ライフサイエンスコーパス: HB-EGF

1 HB-EGF also induced early activation of ERK1/2 in JM-a/C

2 HB-EGF has previously been associated with a number of p

3 HB-EGF induced proliferation of insulin-secreting MIN6 c

4 HB-EGF overexpression and Kras(G12D) together, but neith

5 HB-EGF secretion was measured by enzyme-linked immunosor

6 HB-EGF shedding was assessed by measuring the release of

7 HB-EGF significantly preserved intestinal microvascular

8 HB-EGF, NRG, and TGF-alpha cleavage was not dependent on

9 HB-EGF, often overexpressed in damaged or diseased epith

10 HB-EGF-, but not wounding-, enhanced RhoA activity was s

11 rn analyses showed that release of activated HB-EGF (but neither amphiregulin nor EGF) occured after

12 aling in basal medium, and exogenously added HB-EGF and HGF significantly enhanced wound closure.

13 Unlike exogenously added HB-EGF, LPA stimulated moderate EGFR phosphorylation; th

14 nd closure with or without exogenously added HB-EGF.

15 Exogenously administered HB-EGF stimulated ERK phosphorylation.

16 Neutralizing activities of Y-142 against HB-EGF were evaluated in EGFR and ERBB4 signaling.

17 Remarkably, altering HB-EGF recapitulates the effect of EGFRwt on EGFRvIII ac

18 invasive processes through suppression of an HB-EGF autocrine loop responsible for activating a EGFR-

19 We also uncover an HB-EGF/Ascl1a/Notch/hb-egf(a)-signaling loop that helps

20 ysical association between membrane-anchored HB-EGF and EGFR was observed.

21 ncleavable mutated form of membrane-anchored HB-EGF demonstrated increased survival from anoikis, for

22 e propose a novel role for membrane-anchored HB-EGF in the cytoprotection of epithelial cells.

23 idney cells, expression of membrane-anchored HB-EGF increases cell-cell and cell-matrix adhesion.

24 in binding (HB)-EGF inhibitor (CRM 197), and HB-EGF neutralizing antibody.

25 pha promoter and reduced ADAM17 activity and HB-EGF production, compared to controls.

26 inhibition of the metalloprotease ADAM17 and HB-EGF to regulate cerebral arterial tone and blood flow

27 overed that ligand cleavage by MMP/ADAMs and HB-EGF expression is required for activation of EGFR in

28 lization antibodies against amphiregulin and HB-EGF, the heparin-binding growth factor family of the

29 eport a dual role for EC-derived PDGF-BB and HB-EGF in controlling pericyte recruitment to EC-lined t

30 Combined inhibition of PDGF-BB and HB-EGF-induced signaling in quail embryos leads to reduc

31 ErbB4 was activated by both HRG-beta1 and HB-EGF stimulation; however, compared with HRG-beta1, HB

32 Circulating APN binds to bFGF and HB-EGF, likely inhibiting their protective activity.

33 f colonic APN overlaps with that of bFGF and HB-EGF, which play a protective role in colitis.

34 In contrast COX-2, CYR61, and HB-EGF transcription were regulated in a calcium-depende

35 R is activated by the growth factors EGF and HB-EGF.

36 tid artery was unaffected in HB-EGF(+/-) and HB-EGF(-/-) mice, nor by AG1478.

37 h factor (EGF)-family ligands epiregulin and HB-EGF, the chemokine CX3CL1, and the transcription fact

38 lso activated two other genes epiregulin and HB-EGF.

39 hanced wound maturity were noted in EPR- and HB-EGF-treated wounds transfected with ErbB3.

40 h elevation in the number of macrophages and HB-EGF expression.

41 ulture models, C3 attenuated spontaneous and HB-EGF-induced wound closures, confirmed by delayed woun

42 ng the shedding of EGFR ligands TGFalpha and HB-EGF and, consequently, EGFR signaling activation in O

43 macrophages is the production of angiogenic HB-EGF.

44 ng cancer-derived galectin-1 on DCs and anti-HB-EGF blocking antibodies could, therefore, have therap

45 ing the in vitro biological activity of anti-HB-EGF monoclonal antibody Y-142.

