ライフサイエンスコーパス: HGF

1 HGF concentrations were also lower in islet EC-condition

2 HGF effects were blocked by phosphatidylinositol-3 kinas

3 HGF enhanced co-localization of SphK1/p-SphK1 with actin

4 HGF is a genetically heterogeneous disorder and can be t

5 HGF overexpression conferred resistance to MEKi in paren

6 HGF stimulated SphK1 phosphorylation and enhanced intrac

7 HGF stimulates cell proliferation, cell dispersion, neur

8 HGF-associated deafness is a neurocristopathy but, unlik

9 HGF/Met signaling has recently been associated with basa

10 HGF/MET signaling was elevated in the MEKi-resistant mod

11 HGFs were treated with e-cigarette fluids containing nic

12 Levels of IP-10, HGF, IL-6, MCP-1, MIP-1alpha, IL-12p70, IL-18, VEGF-A, P

13 n with reduction in the PPFs angiopoietin-2, HGF, and EG-VEGF provides potential insight into the mul

14 Last, IL-6, HGF, and VEGF elevations were seen in 5-W MWA and RFA co

15 Our results show that BMF-derived IL-6/HGF and cancer cell-derived TGF-beta1 mediate the intera

16 cell growth and migration as compared with a HGF antagonist in vitro.

17 at Rab7a siRNA inhibition enhances IGF-1 and HGF signalling in beta cells and increases expression of

18 at growth factors such as insulin, IGF-1 and HGF support beta cell growth and survival, but in people

19 in cancer cells was co-related with IL-6 and HGF overexpression in stromal cells in human gastric can

20 owth factor-beta1], AREG [amphiregulin], and HGF [hepatocyte growth factor]) coupled with T-helper ce

21 ate the role of PDGFRalpha-dependent ECM and HGF production in fibroblasts that promotes the remodeli

22 Evaluation of Met, EpCAM, and HGF levels in human tumor samples reveals that EpCAM is

23 a positive feedback loop formed by FOXM1 and HGF/Met and revealed that this loop is a potentially eff

24 FOXM1, and the cross talk between FOXM1 and HGF/Met signaling promoted PDA growth and resistance to

25 oss talk between Forkhead box M1 (FOXM1) and HGF/Met signaling in promotion of PDA growth and resista

26 to measure the expression of MACC1, Met, and HGF messenger RNA in microdissected tumor tissue and cor

27 Two plasma proteins, OSM and HGF, were also associated with multiple sclerosis in com

28 Both Shh and HGF were heterogeneously expressed in PDAC stroma, and o

29 diography, immunohistochemical staining, and HGF ELISA assays confirmed that elevated levels of HGF p

30 enuity pathway analysis identified STAT3 and HGF as top regulator proteins.

31 e consistent with inhibition of the VEGF and HGF pathways.

32 content was blocked with an inhibitory anti-HGF antibody.

33 entrations of HGF in tumors for planning any HGF-targeted therapy, with the potential to improve clin

34 y promoting vascular survival and associated HGF production.

35 ever, blocking PI3K/Akt signaling attenuated HGF-mediated phosphorylation of Spns2.

36 S1P2 or S1P3, with specific siRNA attenuated HGF-induced lamellipodia formation.

37 regulation or inhibition of SphK1 attenuated HGF-induced lamellipodia formation in HLMVECs.

38 In a Pax7 wild type background, HGF stimulation mainly causes ERMS that originate from s

39 e results suggest a novel connection between HGF signaling and deafness via melanocyte deficiencies.

40 dition to IGF1 and IGF2, IGFBP-3 binds bFGF, HGF, neuregulin, and PDGF AB with nanomolar affinity.

41 ecreasing cell survival and inhibiting bFGF, HGF, and IGF1 growth factor rescue and also potentiates

42 ut therapeutic agents that can broadly block HGF ligand binding and exon 14-mutated or amplified MET

43 e form that is similarly capable of blocking HGF/MET activity, but in the absence of any effector fun

44 ochemical assays, 107_A07 competes with both HGF/SF and its truncated splice variant NK1 for MET bind

45 ncreatic cancer and the contribution made by HGF signalling to pancreatic cancer cell motility remain

46 istant subcutaneous tumor growth mediated by HGF/c-Met pathway and VEGF activation.

