ライフサイエンスコーパス: HRG

1 HRG also promotes HA- and CD44-dependent oncogenic event

2 HRG bound specifically to apoptotic Jurkat cells and mat

3 HRG caused prominent induction in the nuclear expression

4 HRG caused the phosphorylation of serine 167 in ERalpha.

5 HRG decreased the dose required for BP-mediated stimulat

6 HRG deficiency was associated with a suppressed antitumo

7 HRG expression levels define a biologically distinct sub

8 HRG has antibacterial activity, and when challenged by H

9 HRG induces tumorigenicity and metastasis of breast canc

10 HRG loss influences macrophage gene regulation, leading

11 HRG mitogenic activity was also impaired by depletion of

12 HRG regulated the association of Ebp1 with E2F promoter

13 HRG siRNA inhibited growth of H1047R but not E545K-expre

14 HRG treatment induced a transient phosphorylation of BRC

15 HRG treatment led to degradation of poly (ADP-ribose) po

16 HRG treatment of SKBr3 cells for 72 h decreased the leve

17 HRG, administered as a single dose, is reasonably well t

18 HRG-1 and HRG-4 are previously unknown transmembrane pro

19 HRG-2 is a type I membrane protein that binds heme and l

20 HRG-3 binds heme and is exclusively secreted by maternal

21 HRG-3 deficiency results either in death during embryoge

22 HRG-beta1 did not activate Akt in MCF-7 cells stably tra

23 HRG-induced Rac activation was phosphatidylinositol 3-ki

24 HRG/M was unable to autophosphorylate the erbB receptors

25 RNA that the growth factor heregulin beta 1 (HRG), a combinatorial ligand for human epidermal growth

26 olocalize within nuclei of heregulin beta 1 (HRG)-stimulated cells and both proteins bind to the endo

27 MCF-7/HRG cells were more than 10-fold resistant to the alkyla

28 itaxel or vincristine) was obtained in MCF-7/HRG cells.

29 ) engineered to overexpress heregulin (MCF-7/HRG), a ligand for the Her-2/3/4 network, we investigate

30 E(2)-induced Erk activation is mediated by a HRG/HER-2/PKC-delta/Ras pathway that could be crucial fo

31 In addition, HRG stimulation caused a significant decrease in BRCA1 m

32 In addition, HRG stimulation of breast cancer cells promoted phosphor

33 n, ATPase activity, and relocalization after HRG treatment could all be blocked by pretreatment with

34 lts suggest the potential use of Hst against HRG-mediated growth of breast cancers with high and low

35 Ebp1 could bind E2F consensus elements in an HRG-inducible manner, leading to transcriptional repress

36 It is thought that an HRG fragment containing the HRR, released via plasmin-me

37 HRG expression in MDA-MB-231 cells using an HRG antisense cDNA.

38 HRG-1 and HRG-4 are previously unknown transmembrane proteins, whi

39 (rs710446, combined p = 9.52 x 10(-22)), and HRG (rs9898, combined p = 1.34 x 10(-11)).

40 pleckstrin homology (PH) domain of Akt, and HRG-beta1 did not induce Akt phosphorylation in the ER-n

41 The combination of BP and HRG also stimulated proliferation of BT-474 cells compar

42 BP and HRG produced a synergistic increase in ERalpha recruitme

43 Butylparaben (BP) and HRG produced a synergistic increase in c-Myc mRNA and pr

44 ndent BRCA1 phosphorylation and that ECM and HRG down-regulate BRCA1 expression in breast cancer cell

45 man breast cancer cells with CXCL12, EGF and HRG, and HMEC-CXCR2 cells with CXCL8 facilitated nuclear

46 esponse to stimulations with ligands EGF and HRG.

47 sized that ECM may affect the expression and HRG-dependent phosphorylation of BRCA1.

48 ression by siRNA reduced Slug expression and HRG-induced EMT.