46 In this study, we utilized the anti-HB-EGF monoclonal antibodies Y-142 and Y-073, which have

47 TNFR1-alpha, TGF-alpha, amphiregulin (AREG), HB-EGF and IL-6Ralpha, from IGROV1-Luc cells, (4.7 nM IC

48 ling through its ability to induce autocrine HB-EGF signaling.

49 finding has high clinical relevance, because HB-EGF signaling is known to be important for human impl

50 imulation; however, compared with HRG-beta1, HB-EGF induced phosphorylation of the 80-kDa cytoplasmic

51 ocephalus; however, the relationship between HB-EGF and hydrocephalus is unclear.

52 nificantly, macrophage depletion or blocking HB-EGF activity results in higher levels of nonrepairabl

53 rapy-induced EGFR activation is regulated by HB-EGF.

54 ry induces decidualization via the canonical HB-EGF and COX-2 pathways.

55 decreased Chi3l1-stimulated epithelial cell HB-EGF production and macrophage MAPK/Erk and PKB/Akt ac

56 Coincident with these changes, HB-EGF significantly decreases mRNA expression of severa

57 Consequently, HB-EGF-treated cells exhibit higher double-strand break

58 Constitutive HB-EGF expression rescued AP-1/NF-kappaB small interferi

59 pression and increases in MMP/ADAM-dependent HB-EGF cleavage are responsible for proteasome inhibitor

60 ffector, ERK1/2 also mediates ADAM-dependent HB-EGF shedding and subsequent EGFR transactivation in r

61 (PKC) cascade that promotes ADAM17-dependent HB-EGF cleavage, EGFR transactivation, and apical exocyt

62 t inhibits A1AR-stimulated, ADAM17-dependent HB-EGF cleavage.

63 cancer angiogenesis through the HS-dependent HB-EGF/EGFR axis that subsequently modulates the express

64 n monocytes, by releasing macrophage-derived HB-EGF, enhance DDR in neighboring cells suffering from

65 nd knockdown of Sp1 substantially diminishes HB-EGF production.

66 d protein kinase activity, and downregulated HB-EGF (heparin-binding EGF-like growth factor) mRNA lev

67 -EGF, epiregulin (EPR), heparin binding EGF (HB-EGF), and heregulin/neuregulin (HRG).

68 ng Amphiregulin (AREG), heparin-binding EGF (HB-EGF), and transforming growth factor alpha (TGFalpha)

69 or-alpha (TGF-alpha) or heparin-binding EGF (HB-EGF), is also often increased in gliomas resulting in

70 factor receptor agonist heparin-binding EGF (HB-EGF), which promotes KV1 channel endocytosis, reduced

71 ription of several EGFR family ligands (EGF, HB-EGF and epiregulin), however only increases in HB-EGF

72 phosphorylation, suggesting that an EGFRvIII-HB-EGF-EGFRwt feed-forward loop regulates EGFRvIII activ

73 y maintained by a continuous EGFRwt-EGFRvIII-HB-EGF loop, potentially an attractive target for therap

74 This suggests that the EGFRvIII-HB-EGF-wild-type EGFR autocrine loop plays an important

75 The consequence of elevated HB-EGF signaling was investigated without the confoundin

76 l pathophysiological mechanism that elevated HB-EGF can elicit VEGF induction and hydrocephalus.

77 Our results support the idea that excess HB-EGF leads to a significant elevation of VEGF and vent

78 CA tissues showed that stromal MFs expressed HB-EGF, whereas EGFR was detected in cancer cells.

79 advantage of transgenic mice that expressed HB-EGF throughout the intestine but developed SPs only i

80 P) in a stable THCE cell line that expressed HB-EGF with AP inserted in the heparin-binding site.

81 hatase (AP) in a stable HCEC line expressing HB-EGF-AP.

82 rneal epithelial (THCE) cell line expressing HB-EGF-AP.

83 of heparin-binding epidermal growth factor (HB-EGF) and activation of EGFR.

84 n of heparin-binding EGF-like growth factor (HB-EGF) and activin AB in LTBI samples.

85 epidermal growth factor)-like growth factor (HB-EGF) and tumor necrosis factor-alpha-converting enzym

86 or a heparin-binding EGF-like growth factor (HB-EGF) antagonist (CRM197) with or without LPA.