47 ted adenoma organoid expansion stimulated by HGF or EGF using adenomas derived from Lgr5(Creert2)/Met

48 ated from crypts and adenomas, stimulated by HGF or EGF, that were derived from mice expressing diffe

49 oduction in human gingival fibroblast cells (HGF) under inflammatory conditions.

50 amatically increased SDF-1 expressing cells, HGF expressing Ym1+ M2 macrophages and CD133+ stem cells

51 In untreated cells, HGF levels correlated significantly with GW-2580 sensiti

52 ncrease in conversion of latent single-chain HGF to active two-chain HGF, coinciding with an increase

53 latent single-chain HGF to active two-chain HGF, coinciding with an increase in the phosphorylation

54 Consequently, HGF/MET-dependent nitric oxide release by neutrophils pr

55 osclerosis (fractalkine/CX3CL1, CCL8, M-CSF, HGF), T-cell development/activation (CD40L, IL-7, CCL25,

56 -induced IL-6 and IL-8 secretion in cultured HGF and HPLF.

57 ated cell surface expression of MET, curbing HGF-independent MET activity, and engaged natural killer

58 d regulation of beta-cell VEGFA and islet EC HGF, these two growth factors are highly integrated in n

59 Elevated HGF induced hepatocyte nuclear factor 4 alpha (Hnf4a), w

60 Limiting endothelial HGF reduced Hnf4a, abolished interference of Hnf4a with

61 These results establish HGF/C-Met as a central organizing signal in blood vessel

62 drenocortical carcinoma cells with exogenous HGF resulted in increased cell proliferation in vitro an

63 key EGFR family members and by facilitating HGF-stimulated EGFR ligand secretion.

64 Last, we identify hepatocyte growth factor ( HGF) as a novel transcriptional target of Prrx1b.

65 The hygroscopic growth factor (HGF) and cloud condensation nuclei (CCN) activity for a

66 tors (GFs) such as hepatocyte growth factor (HGF) and hepato-disruptive GFs such as transforming grow

67 Hepatocyte growth factor (HGF) and its receptor MET represent validated targets fo

68 The hepatocyte growth factor (HGF) and its receptor, c-Met, are actively involved in t

69 g in production of hepatocyte growth factor (HGF) and transforming growth factor (TGF)-beta1 caused b

70 (IL-6) at 6 hours, hepatocyte growth factor (HGF) at 72 hours, and vascular endothelial growth factor

71 The hepatocyte growth factor (HGF) binding antibody rilotumumab (AMG102) was modified

72 ding to its ligand hepatocyte growth factor (HGF) can modulate the apoptosis and immune escape mechan

73 lled induction of the hepatic growth factor (HGF) caused by dysregulated cross talk between pulmonary

74 Hepatocyte growth factor (HGF) induces cell migration and scattering by mechanisms

75 Hepatocyte growth factor (HGF) is a multifunctional protein that signals through t

76 Hepatocyte growth factor (HGF) is responsible for resetting hepatic homeostasis af

77 gulin 1 (NRG1) and hepatocyte growth factor (HGF) provide resistance to MEK inhibition.

78 engagement of the hepatocyte growth factor (HGF) receptor c-Met by heart-produced HGF during priming

79 n of the oncogenic hepatocyte growth factor (HGF) receptor c-MET in PNETs.

80 l cells supply the hepatocyte growth factor (HGF) required for the chemotactic gradient responsible f

81 ature and elevated hepatocyte growth factor (HGF) secretion.

82 found the roles of hepatocyte growth factor (HGF) signaling in stria vascularis development for the f

83 Hepatocyte growth factor (HGF) signaling via c-Met is known to promote endothelial

84 ematically unravel hepatocyte growth factor (HGF) stimulated phosphoinositide-3-kinase (PI3K) and mit

85 kappaB-potentiated hepatocyte growth factor (HGF) to MET proto-oncogene receptor tyrosine kinase (c-M

86 velopment by using Hepatocyte Growth Factor (HGF) to perturb the niche microenvironment.

