factors and immunomodulatory molecules.

49 ) secreted higher VEGF (vascular endothelial growth factor) and lower TSP-1 (thrombospondin-1) levels

50 f HIF-1a, HIF-2a, VEGF (vascular endothelial growth factor), and eNOS (endothelial nitric oxide synth

51 tein subcomponents C1r/C1s, urchin embryonic growth factor, and bone morphogenetic protein 1 domain i

52 e microscopy using conjugates of antibodies, growth factors, and nucleic acids.

53 ; binds integrins, syndecans, collagens, and growth factors; and is assembled by cells into complex f

54 iated cell zone, stable, linear gradients of growth factors are formed across the crypts.

55 regeneration and wound repair than wild-type growth factors, as well as reduced tumour growth (associ

56 Platelet-derived growth factor B (PDGFB) plays a crucial role in recruitm

57 r the influence of a 1.5 kb platelet derived growth factor B (PDGFB) promoter.

58 Chlamydia also upregulates transforming growth factor beta (TGF-beta) expression, whose signalin

59 ercholesterolemia, and abnormal transforming growth factor beta (TGF-beta) signaling in smooth muscle

60 ulin/IGF-1 signaling [IIS]) and transforming growth factor beta (TGF-beta) signaling repress odr-10 e

61 e nitric oxide synthase (iNOS), transforming growth factor beta (TGF-beta), NADPH oxidase isoform 4 (

62 f the antiinflammatory cytokine transforming growth factor beta (TGF-beta).

63 ns poorly understood apart from Transforming Growth Factor beta (TGF-beta1)-mediated induction.

64 ich interact with microbes, and transforming growth factor beta (TGFB) signaling pathway, which is of

65 Here, we found transforming growth factor beta (TGFbeta) and bone morphogenetic prot

66 Transforming Growth Factor Beta (TGFbeta) and insulin-like growth fac

67 ed uterine functions, including transforming growth factor beta (TGFbeta) and LIF interleukin-6 famil

68 D3 to modulate transcription of transforming growth factor beta (TGFbeta)-dependent genes and thereby

69 preferred partner (LPP) mediate transforming growth factor beta (TGFbeta)-induced breast cancer cell

70 FA) had decreased expression of transforming growth factor beta 1 (TGF-beta1) because of interleukin-

71 which reduced the production of transforming growth factor beta 1 (TGF-beta1), a cytokine known to in

72 ed by T-helper type 2 cells and transforming growth factor beta 1 (TGFbeta1) contribute to the develo

73 monocyte chemotactic protein 1, transforming growth factor beta 1, TIR-domain containing adapter indu

74 transcription modulator of the transforming growth factor beta pathway, which activates autophagy an

75 ression of alphaSMA, PDGFbetaR, transforming growth factor beta receptor 1 (TGFbetaR1), collagen 1alp

76 on protein that binds to select transforming growth factor beta superfamily ligands, may enhance eryt

77 e profibrotic agonist, TGFbeta (transforming growth factor beta), additively upregulated myofibroblas

78 Transforming growth factor beta-1 (TGFbeta1) is a major regulator of

79 exquisite specificity to latent transforming growth factor-beta (L-TGF-beta).

80 Transforming growth factor-beta (TGF-beta) is well-known to induce br

81 , which is capable of enhancing transforming growth factor-beta (TGF-beta) mediated tenogenesis in hu

82 Transforming growth factor-beta (TGF-beta) promotes tumor invasion an

83 Here we found that transforming growth factor-beta (TGF-beta) superfamily member activin

84 n stimulation of fibroblasts by transforming growth factor-beta (TGFbeta) play a critical role in wou

85 a key role in the activation of transforming growth factor-beta (TGFbeta), a pro-fibrotic mediator th

86 ent - such as the activation of transforming growth factor-beta and the deposition of extracellular m

87 ry T cells (Tregs) and enhanced transforming growth factor-beta production by CD4(+) T cells.