87 and heparin-binding EGF-like growth factor (HB-EGF) are upregulated, and exogenous addition of these

88 izes heparin binding EGF-like growth factor (HB-EGF) blocked wounding-induced HA synthesis by > or =5

89 rmal growth factor (EGF)-like growth factor (HB-EGF) by these macrophages.

90 y of heparin-binding EGF-like growth factor (HB-EGF) defers on-time implantation, leading to compromi

91 uble heparin-binding EGF-like growth factor (HB-EGF) from AT1R/Cl4 cells, and Ang II-induced EGFR act

92 gand heparin-binding EGF-like growth factor (HB-EGF) from HNSCC cells, where soluble HB-EGF enhanced

93 ds, heparin-binding epidermal growth factor (HB-EGF) has emerged as a paracrine factor that contribut

94 and heparin-binding EGF-like growth factor (HB-EGF) induced rapid and strong RhoA activation.

95 e of heparin-binding EGF-like growth factor (HB-EGF) inhibits KC migration in scratch wound assays.

96 epidermal growth factor-like growth factor (HB-EGF) is a member of the EGF growth factor family.

97 epidermal growth factor-like growth factor (HB-EGF) is a member of the epidermal growth factor famil

98 epidermal growth factor-like growth factor (HB-EGF) is a member of the epidermal growth factor famil

99 rmal growth factor (EGF)-like growth factor (HB-EGF) is activated by reduced endothelial shear stress

100 epidermal growth factor-like growth factor (HB-EGF) is an angiogenic factor mediating radial migrati

101 epidermal growth factor-like growth factor (HB-EGF) is produced as a type-I, single-pass transmembra

102 rmal growth factor (EGF)-like growth factor (HB-EGF) is proven to accelerate healing, however precise

103 eparin-binding epidermal-like growth factor (HB-EGF) is rapidly induced in MG residing at the injury

104 nant heparin-binding EGF-like growth factor (HB-EGF) or transforming growth factor (TGF)-alpha, but n

105 rget heparin-binding EGF-like growth factor (HB-EGF) phenocopied miR-132 overexpression in keratinocy

106 epidermal growth factor-like growth factor (HB-EGF) protects the intestines from injury in a rodent

107 Heparin-binding EGF-like growth factor (HB-EGF) shedding was assessed by measuring the release o

108 and heparin binding epidermal growth factor (HB-EGF) was analyzed by immunohistochemistry.

109 rmal growth factor (EGF)-like growth factor (HB-EGF), a ligand of the EGF receptor (EGFR), in nutrien

110 epidermal growth factor-like growth factor (HB-EGF), are sufficient for rapid and complete neoplasti

111 EG), heparin-binding EGF-like growth factor (HB-EGF), betacellulin, epiregulin, and epigen.

112 GFR, Heparin-binding EGF-like growth factor (HB-EGF), in the intestine.

113 and, heparin-binding EGF-like growth factor (HB-EGF), is synthesized as a membrane-anchored precursor

114 ands heparin-binding EGF-like growth factor (HB-EGF), neuregulin (NRG), and transforming growth facto

115 ding heparin binding-EGF-like growth factor (HB-EGF), that upregulate the expression of a patient-spe

116 , or heparin-binding EGF-like growth factor (HB-EGF), we show that both of these EC-derived ligands a

117 ture heparin-binding EGF-like growth factor (HB-EGF), which, in turn, increases cancer progression.

118 of heparin-binding epidermal growth factor (HB-EGF).

119 of heparin-binding epidermal growth factor (HB-EGF).

120 g of heparin-binding EGF-like growth factor (HB-EGF).

121 and heparin-binding EGF-like growth factor (HB-EGF).

122 gand heparin-binding EGF-like growth factor (HB-EGF).

123 ) and heparin-bound epidermal growth factor (HB-EGF).

124 the heparin-binding epidermal growth factor (HB-EGF).

125 ted enhanced nuclear translocation following HB-EGF treatment.

126 the site located at -83/-54 was required for HB-EGF promoter activity.

127 ore effectively than an equal dosage of free HB-EGF.