49 11)In-bsRICs composed of trastuzumab Fab and HRG exhibited specific binding in vitro to tumor cells d

50 rt environmental heme into the intestine and HRG-3, a secreted protein, to deliver intestinal heme to

51 y was accelerated in HRG-deficient mice, and HRG administration abrogated this effect.

52 echanistic link between metabolic stress and HRG/TGZ-induced cell death.

53 Because HRG-mediated HAS isozyme phosphorylation/activation can

54 In breast cancer cells, heregulin beta1 (HRG) causes a strong activation of Rac; however, it does

55 nation with the HER4 ligand heregulin-beta1 (HRG) resulted in apoptosis of BT20 cells providing a nov

56 the HER3-binding peptide of heregulin-beta1 (HRG) with or without a 12- or 24 mer polyethylene glycol

57 Heregulin-beta1 (HRG), a combinatorial ligand for human epidermal growth

58 f MCF-7 cells with 10(-9) M heregulin-beta1 (HRG-beta1) resulted in a rapid phosphorylation of Akt an

59 rowth factor-I (IGF-I), and heregulin-beta1 (HRG-beta1), can modulate the expression and activity of

60 show that inhibitors of c-Src or HSP90 block HRG-induced targeting of MUC1 to mitochondria and integr

61 Although Hst blocked HRG signaling in both parental and HER-2 transfected cel

62 These studies were achieved by blocking HRG expression in MDA-MB-231 cells using an HRG antisens

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

64 ssion strongly stimulated the levels of both HRG receptors.

65 Purified HRG protein induced, but HRG-deficient serum prevented, M1 macrophage differentia

66 tibacterial activity, and when challenged by HRG, sHIP was found to rescue S. pyogenes bacteria.

67 lerate AR mRNA decay was further enhanced by HRG treatment.

68 ere, we show that cellular import of heme by HRG-1-related proteins from worms and humans requires st

69 activity was also significantly increased by HRG treatment.

70 d Slug transcriptional activation induced by HRG or HSF-1 overexpression.

71 Although the invasion induced by HRG-beta1 or CXCL12 is dependent on the EGF/CSF-1 paracr

72 ensitization of the Rac response/motility by HRG are mediated by the transcription factor hypoxia-ind

73 Akt phosphorylation by HRG-beta1 was abrogated by an arginine to cysteine mutat

74 these cells restored Akt phosphorylation by HRG-beta1, suggesting the requirement of ER-alpha.

75 KCalpha attenuated the apoptosis produced by HRG and GF.

76 hed that, surprisingly, activation of Rac by HRG is mediated not only by ErbB3 and ErbB2 but also by

77 fied as developmental were down-regulated by HRG, whereas those involved in transport were up-regulat

78 rovides an explanation for its regulation by HRG, an ErbB3 ligand.

79 , a downstream effector of Ras signaling, by HRG, a growth factor with diverse functions in breast ca

80 the GADD153 promoter was also stimulated by HRG-inducible ATF-4 and activated HER2 but not wild-type

81 Following stimulation by HRG, a strong increase in [(3)H]thymidine incorporation

82 In human breast cancer cells, HRG induced G3BP mRNA and protein expression.

83 Consequently, HRG-induced apoptosis in SKBr3 cells appeared to involve

84 A, thereby confirming a role for HER4 in DAC/HRG-induced apoptosis.

85 We hypothesized that liver-derived HRG is a critical endogenous modulator of hepatic macrop

86 Liver-derived HRG, similar to alarmins, appears to be an endogenous mo

87 Among patients whose tumors had detectable HRG mRNA and low HER2 (n = 57 [38%] of 151 with availabl

88 Exploratory analyses suggest that detectable HRG and low HER2, biomarkers that link directly to the m

89 B-EGF promoted resurfacing greater than EGF, HRG, or controls.

90 er EPR or HB-EGF treatments compared to EGF, HRG, ErbB3 only, or empty vehicle.