88 Here we show that depletion of transforming growth factor-beta receptor 2 (TGFBR2) in CD4(+) T cells

89 Transforming growth factor-beta(1) and vascular endothelial growth fa

90 12], IL-23, IL-6, IL-27, IL-10, transforming growth factor-beta) that expand and differentiate both p

91 ibroblasts as well as TGF-beta (transforming growth factor-beta)-activated myofibroblasts.

92 ed the expression of TGF-beta1 (transforming growth factor-beta-1) and CTGF (connective tissue growth

93 Mutations in transforming growth factor-beta-induced (TGFBI) gene cause clinically

94 Transforming growth factor beta1 (TGFbeta1) has been shown to contrib

95 Transforming growth factor beta1 (TGFbeta1) is a cytokine that exerts

96 TGF-beta1 (transforming growth factor beta1), downstream of neutrophil elastase,

97 or being connected to TGFbeta1 (transforming growth factor beta1), interleukin-1, TNF-alpha, and BDNF

98 Transforming growth factor-beta1 (TGF-beta1) plays a premier role in

99 ) fibronectin on the surface of transforming growth factor-beta1 (TGF-beta1)-activated human myofibro

100 atelet-derived growth factor c, transforming growth factor beta2) and inflammation (tumor necrosis fa

101 r (IGF) transport and uptake by Insulin-like Growth Factor Binding Proteins (IGFBPs)" route in allerg

102 The work presented here further defines the growth factor-binding domain of MAGP-1.

103 ng an increase in stress marker insulin-like growth factor-binding protein 1 (IGFBP-1), were observed

104 itor of metalloproteinase-2 and insulin-like growth factor-binding protein 7 was measured at H0, H6,

105 ibitor of metalloproteinase-2 x insulin-like growth factor-binding protein 7 was poor with respective

106 e for type I collagen], IGFBP7 [insulin-like growth factor-binding protein-7], and GAL-3 [galectin-3]

107 ocalized activity of the clinically licensed growth factor BMP-2.

108 deno-associated virus 8-vascular endothelial growth factor C (AAV8-VEGF-C) was injected into the cist

109 tor of metalloproteinase 1, platelet-derived growth factor c, transforming growth factor beta2) and i

110 loop between PROX1 and vascular endothelial growth factor-C (VEGF-C) signaling.

111 s into latent GDF9 generated a highly potent growth factor, called hereafter Super-GDF9.

112 Neurotrophin-3 growth factor can improve cochlear neuron survival, and

113 Growth factors can stimulate tissue regeneration, but th

114 Under defined growth factor conditions, such adult stem cells (ASCs) g

115 Those growth factors could serve to distinguish the developmen

116 th the well established pain mediator, nerve growth factor, could also modify macrophage gene transcr

117 ulators (CCNB1, CCND1, RABL6), cytokines and growth factors (CSF2, IL-6, TNF, HGF, VEGF, and EGF), AT

118 ng evidence indicates that connective tissue growth factor (CTGF), a multifunctional signaling modula

119 Midkine-a, an injury-induced growth factor/cytokine that is expressed by Muller glia

120 In the adult brain, vascular endothelial growth factor D (VEGFD) is required for structural integ

121 A-MB-231 cells expressing miR-149, epidermal growth factor (EGF) and amphiregulin expression levels w

122 llus axis and is the source of the epidermal growth factor (EGF) family member NEUREGULIN1 (NRG1).

123 librium is feedback control of the epidermal growth factor (EGF) protease Rhomboid (Rho).

124 vitro by the Tyr kinase domain of epidermal growth factor (EGF) receptor.

125 re the increase in growth factor (epithelial growth factor (EGF), hepatocyte growth factor (HGF)) and

126 he molecular mechanism, we utilize epidermal growth factor (EGF)-inducible immediate early genes (IEG

127 neous physical activity were the increase in growth factor (epithelial growth factor (EGF), hepatocyt

128 Fibroblast Growth Factor (FGF) dependent signalling is frequently a

129 he three members of the endocrine-fibroblast growth factor (FGF) family, FGF19, 21, and 23 are circul

130 osttranscriptional attenuation of fibroblast growth factor (FGF) signaling is essential for the estab

131 , we found that components of the Fibroblast Growth Factor (FGF) signaling pathway were enriched in n

132 and myoblasts is mediated by the fibroblast growth factor (FGF) signaling pathway, and exogenous FGF

133 Fibroblast growth factor (FGF) signaling plays pivotal roles in gen

134 ss and trophectoderm cells due to fibroblast growth factor (FGF) signaling.