128 Expression of selected PR target genes (HB-EGF, IRS-1, and STC1) was significantly elevated in c

129 ows: 5-HT --> 5-HT(2A) receptor --> TACE --> HB-EGF shedding --> EGFR --> ERK --> increased DNA conte

130 ow (<8 per thousand of RPLP0/36B4); however, HB-EGF and AREG mRNAs were strongly induced in human ski

131 We show that mice overexpressing human HB-EGF with beta-galactosidase reporter exhibit an eleva

132 mphiregulin, and bound specifically to human HB-EGF, but not to rodent HB-EGF.

133 We have previously identified HB-EGF, a ligand for EGFRwt, as a gene induced specifica

134 ic program in ovarian cancer cells impacting HB-EGF signaling and subsequent expression of angiogenic

135 cosamine 6-O-sulfate levels in HS, impairing HB-EGF-dependent EGFR signaling and diminishing FGF2, IL

136 that were inhibited by approximately 50% in HB-EGF(+/-) and approximately 90% in HB-EGF(-/-) mice.

137 50% in HB-EGF(+/-) and approximately 90% in HB-EGF(-/-) mice.

138 ranscription factor Sp1 is a major factor in HB-EGF production, and knockdown of Sp1 substantially di

139 F and epiregulin), however only increases in HB-EGF were detected at the protein level.

140 n and leukocyte accumulation were reduced in HB-EGF(-/-).

141 ise to regulatory macrophages also result in HB-EGF production.

142 f the right carotid artery was unaffected in HB-EGF(+/-) and HB-EGF(-/-) mice, nor by AG1478.

143 on in colonic epithelial cells and increases HB-EGF levels in blood from WT mice, but not from mice w

144 Thus, increasing HB-EGF leads to a striking increase in EGFRvIII tyrosine

145 factor SP-1 is involved in NPI-0052-induced HB-EGF transcription.

146 LL-37 induced HB-EGF-AP release and EGFR activation in a dose-dependen

147 Wounding-, LPA-, and ATP-induced HB-EGF shedding and EGFR activation were attenuated by t

148 e demonstrated that the chemotherapy-induced HB-EGF was largely dependent on activator protein-1 (AP-

149 rowth factor beta 1, which, in turn, induced HB-EGF expression in HLMFs.

150 We also found that Y-142 inhibited HB-EGF-induced cancer cell proliferation, endothelial ce

151 therapeutic intervention aimed at inhibiting HB-EGF activity may be useful in cancer prevention and t

152 In contrast, inhibiting HB-EGF by siRNA suppressed TADC-mediated cancer progress

153 Interestingly, HB-EGF had no effect on mesenteric arteries, suggesting

154 e designed to test the effects of juxtacrine HB-EGF signaling upon cell survival and epithelial integ

155 re severe phenotype than that of full-length HB-EGF, even though the full-length protein was efficien

156 Transgenic expression of the EGFR ligand HB-EGF in the intestines of mice promoted development of

157 Prolactin and the ErbB4 ligand HB-EGF each induced STAT5A activation, expression of lac

158 phosphatase (AP)-tagged ligands shed mature HB-EGF and TGF-alpha into the supernatant and promoted t

159 ial cell homeostasis through ADAM17-mediated HB-EGF release, leading to transactivation of EGFR.

160 In this model, HB-EGF was sufficient to promote Kras-initiated tumorige

161 Moreover, HB-EGF is augmented at sites of intimal hyperplasia and

162 In addition, Y-142 neutralized HB-EGF-induced phosphorylation of EGFR and ERBB4, and bl

163 FR kinase inhibitor, AG1478, 2) neutralizing HB-EGF, but not amphiregulin, antibodies, heparin, or CM

164 GAGs to bind FGF-1, FGF-2, and VEGF but not HB EGF.

165 modulates multiple biological activities of HB-EGF including cancer cell proliferation and angiogeni

166 eed, we show that inhibiting the activity of HB-EGF, a potent mitogen, with neutralizing antibodies r

167 , which is required for biologic activity of HB-EGF, restores inflammation in APN KO mice.

168 rs through a mechanism requiring cleavage of HB-EGF and activation of EGFR signaling.

169 hypertonic stress led to strong cleavage of HB-EGF and NRG but only moderate cleavage of TGF-alpha.

