ライフサイエンスコーパス: HGF

1 HGF and MET are expressed in fetal and adult enteric ner

2 HGF concentrations were also lower in islet EC-condition

3 HGF effects were blocked by phosphatidylinositol-3 kinas

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

5 HGF inhibited TGF-beta1-stimulated collagen-1 and alpha-

6 HGF is a genetically heterogeneous disorder and can be t

7 HGF secreted by fibroblasts was also found sequestered w

8 HGF signaling via MET reduced levels of the receptor-int

9 HGF stimulated SphK1 phosphorylation and enhanced intrac

10 HGF, in a dose-dependent manner, induced c-Met phosphory

11 HGF-induced resistance was due to restoration of physiol

12 HGF/Met signaling has recently been associated with basa

13 HGFs were treated with e-cigarette fluids containing nic

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

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

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

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

18 Aberrant HGF-MET (hepatocyte growth factor-met proto-oncogene) si

19 endothelial barrier properties and abolished HGF-activated cortical actin dynamics.

20 LY294002, an inhibitor of PI3k, abolished HGF-induced PI3k (Tyr-458), and Akt (Thr-308 and Ser-473

21 In addition, HGF stimulated peripheral MT growth in an IQGAP1-depende

22 niques to investigate the factors that alter HGF signaling in colon cancer cells and its effects on c

23 tem, and by combining anti-MET drugs with an HGF neutralizing antibody (ficlatuzumab) in human HGF kn

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

25 n response to interaction between CD44v6 and HGF.

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

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

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

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

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

31 n amplifying the fibroblast-derived NRG- and HGF-mediated PI3K/AKT (phosphatidylinositol 3'-kinase/AK

32 y reverses the protective effect of NRG1 and HGF in trametinib-treated cells.

33 g ERBB3 and cMET, the receptors for NRG1 and HGF, respectively, overcome resistance to trametinib pro

34 edium from fibroblasts that produce NRG1 and HGF.

35 evaluated on S. epidermidis growth rate and HGF viability, gene expression, collagen production, rea

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

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

38 ng in human clinical studies of cancer: anti-HGF monoclonal antibodies, MET monoclonal antibodies, an

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

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

41 dentifies the secreted factor responsible as HGF.

42 owth factor sensitization to EGF, as well as HGF and IGF, and increased resistance to EGFR and Met in

43 signaling axis and NADPH oxidase attenuated HGF- induced lamellipodia formation, ROS generation and

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

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

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

47 w GPRC5B is carried by exosomes and augments HGF-induced morphogenesis.

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

49 udy, we investigated the association between HGF/cMET expression and cancer hallmarks of adrenocortic

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

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

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

53 i-MET antibody that, in addition to blocking HGF/MET signaling, also kills MET-overexpressing cancer

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

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

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

57 Activation of MET by HGF plays a key role in tumor progression.

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

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

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

61 es a therapeutic advantage over conventional HGF/MET signaling blockade and generates proof-of-concep

62 Conversely, HGF administration in WT Ppx mice further accelerated be

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

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

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

66 es (ECMs) and when degraded this ECM-derived HGF stimulated cancer cell migration (1.5- to 24-fold).

67 tion, recombinant HGF and fibroblast-derived HGF negligibly affect c-MET phosphorylation on Tyr(1234)

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

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

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

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

72 In all models examined, HGF promoted resistance to MET-targeted agents, affectin

73 fibroblasts and to a lesser extent exogenous HGF.

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

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

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

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

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

79 Hepatocyte growth factor (HGF) and its receptor cMET augment cancer growth and res

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

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

82 he hypothesis that hepatocyte growth factor (HGF) and the HGF receptor MET might support some types o

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

84 Hepatocyte growth factor (HGF) and vascular endothelial growth factor A (VEGFA) ar

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

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

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

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

89 s mutations in the hepatocyte growth factor (HGF) gene.

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

91 Hepatocyte growth factor (HGF) is a mitogen required for beta-cell replication dur

92 Hepatocyte growth factor (HGF) mediated signaling promotes cell proliferation and

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

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

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

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

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

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

99 Hepatocyte growth factor (HGF) signaling promotes tumor invasiveness in renal cell

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

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

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

103 actor (FGF-basic), hepatocyte growth factor (HGF), and migration inhibition factor (MIF) may provide

104 asts was driven by hepatocyte growth factor (HGF), and platelet activation was followed by HMGB1/TLR-

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

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

107 ET and its ligand, hepatocyte growth factor (HGF), has been implicated in malignant progression of ca

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

109 inase receptor for hepatocyte growth factor (HGF), is known to function as a potent antiapoptotic med

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

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

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

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

114 of the MET ligand, hepatocyte growth factor (HGF), which is abundant in the tumor microenvironment.

115 l factors, such as hepatocyte growth factor (HGF), which restrains hepatic injury and facilitates rev

116 EGFR signaling on hepatocyte growth factor (HGF)-stimulated migration and invasion.

117 ponse functions to Hepatocyte Growth Factor (HGF).

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

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

120 ucing signals like Hepatocyte Growth Factor (HGF).

121 ng them to secrete hepatocyte growth factor (HGF).

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

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

124 sregulation of the hepatocyte growth factor (HGF)/MET pathway promotes tumour growth and metastasis.