135 in self-renewal in the absence of fibroblast growth factor (FGF) signalling.

136 Fibroblast growth factors (FGF) act as proangiogenic and mitogenic

137 Here we show that acidic fibroblast growth factor (FGF1) derived from cancer-associated fibr

138 Most fibroblast growth factors (FGFs) function as receptor ligands throu

139 d similarly sized domains, such as Epidermal Growth Factor, Fibronectin Type 3, Immunoglobulin, and T

140 A reliable detection of the growth factor from each embryo culture medium of such a

141 of the EGFR ligand heparin-binding EGF-like growth factor (HB-EGF) in the beta-cell proliferative re

142 Heparin-binding epidermal growth factor like growth factor (HB-EGF), a crucial regulator of heart val

143 Hepatocyte growth factor (HGF) is a multifunctional protein that si

144 (epithelial growth factor (EGF), hepatocyte growth factor (HGF)) and the activation of the signallin

145 Co-occurrence of aberrant hepatocyte growth factor (HGF)/MET proto-oncogene receptor tyrosine

146 How Na(V) -CaM, CaMKII and FGF/fibroblast growth factor homologous factor interactions affect the

147 nase with immunoglobulin-like loop epidermal growth factor homology domain 2, vascular endothelial gr

148 Circulating insulin-like growth factor I (IGF-I) is positively associated with th

149 Insulin-like growth factor (IGF) binding protein 2 (IGFBP2) was disco

150 ch display dysregulation of the insulin-like growth factor (IGF) system.

151 nrichment of the "Regulation of Insulin-like Growth Factor (IGF) transport and uptake by Insulin-like

152 ong with higher serum levels of insulin-like growth factor (IGF)-1 as well as IGF-binding protein (IG

153 genes including LXR (lipid X receptor), the growth factor IGF1 (insulin-like growth factor-1), and t

154 presenting cells, they express the autocrine growth factor IL-2 which transforms them into rapidly di

155 BMPs are multifunctional growth factors implicated in regulating the ovarian func

156 EGFR degradation when activated by epidermal growth factor, increased EGFR protein expression, and co

157 ound that EC-specific YY1 ablation inhibited growth factor-induced angiogenesis.

158 suggests that nuclear Akt activity mediates growth factor-induced nuclear translocation of Raptor, a

159 We find that Vgf nerve growth factor inducible gene up-regulation is a common t

160 orphogenetic activity, with syndecan-binding growth factors inducing greater bone regeneration and wo

161 o secrete various cytokines, chemokines, and growth factors, initiating and perpetuating inflammatory

162 with intravitreal anti-vascular endothelial growth factor injection was observed in 4 patients.

163 iving intravitreal anti-vascular endothelial growth factor injections from July 1, 2013, to September

164 ome combination of anti-vascular endothelial growth factor injections, photodynamic therapy, topical

165 Physiologically, growth factor interactions with the extracellular matrix

166 and activity, which are further activated by growth factors involved in RMS development.

167 The lens epithelium-derived growth factor (LEDGF) is a cellular factor that binds IN

168 y of ADAM17 toward Heparin-binding epidermal growth factor like growth factor (HB-EGF), a crucial reg

169 Modulation of vascular endothelial growth factor-mediated immune suppression via angiogenes

170 ouse models of beta-cell failure acting as a growth factor necessary for beta-cell adaptation to high

171 In this study, we test nerve growth factor (NGF) as an understudied therapeutic for f

172 in E(2) (PGE(2)), bradykinin (BK), and nerve growth factor (NGF) as well as multiple kinases, includi

173 Nerve growth factor (NGF) regulates many aspects of neuronal b

174 a control by stimulating expression of nerve growth factor (NGF), a neurotrophin associated with airw

175 partly through androgen-driven expression of growth factors (Nrg2, Rspo3) by mesenchymal cells acting

176 y, these results highlight the importance of growth factors of the insulin family during two distinct

177 d signaling proteins that, when activated by growth factors or by mutation, drive oncogenic processes

178 onse to leucine whereas mTORC1 activation by growth factors or eccentric contractions was preserved.