87 factor (VEGF) and hepatocyte growth factor (HGF) with the aim of disrupting the tumor microenvironme

88 owth factor (EGF), hepatocyte growth factor (HGF)) and the activation of the signalling pathways (STA

89 h factor (EGF) and hepatocyte growth factor (HGF), and across wide ranges of background stimuli.

90 of the MET ligand, hepatocyte growth factor (HGF), by tissues innervated by vagal motor neurons durin

91 urvival effects of hepatocyte growth factor (HGF), ciliary neurotrophic factor (CNTF), and Artemin th

92 s the receptor for hepatocyte growth factor (HGF), has been implicated in ovarian tumorigenesis and h

93 her by its ligand, hepatocyte growth factor (HGF), or via ligand-independent mechanisms, such as MET

94 on of c-Met and/or hepatocyte growth factor (HGF), the amplification of the MET gene, and mutations i

95 ulation of EGF and hepatocyte growth factor (HGF), two promoting factors for breast cancer progressio

96 owth factor (EGF), hepatocyte growth factor (HGF), vascular endothelial growth factor (VEGF) showed t

97 was performed for hepatocyte growth factor (HGF), vascular endothelial growth factor (VEGF), and c-M

98 eukin-6 (IL-6) and hepatocyte growth factor (HGF), whereas cancer cells produced high level of transf

99 the MET receptor, hepatocyte growth factor (HGF).

100 ponse functions to Hepatocyte Growth Factor (HGF).

101 ate in response to hepatocyte growth factor (HGF).

102 onse to its ligand hepatocyte growth factor (HGF).

103 tokines, including hepatocyte growth factor (HGF).

104 , the receptor for hepatocyte growth factor (HGF).

105 rrence of aberrant hepatocyte growth factor (HGF)/MET proto-oncogene receptor tyrosine kinase (MET) a

106 Hepatocyte growth factor (HGF)/Met signaling has critical roles in pancreatic duct

107 = 0.40, P = .001), hepatocyte growth factor (HGF; r = 0.31, P = .02), and endocrine gland-VEGF (EG-VE

108 tor Hepatocyte Growth Factor/Scatter Factor (HGF/SF) and its receptor, the product of the MET proto-o

109 ral angiogenesis-related factors (CD26, FGF, HGF, MMP-8, MMP-9, OPN, PF4, SDF-1) and cytokines (IL-1r

110 is using primary human gingival fibroblasts (HGFs) and human periodontal ligament fibroblasts (HPLFs)

111 the coculture of human gingival fibroblasts (HGFs) and U937 human monocytic cells; however, the respo

112 okine release by human gingival fibroblasts (HGFs) remains underexplored.

113 host response of human gingival fibroblasts (HGFs) to two featured isoforms of tetra-acylated PgLPS14

114 demonstrated in human gingival fibroblasts (HGFs).

115 ling capacity of human gingival fibroblasts (HGFs).

116 Hereditary gingival fibromatosis (HGF) is the most common genetic form of gingival fibroma

117 nal model (the Hierarchical Gaussian Filter, HGF), to choices made during slot machine game play as w

118 downregulation of Rac GTP loading following HGF stimulation and enhanced inhibition of Rac-dependent

119 Lungs were evaluated for HGF (hepatocyte growth factor), a protein involved in al

120 Here, we report a role for HGF-induced intracellular sphingosine-1-phosphate (S1P)

121 er, these data suggest an important role for HGF/cMET signaling in adrenocortical carcinoma growth an

122 ice with inducible deletion of MET, we found HGF receptor signaling to regulate intestinal homeostasi

123 at both mAbs engaged a pathway distinct from HGF-induced receptor degradation and protease-mediated s

124 cells into the SV depends on signaling from HGF/MET.

125 ed with antibodies are refractory to further HGF stimulation due to antibody-mediated MET depletion.