91 ct activation profiles in response to either HRG or EGF, with obvious differences in both the intensi

92 Here we show that Caenorhabditis elegans HRG-3 is required for the delivery of maternal heme to d

93 e expression of Hst in MCF7 cells eliminated HRG signaling through both mitogen-activated protein kin

94 Inhibition of PKC function enhanced HRG-induced apoptosis, leading to synergistic down-regul

95 of classical PKC isoforms (Go6976) enhanced HRG-induced apoptosis, whereas the PKCdelta selective in

96 F) and Ro318425 (Ro), significantly enhanced HRG-induced apoptosis as determined by flow cytometric a

97 These findings suggest that ECM enhances HRG-dependent BRCA1 phosphorylation and that ECM and HRG

98 ning significant signals were located on F5, HRG, KNG1, F11, F12 and ABO and have been previously rep

99 bB3) is physically linked to ErbB2 following HRG stimulation.

100 ing an evolutionarily conserved function for HRG-1.

101 milar receptor requirements are observed for HRG-induced actin cytoskeleton reorganization and mitoge

102 lidate this finding and should preselect for HRG expression and focus on cancers with low HER2 levels

103 Our results establish a role for HRG-3 as an intercellular heme-trafficking protein.

104 A-induced thrombin generation in plasma from HRG-deficient and wild-type mice.

105 ombin generation was enhanced in plasma from HRG-deficient mice, and accelerated clotting was restore

106 of the antiangiogenic cleavage product from HRG.

107 Furthermore, HRG expression is higher in recurrent SCCHN compared to

108 Furthermore, HRG treatment resulted in G3BP translocation to the nucl

109 the expression of hypoxic responsive genes (HRG) PYRUVATE DECARBOXYLASE (VvPDC), ALCOHOL DEHYDROGENA

110 Although multiple heme-responsive genes (HRGs) have been characterized within the free-living nem

111 we showed that histidine-rich glycoprotein (HRG) binds FXIIa and attenuates its capacity to trigger

112 Histidine-rich glycoprotein (HRG) is a 75-kDa heparin-binding plasma protein implicat

113 Histidine-rich glycoprotein (HRG) is a plasma protein consisting of 6 distinct functi

114 Histidine-rich glycoprotein (HRG) is an abundant serum protein that exhibits many fun

115 interacts with histidine-rich glycoprotein (HRG), and the name sHIP (streptococcal histidine-rich gl

116 plasma protein, histidine-rich glycoprotein (HRG), was demonstrated, in mouse tumor models, to mediat

117 at targeting prevention to high-risk groups (HRG) could be very effective.

118 titis significantly up-regulated hepatocytic HRG expression, which was associated with M1 polarizatio

119 Heregulin (HRG) is an activator of the erbB2-, erbB3- and erbB4-(er

120 Heregulin (HRG)-induced cell responses are mediated by the ErbB fam

121 HER-2 (erbB2) leads to amplified heregulin (HRG) signaling, promoting more aggressive breast cancer

122 creased with HER ligands, such as heregulin (HRG).

123 ng, the protein was identified as heregulin (HRG)alpha.

124 eceptor (HER) 3 (ErbB3), blocking heregulin (HRG) -mediated ErbB3 signaling and inducing ErbB3 recept

125 y an antibody against HER-2 or by heregulin (HRG) depletion from the conditioned medium through immun

126 e effects of ErbB-2 activation by heregulin (HRG) on BRCA1 function.

127 The growth factor heregulin (HRG), a ligand of ErbB3 and ErbB4 receptors, contributes

128 The growth factor heregulin (HRG), expressed in about 30% of breast cancer tumors, ac

129 The ErbB3/4 ligand heregulin (HRG) profoundly affects cell growth and differentiation,

130 es crosstalk between ErbB3 ligand heregulin (HRG)-triggered signaling and the AR axis, affecting biol

131 upregulated the HER3/HER4 ligand heregulin (HRG).