179 aches for simultaneously delivering multiple growth factors or molecules from a single construct to a

180 Midkine is a heparin-binding growth factor, originally reported as the product of a r

181 Inhibition of multiple growth factor pathways may postpone resistance and exten

182 TRIM28 and TRIM27 inhibited platelet-derived growth factor (PDGF)-induced migration in human VSMCs.

183 increases the expression of platelet-derived growth factor (PDGFB) in human pulmonary arterial endoth

184 c bone marrow cell populations in vivo using growth factor pharmacotherapy show that cf-mRNA reflects

185 g enamel matrix derivative, platelet-derived growth factor, platelet concentrates, and fibroblast-gro

186 The human hepatocyte growth factor receptor (c-MET) signaling pathway is dysr

187 Epidermal growth factor receptor (EGFR) and human epidermal growth

188 irectly bind and activate cellular epidermal growth factor receptor (EGFR) and integrin beta1, respec

189 oss impacts recycling of the RTKs, epidermal growth factor receptor (EGFR) and proto-oncogene c-Met (

190 We apply this model to epidermal growth factor receptor (EGFR) antibodies and find that t

191 inases, including signaling by the epidermal growth factor receptor (EGFR) family (EGFR1-4 or the hum

192 Asymmetric dimer formation of epidermal growth factor receptor (EGFR) is crucial for EGF-induced

193 c tyrosine residue in STING by the epidermal growth factor receptor (EGFR) is required for directing

194 Acquired drug resistance in epidermal growth factor receptor (EGFR) mutant non-small-cell lung

195 nterleukin 6 receptor (IL-6R), and epidermal growth factor receptor (EGFR) signaling.

196 Targeting epidermal growth factor receptor (EGFR) through an allosteric mech

197 Several epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors

198 rosine kinases (RTKs), such as the epidermal growth factor receptor (EGFR), locally increases the abu

199 ly (ADP-ribose) polymerase (PARP), epidermal growth factor receptor (EGFR), Vascular endothelial grow

200 attenuation of the pro-tumorigenic Epidermal Growth Factor Receptor (EGFR)-Akt axis, and finally cell

201 n in a Drosophila genetic model of epidermal growth factor receptor (EGFR)-driven tumorigenesis simil

202 ncing KSHV infectivity through the epidermal growth factor receptor (EGFR).

203 egy for tumours overexpressing the epidermal growth factor receptor (EGFR).

204 We assessed actions of fibroblast growth factor receptor (FGFR) 2 in urothelium after cycl

205 tional optogenetic design for the fibroblast growth factor receptor (FGFR).

206 expression of numerous genes including nerve growth factor receptor (NGFR), which becomes transcripti

207 Platelet Derived Growth Factor Receptor (PDGFR) signaling is a central mi

208 Platelet-derived growth factor receptor (PDGFR)-alpha plays roles in cell

209 static RCC treated with vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitor

210 h included enhanced expression of fibroblast growth factor receptor 1 (FGFR1) and axonal guidance mol

211 Hypoxia induced increased fibroblast growth factor receptor 1 (FGFR1) expression in NSCLC cel

212 d whether dual versus single human epidermal growth factor receptor 2 (HER2) -targeting drugs added t

213 Human epidermal growth factor receptor 2 (HER2)-amplified breast cancers

214 RCA1/2 mutation (gBRCAm) and human epidermal growth factor receptor 2 (HER2)-negative metastatic brea

215 ormone receptor-positive and human epidermal growth factor receptor 2 (HER2)-negative metastatic brea