126 h HGF remain competent to respond to further HGF stimulation, cells pre-treated with antibodies are r

127 Further, HGF enhanced association of Spns2 with S1P1 that was blo

128 For normal hearing, HGF levels must be fine-tuned as an excess or deficiency

129 r an EGFR tyrosine kinase inhibitor hindered HGF-stimulated pancreatic carcinoma cell chemotaxis and

130 However, HGF/MET inhibitors being explored as cancer therapeutics

131 rt the characterization of recombinant human HGF (rh-HGF) as a PET tracer for detection of c-Met expr

132 more, implanted hUC-MSC sheets secrete human HGF continuously to the murine target tissue.

133 s prostate cancer cell adhesiveness, impairs HGF-mediated cell migration and reduces 3D invasion.

134 es was positively associated with changes in HGF, IGF1, and extracellular matrix genes.

135 encing also increased OPG gene expression in HGF only.

136 was noted that CSCs demonstrated 3.2-fold in HGF, 2.9-fold in VEGF and 8.7-fold in PDGF-B higher gene

137 migration, and inhibition of tumor growth in HGF-dependent and -independent mouse xenograft models.

138 6 and IL-8 was not influenced by losartan in HGF or HPLF.

139 cription of IL-6 and IL-8 in HPLF but not in HGF.

140 s factor-alpha, and osteoprotegerin (OPG) in HGF and HPLF.

141 3.3 %ID/g, demonstrating selective uptake in HGF-positive tumors.

142 In humans, noncoding variants in HGF are associated with nonsyndromic deafness DFNB39 How

143 aluate the mRNA levels of CD147 and MMP-2 in HGFs and U937 cells.

144 MMP-2 enzyme activities in HGFs were also significantly increased by the coculturin

145 to evaluate the release of soluble CD147 in HGFs after coculturing with U937 cells and its functiona

146 The protein and mRNA expression of CD147 in HGFs were enhanced after transwell coculturing with U937

147 adenosine dampens IL-1beta-induced CXCL8 in HGFs and involves HO-1 and pAMPK signaling.

148 oxidant defense and cytoskeletal dynamics in HGFs, and thereby enhances our understanding of periodon

149 oxidant defense and cytoskeletal dynamics in HGFs.

150 exogenous CD147 enhanced MMP-2 expression in HGFs, whereas treatment with cyclosporine-A, which inhib

151 ct on the enhancement of MMP-2 expression in HGFs.

152 ole in monocyte-enhanced MMP-2 expression in HGFs.

153 n, reduced U937-enhanced MMP-2 expression in HGFs.

154 n multiple mouse models of cancer, including HGF-dependent and -independent tumor xenografts, we dete

155 by myofibroblast-secreted factors, including HGF.

156 Disruption of the DATE increased HGF signaling via MET and reduced levels of receptor-int

157 tochemical analyses indicated that increased HGF/cMET expression in human adrenocortical carcinoma sa

158 The antibody, 107_A07, inhibited HGF/SF-induced cell migration and proliferation in vitro

159 ng, as knocking down either ligand inhibited HGF-mediated migration and invasion.

160 gand-independent Met signaling by inhibiting HGF binding to Met and inducing receptor down-regulation

161 enting fibrinolysis, elevated PAI-1 inhibits HGF's activation by u-PA and the resultant anti-inflamma

162 Interestingly, HGF/c-Met-mediated signaling could not induce PD-L1 at t

163 ved from the compound mice and controls into HGF-transgenic mice further uncovered that HGF induces p

164 At the level of cell-to-cell junctions, HGF attenuates the linkage of stress fibers to cell-to-c

165 At the level of cell-to-substrate junctions, HGF augments the linkage of stress fibers to cell-to-sub

166 iated astrocytes to secrete the c-Met ligand HGF.

167 he initial effects of binding to its ligand, HGF.

168 c inhibition using AT1R antagonist losartan, HGF and HPLF were stimulated by IL-1beta for 3 (messenge

169 tely 4-7 %ID/g), which corresponded with low HGF levels in these tumors (ex vivo ELISA).