132 3) integrin and overexpression of Heregulin (HRG), a growth factor associated with breast cancer aggr

133 r cells exhibiting high levels of Heregulin (HRG), a growth factor closely associated with a metastat

134 epidermal growth factor (EGF) or heregulin (HRG) results in marked upregulation of MUC1-C translatio

135 epidermal growth factor (EGF) or heregulin (HRG), significantly improves prediction of cell migratio

136 with these results, we show that heregulin (HRG), a ligand for ErbB receptors, activates c-Src and,

137 We now show that heregulin (HRG), but not EGF, stimulates p95ErbB2 phosphorylation i

138 hese mechanisms, we observed that heregulin (HRG)-mediated activation of HER2, or HER2 overexpression

139 Addition of the ErbB-ligand, Heregulinbeta1 (HRG), to breast tumour-derived T47D cells promotes D-cyc

140 have shown that recombinant heregulinbeta1 (HRG) induces apoptosis in SKBr3 breast cancer cells that

141 to quantify the contribution of heterosexual HRGs and the potential impact of focused interventions t

142 We show that high HRG expression is associated with activated HER3, wherea

143 (PE)HRG214 (HRG) is a polyclonal antibody preparation produced by im

144 Caenorhabditis elegans and human HRG-1-related proteins are conserved, membrane-bound per

145 w, by exploiting this auxotrophy to identify HRG-1 proteins in C. elegans, that these proteins are es

146 ctional blockade of alpha(v)beta(3) impaired HRG-promoted hyperactivation of ERK1/ERK2 MAPK without a

147 Taken together, our results implicate HRG-2 as a facilitator of heme utilization in the Caenor

148 In HRG-induced UBs, however, the expression of GFRalpha1 wa

149 Cytochrome heme profiles are aberrant in HRG-2-deficient worms, a phenotype that was partially su

150 lusion after FeCl3 injury was accelerated in HRG-deficient mice, and HRG administration abrogated thi

151 further evidence of a key role for CYR61 in HRG-dependent alpha(v)beta(3) overexpression.

152 Forced expression of CYR61 in HRG-negative MCF-7 cells notably upregulated the express

153 f Bcl-2 protein and further degraded PARP in HRG-treated cells.

154 dium-hydrogen exchanger2 was up-regulated in HRG-treated UBs compared with UBs grown in the presence

155 ivity, demonstrating a direct causal role in HRG induction of tumorigenicity.

156 oss after tail tip amputation was similar in HRG-deficient and wild-type mice, carotid artery occlusi

157 tic and proliferative cascades and inhibited HRG-induced Her-2/3 phosphorylation.

158 -activating protein beta2-chimerin inhibited HRG-induced ERK activation, mitogenicity, and migration

159 MDM, while DNA, but not chromatin, inhibited HRG binding to apoptotic cells, and either anti-FcgammaR

160 Anti-FcgammaRI mAb inhibited HRG binding to HMDM, while DNA, but not chromatin, inhib

161 The PI3K inhibitor BEZ235 markedly inhibited HRG and pAKT levels and, in combination with lapatinib,

162 ic small interfering RNAs) not only inhibits HRG-mediated HAS phosphorylation/activation and HA produ

163 Interestingly, HRG expression in tumor biopsies from invasive breast ca

164 In this study we have investigated HRG activation of ErbB2, extracellular signal-regulated

165 and VWF, with the leading variants in KNG1, HRG and F12 being the same as in the EAs; the significan

166 significant signals were identified in KNG1, HRG, F12, ABO and VWF, with the leading variants in KNG1

167 previously reported associations with KNG1, HRG and F12 in EAs.

168 previously reported associations with KNG1, HRG, F11, F12, and ABO were confirmed.