170 Active cleavage of HB-EGF in TADCs by ADAM9 and ADAM17 is associated with i

171 istate-13-acetate (TPA) -induced cleavage of HB-EGF, NRG, and TGF-alpha was dependent on PKC and sens

172 Mice that expressed a combination of HB-EGF and US28 (a constitutively active, G-protein-coup

173 47(phox) inhibited FINR, whereas deletion of HB-EGF abolished nuclear factor kappaB activation in smo

174 Our current goal was to assess the effect of HB-EGF on intestinal microvascular blood flow and intest

175 Enhancement of HB-EGF production in TADCs increased the proliferation,

176 ogether, our data suggest that expression of HB-EGF in human KCs triggers a migratory and invasive ph

177 mbrane domain to release the soluble form of HB-EGF (s-HB-EGF) by sheddases, including matrix metallo

178 own to be a precursor of the soluble form of HB-EGF (sHB-EGF), which promotes cell proliferation and

179 Conversely, the secreted form of HB-EGF improved islet function, but had severe fibrotic

180 nsgenic overexpression of the active form of HB-EGF.

181 Induction of HB-EGF expression and ectodomain shedding synergisticall

182 hat stress signaling leading to induction of HB-EGF expression and increases in MMP/ADAM-dependent HB

183 The induction of HB-EGF in regulatory macrophages is due to new transcrip

184 Furthermore, we discover that induction of HB-EGF is dependent on reactive oxygen species and p38-M

185 EGFR) phosphorylation, whereas inhibition of HB-EGF expression by use of the HB-EGF inhibitor (CRM197

186 Inhibition of HB-EGF shedding using a MMP inhibitor, GM6001, also dram

187 superior to bevacizumab in the inhibition of HB-EGF-induced tube formation.

188 o understand the function of each isoform of HB-EGF, we made transgenes expressing either a constitut

189 Knockdown of HB-EGF expression by siRNA suppresses p40 effects on tra

190 gulin, partially compensates for the loss of HB-EGF during implantation.

191 HB-EGF and found that this specific loss of HB-EGF in the uterus still defers on-time implantation w

192 ory role of amphiregulin for uterine loss of HB-EGF, preventing complete failure of pregnancy.

193 cing indicated that PIKfyve is a mediator of HB-EGF-stimulated EGFR nuclear trafficking, EGFR binding

194 Modulation of HB-EGF activity might have a therapeutic potential in th

195 and markedly inhibited by neutralization of HB-EGF.

196 otility and proliferation, overexpression of HB-EGF also reduced KC growth by >90%.

197 oupled receptor that increases processing of HB-EGF from the membrane) rapidly developed large cecal

198 induces decidualization via up-regulation of HB-EGF and COX-2.

199 Significant up-regulation of HB-EGF has been seen in tumor-infiltrating CD11c(+) dend

200 hypothesized that strain-induced release of HB-EGF and TGF-alpha is mediated via integrin-ADAM17/TAC

201 mediated through EGFR (ErbB1) via release of HB-EGF and TGF-alpha ligands.

202 of MMP14 also results in membrane release of HB-EGF and the activation of EGFR.

203 The release of HB-EGF assessed by AP activity increased significantly i

204 that coacervate-based controlled release of HB-EGF may serve as a new therapy to accelerate healing

205 thickness wound model, controlled release of HB-EGF within the wound significantly accelerated wound

206 o wounding, LPA, or both, and the release of HB-EGF-AP induced by LPA was inhibited by PP2 and GM6001

207 II cell cultures did not enhance release of HB-EGF.

208 reased expression and ectodomain shedding of HB-EGF and reduced incidence of cancer development, resu

209 l differentiation via ectodomain shedding of HB-EGF and TGF-alpha.

210 on the expression and ectodomain shedding of HB-EGF by TNFalpha-converting enzyme/a disintegrin and m

211 ile, we found that the enzymatic shedding of HB-EGF was also regulated by chemotherapy treatment, res

212 Wound- and LPA-induced shedding of HB-EGF was assessed by measuring the release of alkaline

213 und that macrophages are the major source of HB-EGF production in pancreatic cancer tissue samples, a

214 ime that human and mouse DCs are a source of HB-EGF, an EGFR ligand with tumorigenic properties.