216 Methods: Patients with ER+/human epidermal growth factor receptor 2 (HER2)-negative metastatic brea

217 R2CLIMB study, patients with human epidermal growth factor receptor 2 (HER2)-positive breast cancer w

218 Patients with human epidermal growth factor receptor 2 (HER2)-positive metastatic brea

219 Conclusion Human epidermal growth factor receptor 2 (HER2)-targeted imaging with zi

220 Background Human epidermal growth factor receptor 2 (HER2)-targeted therapies are s

221 n site and the tumor markers human epidermal growth factor receptor 2 and estrogen receptor had an im

222 Ramucirumab-an IgG1 vascular endothelial growth factor receptor 2 antagonist-plus docetaxel was p

223 targeted therapies exist for human epidermal growth factor receptor 2 positive (HER2 +) breast cancer

224 t activation of VEGFR2 (vascular endothelial growth factor receptor 2) and decreases blood levels of

225 Other anti-fibroblast growth factor receptor 3 (FGFR3) compounds are showing p

226 Fibroblast growth factor receptor 3 (FGFR3) was also identified as

227 h factor receptor (EGFR) and human epidermal growth factor receptor 3 (HER3) have been investigated a

228 3K interactors, such as the platelet-derived growth factor receptor A (PDGFRA), as well as novel RNA-

229 (ICC), and cells expressing platelet-derived growth factor receptor alpha (PDGFRalpha(+) cells).

230 at p-Ezrin (T567) is controlled by epidermal growth factor receptor and MET.

231 ing insulin-like growth factor 1, fibroblast growth factor receptor and WNT signalling are similar to

232 een Target of Rapamycin (TOR) and Fibroblast growth factor receptor b (Fgfrb) signaling in ring muscl

233 is selectively mediated by platelet-derived growth factor receptor signaling.

234 everely disrupt PM association of fibroblast growth factor receptor substrate 2alpha but do not elimi

235 lore the novel hypothesis that regulation of growth factor receptor trafficking can be used to promot

236 The oncogene epidermal growth factor receptor variant III (EGFRvIII) is frequen

237 eins, including apolipoprotein E4, epidermal growth factor receptor, CD71 and programmed death-ligand

238 gesterone receptor (PR), and human epidermal growth factor receptor-2 (HER2) are the three crucial bi

239 e the linker for activation of T cells (LAT):growth-factor-receptor-bound protein 2 (Grb2):son of sev

240 e progenitors (APs) express platelet-derived growth factor receptors (PDGFRs), PDGFRalpha and PDGFRbe

241 n beta cells and increases expression of the growth factor receptors IGF-1R and c-Met.

242 h factor-beta-1) and CTGF (connective tissue growth factor), reduced fibroblast proliferation, and de

243 on and further investigated hepatoma-derived growth factor-related protein 3 (HRP3 or HDGFRP3).

244 PEA-OXA administration enhanced neurotrophic growth factor release and decreased the astroglial and m

245 The measurement of growth factors released in a culture medium is considere

246 ined media for the continued optimization of growth factors required to support the primary isolation

247 survival and inhibiting bFGF, HGF, and IGF1 growth factor rescue and also potentiates the activity o

248 Growth factor sequestration by IGFBP-3-Fc enhances the a

249 ing of PP2A-B56 to ADAM17 protease decreases growth factor signaling and tumor development in mice.

250 9 downregulation in TNBC enhances reciprocal growth factor signaling between macrophages and cancer c

251 d a minimal mathematical model demonstrating growth factor signaling is sufficient to guarantee this

252 ta support the model that the amino acid and growth factor signaling pathways converge on the Rag GTP

253 Pase acts in both the amino-acid-sensing and growth factor signaling pathways to control TORC1 activi

254 sters, direct crosstalk between integrin and growth-factor-signaling, and clarifies how compartmental

255 Anabolic metabolism mediated by aberrant growth factor signalling fuels tumour growth and progres

256 Growth factor signalling is also controlled at the cell

257 Growth factor signalling is dependent on the presence of

258 ix synthesis downstream of biomechanical and growth factor signals.