169 Transfection of full-length HRG cDNA into the estrogen (E2)-dependent cell line MCF-

170 re we explore the hypothesis that high-level HRG expression defines a subpopulation of SCCHNs with ac

171 ng to EGFR and HER3, suggest that high-level HRG expression was associated with clinical response in

172 MTLn3 cells in response to the ErbB3 ligand HRG-beta1.

173 Our findings suggest that Ebp1, by linking HRG activation of membrane receptors to E2F gene activit

174 associated with activated HER3, whereas low HRG expression is associated with low HER3 activation in

175 h of HRG-overexpressing cells, while the low-HRG-expressing 231/AS31 cells did not show a significant

176 ve shown that the heme transporter B. malayi HRG-1 (BmHRG-1) is indeed functional in B. malayi In add

177 ls were seeded on laminin (LAM) or Matrigel, HRG induced a significantly higher proliferation than it

178 ting a role of oxidative stress in mediating HRG/TGZ-induced cell death.

179 Therefore, in a nucleic acid-driven model, HRG inhibits thrombosis by modulating the intrinsic path

180 Moreover, HRG expression in MCF-7 cells renders the cells sensitiv

181 Moreover, HRG promoted growth of UBs cultured in the absence of GD

182 Moreover, HRG-deficient mice showed significantly enhanced hepatic

183 -7 cells overexpressing a structural mutated HRG isoform.

184 ding EGF (HB-EGF), and heregulin/neuregulin (HRG).

185 Notably, HRG treatment upregulates surface expression levels of C

186 Her-2 phosphorylation, the majority (67%) of HRG-overexpressing and Her-2 tumors (n = 57; 30%) were i

187 oph that requires the coordinated actions of HRG-1 heme permeases to transport environmental heme int

188 sociation of the tumor-promoting activity of HRG from the sensitization to Doxo, that is, although th

189 ture confirmed the proliferative activity of HRG.

190 We demonstrate that assessment of HRG expression and Her-2 activation define a particular

191 sion was noticeably decreased by blockade of HRG expression in the 231/ASPOOL, 231/AS31 and Hs578T/AS

192 -2 overexpression concludes that blockage of HRG expression suppresses the aggressive phenotype of MD

193 earch for the mechanism by which blockage of HRG reverts this aggressive phenotype, we discovered tha

194 Taken together, the combination of HRG and TGZ may provide a basis for the development of a

195 estion, while neutralization or depletion of HRG from sera reduced this effect.

196 the effects exerted by the downregulation of HRG expression as well as by functional blockade of alph

197 empt to dissociate the tumorigenic effect of HRG from the sensitizing effect to chemotherapy, we cons

198 d in apoptosis, which mimicked the effect of HRG treatment.

199 as PI 3-K inhibitors, blocked the effect of HRG-beta1 on ER-alpha expression and activity and on the

200 bB inhibitors demonstrate that the effect of HRG-beta1 on ER-alpha expression and activity is also me

201 titutively active Akt mimicked the effect of HRG-beta1.

202 be a downstream modulator of the effects of HRG on cell cycle progression.

203 B2 is the primary mediator of the effects of HRG-beta1 on ER-alpha regulation.

204 The preadministration of an excess of HRG decreased uptake in MDA-MB-468 (HER2-negative/HER3-p

205 as HC, induce transiently the expression of HRG and VvFT and hasten the sprouting of endodormant gra

206 ation, induces transiently the expression of HRG and VvFT, and in the long-term, along with the advan

207 We propose that high-level expression of HRG is associated with constitutive activation of HER3 i

208 dimerization and high-level co-expression of HRG.

209 echanism underlying the diverse functions of HRG is not well established but is believed to depend on

210 in the modulation of uncontrolled growth of HRG-overexpressing breast carcinomas.

211 ility and anchorage-dependent cell growth of HRG-overexpressing cells, while the low-HRG-expressing 2

212 we examined whether CYR61, independently of HRG, actively regulates breast cancer cell survival and

213 To date, structural information of HRG has largely come from sequence analysis and spectros

214 SCCHN tumors express the highest levels of HRG compared to a diverse collection of other tumor type

215 Therefore, controlling tissue levels of HRG or PGF might be a promising strategy in chronic infl

216 cells expressing endogenously high levels of HRG.