170 ong those, the hepatocyte growth factor/MET (HGF/MET) axis is emerging as a critical player not only

171 We studied the c-MET/HGF axis as a mediator of tumor-stromal interaction in o

172 ion and pharmacological studies point to MET/HGF signaling for antero-posterior migration of esophagu

173 87MG (HGF-positive, MET-positive) and MKN45 (HGF-negative, MET-positive) and 4 patient-derived xenogr

174 protects MET from degradation, and modulates HGF-induced phosphatidylinositol-3-kinase and mitogen-ac

175 Moreover, HGF mRNA levels were measured by quantitative reverse tr

176 Moreover, HGF-induced migration of HLMVECs was attenuated by down-

177 in distinct subsets of lumbar motor neurons: HGF supports hindlimb motor neurons through c-Met; CNTF

178 In the absence of HGF, cell trajectories are highly tortuous whereas in th

179 , we investigated the aberrant activation of HGF/MET and Wnt/beta-catenin cascades in prostate tumori

180 pression of FOXM1 enhanced the activation of HGF/Met signaling and its downstream pathways, including

181 ver, the mechanism of aberrant activation of HGF/Met signaling and resistance to Met inhibition in PD

182 Furthermore, activation of HGF/Met signaling increased the expression and transcrip

183 Blockade of HGF/Met, Janus kinase 2 (JAK2)/STAT3 and TGF-beta1 signa

184 tients with elevated local concentrations of HGF in tumors for planning any HGF-targeted therapy, wit

185 s that react to increasing concentrations of HGF, in Madin-Darby canine kidney (MDCK) cells, grown as

186 be fine-tuned as an excess or deficiency of HGF cause deafness in mouse.

187 In mice, a deficiency of HGF expression limited to the auditory system, or an ove

188 Depletion of HGF or MET restored sensitivity of MEKi-resistant cells

189 Genetic dissection of HGF signaling via c-MET reveals that the incorporation o

190 duction in Akt phosphorylation downstream of HGF signalling.

191 fically identified to function downstream of HGF-mediated c-Met activation in a PI3K dependent manner

192 , truncation of DATE activated expression of HGF, resulting in its autocrine signaling via MET.

193 other functions, PAI-mediated inhibition of HGF activation prohibits the resolution of inflammation

194 erties that demonstrate potent inhibition of HGF-mediated c-Met phosphorylation in a mouse liver phar

195 on in Met-driven cancer cells, inhibition of HGF-mediated cancer cell migration, and inhibition of tu

196 ll quiescence via intramuscular injection of HGF increases the penetrance of sarcoma formation at the

197 variants in the 3'UTR of a short isoform of HGF encoding hepatocyte growth factor.

198 elopment for the first time and that lack of HGF signaling in the inner ear leads to profound hearing

199 tion of patients having high local levels of HGF in tumors.

200 In the inner ear, levels of HGF must be fine-tuned for normal hearing.

201 High levels of HGF protein in tumor tissues correlated with lower level

202 not been performed using the local levels of HGF protein in tumors.

203 noninvasively determine the local levels of HGF protein in tumors.

204 ISA assays confirmed that elevated levels of HGF protein were present only in U87MG tumors and that (

205 cumulate in tumors with high local levels of HGF protein.

206 a-knockout mice demonstrated lower levels of HGF.

207 the auditory system, or an overexpression of HGF, causes neurosensory deafness.

208 e highly tortuous whereas in the presence of HGF, they become far less so, resembling free expansion

209 ver, extracellular proteolytic regulation of HGF activation, which is influenced by the tumor microen

210 ibiting an extracellular signal regulator of HGF, which is typically activated by tumor-stromal inter

211 nhibitor combination reversed the release of HGF.

212 These results indicate a role of HGF/MET in beta-catenin-mediated prostate cancer cell gr

213 addition of CSF1 increased the secretion of HGF and other cytokines in conditioned media from AML pa

214 leukemia population through the secretion of HGF and other cytokines.

215 sulin content, and in IUGR ECs, secretion of HGF was diminished.