259 COVID-19 were enriched in tissue reparative growth factor signature A, whereas the profiles of those

260 ctor homology domain 2, vascular endothelial growth factor, soluble fms-like tyrosine kinase, von Wil

261 Reversely, upon growth factor stimulation, Exo70 is phosphorylated by ER

262 Upon growth factor stimulation, the guanine-nucleotide exchan

263 in nuclear mTORC1 activity in the absence of growth factor stimulation.

264 luding cytokines such as IL-1beta and IL-18, growth factors such as fibroblast growth factor 2 (FGF2)

265 It is known that growth factors such as insulin, IGF-1 and HGF support be

266 ing to reduced secretion of cancer-promoting growth factors, such as chemokines.

267 th similar normal morphologic features, some growth factors, such as IL-1beta, might exhibit differen

268 e transcription factor HIF or HIF-responsive growth factors, such as VEGF, for the treatment of cance

269 -function mechanism, augmenting transforming growth factor (TGF) beta signaling.

270 orneal fibroblasts treated with transforming growth factor (TGF) beta-1 or generated directly from cu

271 ced the pro-fibrotic effects of transforming growth factor (TGF)-beta as a potential mechanism for in

272 line-derived neurotrophic factor (GDNF) is a growth factor that regulates the health and function of

273 The ability of hepatocyte growth factor, the ligand for MET, to promote AKT activa

274 equiring bilateral anti-vascular endothelial growth factor therapy were included.

275 gulated during HCMV infection but not during growth factor treatment.

276 that sequential inputs from amino acids and growth factors trigger PA production required for mTORC1

277 ed regions with distinct microstructures and growth factor types.

278 had increased baseline vascular endothelial growth factor (VEGF) (880.0 pg/mL vs 245.4 pg/mL; P = .0

279 Vascular endothelial growth factor (VEGF) and semaphorin-binding receptor Neu

280 r-1 alpha (HIF-1alpha), vascular endothelial growth factor (VEGF) and tumor necrosis factor-alpha (TN

281 ilized with heparin and vascular endothelial growth factor (VEGF) could be implanted into the arteria

282 cy and switches in anti-vascular endothelial growth factor (VEGF) drug.

283 iogenic drugs targeting vascular endothelial growth factor (VEGF) has transformed therapy for these p

284 ce, predicted polarized vascular endothelial growth factor (VEGF) secretion, and matched iPSC-RPE mon

285 sensitive to increased vascular endothelial growth factor (VEGF) stimulation due to a reduced capaci

286 his study assessed anti-vascular endothelial growth factor (VEGF) therapy intensity and its relations

287 Anti-vascular endothelial growth factor (VEGF) treatment of neovascular age-relate

288 and stable secretion of vascular endothelial growth factor (VEGF), brain-derived neurotrophic factor,

289 factor receptor (EGFR), Vascular endothelial growth factor (VEGF), etc.

290 target genes, including vascular endothelial growth factor (VEGF), where it enhances local histone H3

291 is a novel inhibitor of vascular endothelial growth factor (VEGF)-C and VEGF-D.

292 ein, we identified that vascular endothelial growth factor (VEGF)-C, a potent lymphangiogenic factor,

293 (S1PRs), which restrain vascular endothelial growth factor (VEGF)-induced angiogenesis, spatially res

294 Furthermore, vascular endothelial growth factor (VEGF)-induced EC migration was diminished

295 lete absence of hepatic vascular endothelial growth factor (VEGF)-stromal cell-derived factor 1 (sdf1

296 by chronic elevation of vascular endothelial growth factor (VEGF).

297 the angiogenic markers vascular endothelial growth factor (VEGFA) and CD31 and the proliferation mar

298 = 27) with 1 exception (vascular endothelial growth factor) were overexpressed with BAL neutrophilia

299 pid mediators, tissue injury and repair, and growth factors with immunoassay (enzyme-linked immunosor

300 real injections of anti-vascular endothelial growth factor without significant improvement of best-co