217 Here we report molecular mechanisms of HRG-induced apoptosis.

218 tablished that Rac is a critical mediator of HRG mitogenic signaling in breast cancer cells and highl

219 treatment with LY294002 reduces migration of HRG-stimulated cells but not EGF-stimulated cells, despi

220 Transfection of the deletion mutant of HRG described in this study (HRG/M) into MCF-7 cells res

221 constructed a structural deletion mutant of HRG.

222 hich PKC isoform(s) mediated potentiation of HRG-induced apoptosis, the profile of PKC isoforms was m

223 c, cytoplasmic, and transmembrane regions of HRG-1-related proteins.

224 To investigate the role of HRG as a regulator of the intrinsic pathway, we compared

225 dominantly mediated through the secretion of HRG and activation of HER-2 by an autoctine/paracrine me

226 beta(3) in the proliferation and survival of HRG-overexpressing breast cancer models.

227 show that macrophages are a direct target of HRG.

228 RG-1, BmHRG-2, and BmMRP-5 (all orthologs of HRGs in C. elegans) are down-regulated in heme-treated B

229 n accordance, expression arrays conducted on HRG-treated peritoneal macrophages showed induction of g

230 invasion induced by EGF is not dependent on HRG-beta1 or CXCL12 signaling, showing an asymmetrical r

231 ssed in SKBr3 cells, the effect of Go6976 on HRG-induced apoptosis largely related to inhibition of P

232 tigate the impact of this HER-2 inhibitor on HRG-induced signaling, proliferation, and sensitivity to

233 s an important molecular interaction site on HRG, possesses a cystatin-like fold composed of a 5-stra

234 in competition assays with unlabeled Fab or HRG on cells expressing one or both receptors.

235 ut the preadministration of unlabeled Fab or HRG to determine the specificity of uptake.

236 Purified HRG or HRG in sera increased the number of HMDM-containing apop

237 of short gene lengths, multiple exons, other HRGs in B. malayi (BmHRG-3-6) remain unidentified.

238 reast cancer cells engineered to overexpress HRG, and significantly increased their sensitivity to Ta

239 heterologous plasma membrane heme permease (HRG-4), but the mode of suppression mediated by the Nce1

240 a isoform alone was sufficient to potentiate HRG-induced apoptosis.

241 rotein kinase and Akt pathways and prevented HRG-mediated proliferation.

242 tant, or small molecule inhibitors prevented HRG-induced HSF-1 activation and Slug expression.

243 was facilitated by the transmembrane protein HRG-2.

244 Purified HRG or HRG in sera increased the number of HMDM-containi

245 Purified HRG protein induced, but HRG-deficient serum prevented,

246 re of the N2 domain of serum-purified rabbit HRG.

247 The addition of recombinant HRG to the isolated UB grown in three-dimensional cultur

248 e trastuzumab coexposure completely reversed HRG-promoted CDDP resistance.

249 erapy efficacy in cells that did not secrete HRG, such as MCF-7 cells overexpressing a structural mut

250 ng alpha(v)beta(3) and its driven signaling, HRG blockade led to decreased levels of CYR61 in 231/ASP

251 etion mutant of HRG described in this study (HRG/M) into MCF-7 cells resulted in the dissociation of

252 In this phase I study, HRG was administered intravenously as a single dose (1,

253 ed Hst inhibited HER-3 levels and suppressed HRG-induced proliferation of MCF7 and BT474 breast cance

254 hat breast cancer cells exposed to sustained HRG treatment show markedly enhanced Rac1 activation and

255 rt and serves as a proof of the concept that HRG is a key promoter of breast cancer tumorigenicity an

256 To confirm that HRG modulates the contact system, we used DNase, RNase,

257 In this study, we demonstrate that HRG-beta1 increased secretion of VEGF from breast cancer

258 It was previously demonstrated that HRG induced the phosphorylation of BRCA1, which was medi

259 We demonstrated that HRG stimulation of mammary epithelial cells induces the

260 gether, these findings clearly indicate that HRG activation of ErbB2-ERK signaling modulates HAS phos