216 fetal development reveal potential sites of HGF-MET interaction.

217 However, both sources of HGF increased the phosphorylation of c-MET on Tyr(1349),

218 Targeted therapy of HGF in combination with gemcitabine in a preclinical mod

219 Because recent clinical trials of HGF-targeting therapies have been largely unsuccessful i

220 btained a measure of the ultrasensitivity of HGF-responsive genes, identifying a subset with higher a

221 to rule out the effect of direct contact of HGFs and U937 cells.

222 Primary cultures of HGFs were grown on Type I collagen matrices previously t

223 hat enhanced tumor promotion is dependent on HGF-Met signaling in mucosa of Ikkbeta-mutant animals.

224 The negative effect on HGF-mediated growth was overcome by expression of CD44v4

225 st that PIPKIgamma, downstream of EGF and/or HGF receptor, participates in breast cancer progression

226 Crypts incubated with EGF or HGF expanded into self-organizing mini-guts with similar

227 Adenoma organoids stimulated with EGF or HGF expanded to almost twice the size of nonstimulated o

228 lowing: chromosome 7 copy gain, focal MET or HGF gene amplification, or MET kinase domain mutations.

229 n a domain (Ig1) not reported to bind NK1 or HGF/SF.

230 We show that persistent HGF treatment stimulates the clonogenic activity of ICAM

231 ic-associated gene (VEGF, VEGFR2, BFGF, PGF, HGF, Ang-1, VWF, PECAM-1 and ENOS) expression analysis a

232 4 patient-derived xenografts (MET-positive, HGF unknown).

233 verlapping but distinct epitopes, preventing HGF interaction with MET and triggering receptor ubiquit

234 d7 in Ikkbeta-deficient fibroblasts prevents HGF secretion, and pharmacological inhibition of Met dur

235 press the induction effect of TMPRSS2 on pro-HGF activation, extracellular matrix degradation and pro

236 n of c-Met, Gab1 and AKT, in response to pro-HGF, which functionally leads to attenuated proliferatio

237 In this local process, HGF is known to attenuate local cadherin-dependent adhes

238 actor (HGF) receptor c-Met by heart-produced HGF during priming in the lymph nodes instructs T cell c

239 idated exosome proteins of interest (pSTAT3, HGF, and IL6) in HGSOC samples of origin-based cell line

240 Finally, recombinant HGF and HS-5-conditioned media rescued cell viability af

241 rh-HGF was expressed in human embryonic kidney 293 cells an

242 The fact that sonication-denatured rh-HGF had significantly lower uptake in U87MG tumors, alon

243 haracterization of recombinant human HGF (rh-HGF) as a PET tracer for detection of c-Met expression i

244 cific and prominent uptake of (64)Cu-NOTA-rh-HGF in c-Met-positive U87MG tumors (percentage injected

245 rovided initial evidence that (64)Cu-NOTA-rh-HGF visualizes c-Met expression in vivo, an application

246 rmed the c-Met specificity of (64)Cu-NOTA-rh-HGF.

247 ominantly increased periablational and serum HGF and downstream distant tumor VEGF levels.

248 Y23 and Y333 in response to stromal signals HGF and IGF-1, respectively, and IGF-1 expression was re

249 Similarly, HGF-mediated expansion of adenoma organoids required CD4

250 on, down-regulation of Spns2 also suppressed HGF-induced lamellipodia formation, suggesting a key rol

251 ces the responsiveness to NRG1 and sustained HGF-mediated activation of AKT.

252 to select patients for therapies that target HGF-MET signaling.

253 We further determined that HGF induced secretion of AREG, which is dependent on int

254 We found that HGF/c-Met-mediated signaling activated the Ras/Raf pathw

255 We have previously reported that HGF stimulates lamellipodia formation and motility of hu

256 Taken together, these results suggest that HGF/c-Met-mediated lamellipodia formation, and perhaps m

257 These results suggest that HGF/MET signaling is important for development and funct

258 o HGF-transgenic mice further uncovered that HGF induces prostatic oncogenic transformation and cell

259 The HGF at 90% RH is in the range of 1.3 to 1.8 for alkylami

260 The HGF receptor was not different between control and IUGR

261 The HGF was superior in accounting for the behaviour of our

262 The HGF-mediated phosphorylation of SphK1 and its localizati

263 The HGF/MET pathway is frequently activated in a variety of

264 um carboxylate aerosols was derived from the HGF and CCN results and theoretically calculated.