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

126 d regulator of the hepatocyte growth factor (HGF)/Met/mitogen-activated protein kinase pathway, which

127 = 0.40, P = .001), hepatocyte growth factor (HGF; r = 0.31, P = .02), and endocrine gland-VEGF (EG-VE

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

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

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

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

132 demonstrated in human gingival fibroblasts (HGFs).

133 ling capacity of human gingival fibroblasts (HGFs).

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

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

136 eased c-Met, suggesting a potential role for HGF/c-Met in beta-cell proliferation in situations of re

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

138 Thus, quercitrin was not toxic for HGFs; increased collagen IIIalpha1 and decorin levels; d

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

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

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

142 Patients with periodontitis showed higher HGF concentrations in saliva, GCF, and serum (P <0.001);

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

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

145 eutralizing antibody (ficlatuzumab) in human HGF knock-in mice bearing c-MET-amplified tumors.

146 -38877605, crizotinib, and DN30 Fab in human HGF knock-in mice.

147 Ectopic production of human HGF in CCIC xenografts rendered the xenografts susceptib

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

149 f HGF receptor MET on MSC, thereby impairing HGF-driven MSC recruitment.

150 encing also increased OPG gene expression in HGF only.

151 6 and IL-8 was not influenced by losartan in HGF or HPLF.

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

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

154 3.3 %ID/g, demonstrating selective uptake in HGF-positive tumors.

155 IL-6 and stimulated NF-kappaB activation in HGFs.

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

157 oxidant defense and cytoskeletal dynamics in HGFs.

158 significantly increased MMP-1 production in HGFs, whereas adding EGCG significantly attenuated this

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

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

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

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

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

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

165 ng of these hotspots effectively interrupted HGF/MET signaling in multiple cell-based biochemical and

166 This study investigates HGF expression and its relationship to subgingival micro

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

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

169 fied 1 hotspot that coincides with the known HGF beta chain binding site on blades 2-3 of the SEMA do

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

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

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

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

174 87MG (HGF-positive, MET-positive) and MKN45 (HGF-negative, MET-positive) and 4 patient-derived xenogr

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

176 there are three approaches toward modulating HGF/MET signaling in human clinical studies of cancer: a

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

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

179 human, monoclonal antibody that neutralises HGF.

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

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

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

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

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

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

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

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

188 duction in Akt phosphorylation downstream of HGF signalling.

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

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

191 liminary clinical benefit from inhibition of HGF or MET has been reported.

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

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

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

195 from normal ovaries secreted high levels of HGF (1500-3800 pg/ml) as compared with tumor-derived fib

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

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

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

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

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

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

202 ) was analyzed in the absence or presence of HGF, in a stroma-tumor coculture system, and by combinin

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

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

205 by HMGB1/TLR-4-dependent down-regulation of HGF receptor MET on MSC, thereby impairing HGF-driven MS

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

207 r of HAI-1, which is a critical regulator of HGF/c-MET signaling.

208 nhibitor combination reversed the release of HGF.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

225 4 patient-derived xenografts (MET-positive, HGF unknown).

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

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

228 thway in response to fibroblast-secreted pro-HGF.

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

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

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

232 stitutive c-MET phosphorylation, recombinant HGF and fibroblast-derived HGF negligibly affect c-MET p

233 d found that Pim-1 kinase activity regulates HGF-induced tumor cell migration, invasion, and cell sca

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

235 The concentrated rh-HGF was conjugated to 2-S-(4-isothiocyanatobenzyl)-1,4,7

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

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

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

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

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

241 Flow cytometry examination confirmed that rh-HGF had a strong and specific capacity to bind to c-Met.

242 The rh-HGF expression yield was 150-200 mug of protein per 5 x

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

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

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

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

247 ortactin association with EB1 and suppressed HGF-induced endothelial cell peripheral actin cytoskelet

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

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

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

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

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

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

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

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

256 The HGF receptor was not different between control and IUGR

257 The HGF-mediated phosphorylation of SphK1 and its localizati

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

259 The HGF/MET signaling pathway is critical in mediating a wid

260 that hepatocyte growth factor (HGF) and the HGF receptor MET might support some types of enteric neu

261 down by small interfering RNA attenuated the HGF-induced increase in endothelial barrier properties a

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

263 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

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

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

266 y deoxyadenosine tract element (DATE) of the HGF gene promoter.

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

268 terized mice with pancreatic deletion of the HGF receptor, c-Met (PancMet KO mice), in two models of

269 resistance mediated by up-regulation of the HGF receptor, MET.

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

271 mal development and the association with the HGF phenotype.

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

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

274 ns 2-3, both of which are thought to bind to HGF alpha chain.

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

276 ction of IKKbeta/NF-kappaB in CAFs linked to HGF release and raise potential concerns about the use o

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

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

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

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

281 ne circuits requiring nonlinear responses to HGF signalling.

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

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

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

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

286 ucible nitric oxide synthase production upon HGF stimulation.

287 In vitro, HGF increased enteric neuron differentiation and neurite

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

289 We also analyzed whether HGF administration could accelerate beta-cell regenerati

290 To determine whether HGF/c-Met signaling is required for beta-cell regenerati

291 These results reveal a mechanism by which HGF/c-MET signaling promotes tumor formation after tissu

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

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

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

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

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

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

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

299 %ID/g]), whereas uptake in MKN45 xenografts (HGF-negative) was 5.0 +/- 1.3 %ID/g and a control of non

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