261 These results indicate that HRG is regulating alpha(v)beta(3) levels as well as alph

262 The findings indicate that HRG, by acting as a bridge between DNA on apoptotic cell

263 Assay of PKC activity indicated that HRG activated PKC in SKBr3 cells, predominantly affectin

264 In this study, we show that HRG potentiates the ingestion of apoptotic cells by matu

265 ta presented here paradoxically suggest that HRG expression can actually be beneficial when it comes

266 Taken together, the data suggest that HRG supports UB epithelial cell differentiation and non-

267 Taken together, our data suggest that HRG-beta1, bound to the ErbB2 ErbB3 heterodimer, in the

268 d either anti-FcgammaRI or DNA abrogated the HRG-dependent ingestion.

269 (O-t-butyl)-Ala-leucinal] inhibited also the HRG-induced down-regulation of BRCA1 protein in breast c

270 r, blockade of CYR61 expression impaired the HRG-induced hyperactivation of ERK1/ERK2 MAPK without al

271 a(5) and alpha(v)beta(6) was assessed in the HRG-overexpressing breast cancer cells MDA-MB-231, Hs578

272 oteosome inhibitor lactacystin inhibited the HRG-induced down-regulation of BRCA1 mRNA expression.

273 naling corresponded to downregulation of the HRG receptors, HER-3 and HER-4, whereas HER-2 overexpres

274 The activation of the HRG signaling axis has been considered as a poor prognos

275 fected with the antisense orientation of the HRG-beta2 full-length cDNA (231/ASPOOL, 231/AS31 and Hs5

276 Electron microscopic examination of the HRG-induced UB revealed the presence of structurally mat

277 EBP) homologous protein (CHOP) as one of the HRG-inducible genes.

278 Furthermore, our data indicate that the HRG-induced ErbB2.ErbB4 complexes stimulate ErbB2 tyrosi

279 Our data show that the HRG/M sequences are sufficient to sensitize MCF-7 cells

280 ecipitation of phospho-HER3, was compared to HRG expression in SCCHN samples.

281 Conjugation of Fab to HRG was confirmed by sodium dodecyl sulphate polyacrylam

282 ge function, indicating that invasiveness to HRG-beta1 is dependent on the EGF/CSF-1 paracrine loop.

283 hosphorylated wild-type BRCA1 in response to HRG in T47D cells, Cdk4 failed to phosphorylate the trun

284 orylation of p95ErbB2 and AKT in response to HRG was abrogated to varying degrees by GW572016.

285 m HCC-1937 cells was observed in response to HRG.

286 ot only was the elevated ErbB3 responsive to HRG-beta1-induced enhanced signaling mechanism, but also

287 TLn3-ErbB3 and transgenic MMTV-Neu tumors to HRG-beta1 is inhibited by blocking EGF receptor, CSF-1 r

288 able fraction (PAF) of HIV infections due to HRGs, or (b) the number per capita or fraction of HIV in

289 During the first 24 h after treatment, HRG and VvFT were strongly induced by hypoxia, subsequen

290 e combination of heregulin and troglitazone (HRG/TGZ) induced both apoptosis and necrosis, the main m

291 of BRCA1 and decreased BRCA1 expression upon HRG stimulation while overexpression of truncated BRCA1

292 was mediated through alpha(6) integrin upon HRG stimulation.

293 Our investigation into whether HRG is a factor likely to promote tumor formation indepe

294 e Her-2/3/4 network, we investigated whether HRG-induced transactivation of Her-2 affected breast can

295 otype, we discovered that the cells in which HRG is blocked exhibit a marked decrease in erbB activat

296 d HB-EGF stimulation; however, compared with HRG-beta1, HB-EGF induced phosphorylation of the 80-kDa

297 lerated clotting was restored to normal with HRG reconstitution.

298 BRCA1 in T47D cells 4 h after treatment with HRG compared to its level in control nontreated T47D cel

299 is-phenotypes that are fully rescued by worm HRG-1.

300 nt yeast strain, ectopically expressing worm HRG-2, revealed significantly improved growth at submicr