215 Egr-1 increased the transcription of HB-EGF (epidermal growth factor), amphiregulin and epire

216 nto a therapeutic agent for the treatment of HB-EGF-dependent cancers.

217 The effects of p40 on HB-EGF release and ADAM17 activation in vivo are examine

218 cleavage was not dependent on PKC, and only HB-EGF and NRG cleavage were inhibited by BB94.

219 ouse model, we show that exogenous ADAM17 or HB-EGF restores cerebral arterial tone and blood flow re

220 Silencing EGFRwt or HB-EGF leads to a striking inhibition of EGFRvIII-induce

221 d tumorigenicity, while increasing EGFRwt or HB-EGF levels resulted in accelerated EGFRvIII-mediated

222 sfected with additional ErbB3, either EPR or HB-EGF promoted resurfacing greater than EGF, HRG, or co

223 re abolished in the presence of gefitinib or HB-EGF-neutralizing antibody.

224 ithout treating HC11 cells with prolactin or HB-EGF, s80(HER4) (expressed from a cDNA construct) loca

225 breast cancer cells 4-fold over TGFalpha or HB-EGF exosomes and 5-fold over equivalent amounts of re

226 greater membrane stability than TGFalpha or HB-EGF.

227 3 microM PP2 effectively inhibited wound- or HB-EGF-induced AKT phosphorylation.

228 implantation estrogen secretion from ovarian HB-EGF deficiency is a cause of sustained expression of

229 Y-142 has a potent HB-EGF neutralizing activity that modulates multiple bio

230 Moreover, up-regulation of E-cadherin by pro-HB-EGF not only resulted in cellular morphologic change

231 necrosis factor alpha-converting enzyme (pro-HB-EGF sheddase), increased phosphorylation of EGF recep

232 Expression of noncleaved pro-HB-EGF in pancreatic cells resulted in the up-regulation

233 oxygen species, increased expression of pro-HB-EGF and tumor necrosis factor alpha-converting enzyme

234 e clearly indicated the distinct role of pro-HB-EGF in the regulation of E-cadherin expression and th

235 ely, our data defined a distinct role of pro-HB-EGF in the regulation of E-cadherin, suggesting that

236 tudied extensively; however, the role of pro-HB-EGF in tumor progression is unknown, despite the fact

237 e the fact that a considerable amount of pro-HB-EGF remains on the cell membrane.

238 We showed here that the expression of pro-HB-EGF was associated with the differentiation status in

239 nthesized as a membrane-bound precursor (pro-HB-EGF), it is cleaved at the juxtamembrane domain to re

240 MG residing at the injury site and that pro-HB-EGF ectodomain shedding is necessary for retina regen

241 In vitro, HLMFs produced HB-EGF and their conditioned media induced EGFR activati

242 lipopolysaccharide, with some pups receiving HB-EGF (800 microg x kg(-1) x dose(-1)) added to the fee

243 Expression of APN and its receptors, HB-EGF, and basic fibroblast growth factor (bFGF) messen

244 Y-142 recognized HB-EGF as well as the EGFR ligand amphiregulin, and boun

245 Released HB-EGF induced the formation of invadopodia, cellular st

246 In conclusion, mechanical strain releases HB-EGF and TGF-alpha and promotes fetal type II cell dif

247 etal epithelial cells actives TACE, releases HB-EGF and TGF-alpha, and promotes differentiation.

248 Remarkably, HB-EGF stimulates the formation of multipotent MG-derive

249 Immunostaining revealed HB-EGF-induced expression of the mesenchymal protein vim

250 ultiple NFAT targets, including Rcan1, Rgs2, HB-EGF, Lif, and Gem, were validated by chromatin immuno

251 cifically to human HB-EGF, but not to rodent HB-EGF.

252 ain to release the soluble form of HB-EGF (s-HB-EGF) by sheddases, including matrix metalloproteinase

253 The tumorigenic potential of s-HB-EGF has been studied extensively; however, the role o

254 A2780 cells, attenuated growth factor (SDF1, HB-EGF, VEGF(165) and HGF) mediated cell migration and i

255 rs by magnetic beads activated TACE and shed HB-EGF and TGF-alpha.