265 s in the range of 0.06-1.37 derived from the HGF measurements at 90% RH, 0.05-0.49 derived from the C

266 most effectively blocked, by inhibiting the HGF/C-Met signaling pathway between endothelial cells an

267 ressed SPINT2 in melanoma cells inhibits the HGF-induced MET-AKT (v-Akt murine thymoma viral oncogene

268 mples contain alterations in the DATE of the HGF promoter.

269 th an increase in the phosphorylation of the HGF receptor (HGFR or MET, encoded by the MET gene), as

270 a significant role in the suppression of the HGF-MET pathway and malignant melanoma progression.

271 he cross-talk between LSECs and CECs via the HGF/c-MET axis.

272 mal development and the association with the HGF phenotype.

273 one gene (SOS1) has been associated with the HGF trait observed to segregate in a dominant inheritanc

274 _A07 Fab comes into close proximity with the HGF/SF-binding SEMA domain when MET is in the "compact",

275 tokines and growth factors (CSF2, IL-6, TNF, HGF, VEGF, and EGF), ATM and p53 signaling pathways.

276 poptosis-associated proteins CASP8, TNFSF14, HGF, and TGFB1, with HGF discriminating between ICU and

277 n, and the relevance of this conformation to HGF/SF binding and signaling.

278 ficient adenoma organoids did not respond to HGF stimulation, but did respond to EGF.

279 r cells have a specific motility response to HGF both in 2D and 3D physiomimetic organotypic assays;

280 that EGFR was phosphorylated in response to HGF stimulation that is dependent on EGFR kinase activit

281 owever, c-Met phosphorylation in response to HGF was unaffected by EGFR signaling.

282 ne circuits requiring nonlinear responses to HGF signalling.

283 first time that DCC-2701 may be superior to HGF antagonists that are in clinical trials and that pTy

284 Together, HGF induces both structural changes in the actin-bound j

285 ere performed on murine xenografts of U87MG (HGF-positive, MET-positive) and MKN45 (HGF-negative, MET

286 tive angiogenic programs such as unregulated HGF-MET signaling and enhanced autocrine signaling throu

287 ucible nitric oxide synthase production upon HGF stimulation.

288 c trafficking of the two NRP1 variants, upon HGF stimulation, is due to loss of N-glycosylation at th

289 In vitro, HGF increased enteric neuron differentiation and neurite

290 graphy and immunohistochemistry, and ex vivo HGF ELISA experiments were performed on murine xenograft

291 cell populations strongly express Met, while HGF is produced by stromal and basal myoepithelial cells

292 ARGX-111 competed with HGF for MET binding, inhibiting ligand-dependent MET act

293 FO-AMG102 uptake was closely correlated with HGF protein levels in tumors.

294 Here we report 11 individuals with HGF from three unrelated families.

295 organoid cultures from ISCs stimulated with HGF or EGF and assessed intestinal differentiation by im

296 ypts from Cd44(+/+) mice on stimulation with HGF, but had the same response to EGF.

297 roteins CASP8, TNFSF14, HGF, and TGFB1, with HGF discriminating between ICU and non-ICU cohorts.

298 Consequently, while cells pre-treated with HGF remain competent to respond to further HGF stimulati

299 ressed transcripts that are involved in WNT, HGF, TGFbeta, IGF, BMP, FGF and estrogen signaling.

300 %ID/g]), whereas uptake in MKN45 xenografts (HGF-negative) was 5.0 +/- 1.3 %ID/g and a control of non

301 t 120 h after injection in U87MG xenografts (HGF-positive) was high (36.8 +/- 7.8 percentage injected