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 coimmunoprecipitates with the transcriptional rep

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

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

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

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

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

8 HB-EGF significantly preserved intestinal microvascular

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

41 macrophages is the production of angiogenic HB-EGF.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

66 (EGF) receptor ligand, heparin-binding EGF (HB-EGF), with no defined immuno-pathophysiological funct

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

82 epidermal growth factor-like growth factor (HB-EGF) as the signal that maintains HSC quiescence and

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

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

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

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

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

88 gand heparin-binding EGF-like growth factor (HB-EGF) in the beta-cell proliferative response to gluco

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

104 epidermal growth factor like growth factor (HB-EGF), a crucial regulator of heart valve development

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

106 epidermal growth factor-like growth factor (HB-EGF), a potent epithelial proliferation and migration

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

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

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

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

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

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

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

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

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

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

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

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

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

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

121 ted enhanced nuclear translocation following HB-EGF treatment.

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

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

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

125 Our findings identify a novel glucose/HB-EGF/EGFR axis implicated in beta-cell compensation to

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

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

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

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

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

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

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

133 50% in HB-EGF(+/-) and approximately 90% in HB-EGF(-/-) mice.

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

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

136 Src family kinases, known to be involved in HB-EGF processing, abrogated glucose-induced beta-cell p

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

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

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

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

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

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

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

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

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

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

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

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

149 t an immunoregulatory function for intrinsic HB-EGF expressed by CD4 T cells in T(H)2 inflammation an

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

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

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

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

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

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

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

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

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

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

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

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

162 roof of concept that local administration of HB-EGF has the potential to be developed as a topical tr

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

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

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

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

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

168 47(phox) inhibited FINR, whereas deletion of HB-EGF abolished nuclear factor kappaB activation in smo

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

170 C57BL/6 J mice, we evaluated the efficacy of HB-EGF treatment (5 ul of 10 ug/ml) solution.

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

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

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

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

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

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

177 fore, we wished to elucidate the function of HB-EGF synthesized by CD4 T cells in the context of alle

178 Induction of HB-EGF expression and ectodomain shedding synergisticall

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

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

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

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

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

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

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

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

187 Furthermore, knockdown of HB-EGF in rat islets blocks beta-cell proliferation in r

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

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

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

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

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

193 and markedly inhibited by neutralization of HB-EGF.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

217 In rat islets, inhibition of EGFR or HB-EGF blocks the proliferative response not only to HB-

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

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

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

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

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

223 greater membrane stability than TGFalpha or HB-EGF.

224 In this study, we show how knocking out HB-EGF expression in CD4 T cells in vivo attenuates IL-5

225 Knocking out HB-EGF in CD4 T cells resulted in increased Bcl-6 bindin

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

254 show that immature LSECs are unable to shed HB-EGF from the cytosolic membrane.

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

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

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

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

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

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

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

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

263 Mechanistically, we demonstrate that HB-EGF mRNA levels are increased in beta-cells in respon

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

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

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

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

268 The results show that HB-EGF delivered post radiation, significantly increased

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

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

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

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

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

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

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

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

277 ied ChREBP binding sites in proximity to the HB-EGF gene.

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

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

280 exposure of isolated rat and human islets to HB-EGF stimulates beta-cell proliferation.

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

282 locks the proliferative response not only to HB-EGF but also to glucose.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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.