256 III tyrosine phosphorylation while silencing HB-EGF attenuates EGFRvIII phosphorylation, suggesting t

257 re we demonstrate that expression of soluble HB-EGF (sHB-EGF) or full-length transmembrane HB-EGF (pr

258 , is necessary to restrict action of soluble HB-EGF away from surrounding tissue.

259 resulting in the elevated release of soluble HB-EGF from the cellular membrane.

260 r, lentivirus-mediated expression of soluble HB-EGF, but not soluble AREG, strongly enhanced KC migra

261 tor (HB-EGF) from HNSCC cells, where soluble HB-EGF enhanced invadopodia ECM degradation in HNSCC but

262 prevented by pretreatment with the specific HB-EGF inhibitor CRM197 or the metalloproteinase inhibit

263 restored by addition of the ADAM17 substrate HB-EGF (heparin-binding epidermal growth factor-like gro

264 nalling and shedding of the ADAM17 substrate HB-EGF.

265 well as two other NGF-induced AP-1 targets (HB-EGF and miR-21) function in positive feedback loops t

266 rkably, all these genes, which include TGFA, HB-EGF, EPHA2, IL8, MAP4K4, FOSL1, EMP1, and DUSP6, infl

267 Our study provides genetic evidence that HB-EGF is critical for normal implantation.

268 We also show by immunohistochemistry that HB-EGF expression correlates with the presence of EGFRvI

269 bjected to experimental NEC, indicating that HB-EGF may play a critical role in the treatment of vari

270 Finally, we show that HB-EGF acts upstream of the Wnt/beta-catenin-signaling c

271 In this study, we show that HB-EGF is induced by EGFRvIII only when EGFRwt is presen

272 We also show that HB-EGF is strongly induced in regenerating epidermis aft

273 We show that HB-EGF mediates its effects via an EGFR/MAPK signal tran

274 These findings suggest that HB-EGF signaling is required for low flow-induced hypert

275 d with the anti-EGFR antibody cetuximab, the HB-EGF inhibitor CRM197, and the anti-vascular endotheli

276 nhibition of HB-EGF expression by use of the HB-EGF inhibitor (CRM197) or siRNA resulted in the suppr

277 to three sites within the first 2 kb of the HB-EGF promoter following stimulation, and the site loca

278 een CCA cells and myofibroblasts through the HB-EGF/EGFR axis contributes to CCA progression.

279 s EGFR activation by regulating the TNFalpha/HB-EGF axis during liver regeneration.

280 on of R142 and Y123 and its high affinity to HB-EGF.

281 me autotaxin (ATX) in pregnant mice leads to HB-EGF and COX-2 down-regulation near embryos and attenu

282 ons in renal epithelial cells in response to HB-EGF.

283 growth factor receptor (EGFR) in response to HB-EGF.

284 B-EGF (sHB-EGF) or full-length transmembrane HB-EGF (proHB-EGF), but not proAREG, results in profound

285 depends on the ratio of cleaved to uncleaved HB-EGF and that the transmembrane intermediate, while de

286 Only JM-a/CYT-2 cells formed tubules upon HB-EGF stimulation.

287 in mice with conditional deletion of uterine HB-EGF and found that this specific loss of HB-EGF in th

288 ore the significance specifically of uterine HB-EGF in implantation, we examined this event in mice w

289 y a role in the resolution of DNA damage via HB-EGF.

290 In vitro, HB-EGF released from the coacervate delivery system disp

291 Whereas HB-EGF shedding was also detected in E18 cells exposed t

292 We thus tested whether HB-EGF contributes to low flow-induced negative hypertro

293 for EGFR, was not released by stretch, while HB-EGF, a ligand for EGFR and ErbB4, was shed by stretch

294 Association of serum APN with HB-EGF and bFGF was studied by coimmunoprecipitation.

295 Moreover, pretreatment of cells with HB-EGF impaired ARPE-19 migration toward HGF in a matrix

296 ionally, TACE was co-immunoprecipitated with HB-EGF.

297 Conversely, pretreatment of ImSt with HB-EGF completely blocked H pylori-induced apoptosis.

298 t with in vitro results, wounds treated with HB-EGF coacervate exhibited enhanced migration of kerati

299 Stressed pups treated with HB-EGF had significantly increased microvascular blood f

300 jury scores, with stressed pups treated with HB-EGF showing decreased histologic injury.