ライフサイエンスコーパス: AREG

1 production of the EGFR ligand amphiregulin (AREG).

2 ssed the tissue repair protein amphiregulin (AREG).

3 factor receptor (EGFR) ligand, amphiregulin (AREG).

4 levels of YAP/TEAD-regulated genes (Ctgf and Areg).

5 -fold over equivalent amounts of recombinant AREG.

6 g is mitigated by systemic administration of AREG.

7 tion of the cytoplasmic C-terminal region of AREG.

8 ase-processed carboxy (C)-terminal domain of AREG.

9 ere selectively blocked by neutralization of AREG.

10 xemestane strongly induced the expression of AREG.

11 imilar to the treatment of recombinant human AREG.

12 stent DNA damage-inducible overproduction of AREG.

13 rca2fl/fl mice rescued HSC defects caused by AREG.

14 d impact of primary tumour location and EREG/AREG.

15 as enriched for reparative factors including Areg.

16 1 promoter enabled ILC2-specific deletion of AREG.

17 ere the most functionally relevant source of AREG.

18 sident regulatory CD4(+) T cells can express AREG.

19 e release of tissue-protective amphiregulin (AREG)(10-12).

20 Amphiregulin (Areg), a growth factor produced by regulatory T (Treg) c

21 hat AGR2 induces expression of amphiregulin (AREG), a growth promoting EGFR ligand.

22 Mechanistically, Treg cell-derived Areg activated pro-fibrotic transcriptional programs in

23 Mechanistically, AREG activated the phosphoinositide 3-kinases (PI3K)/AKT

24 s EGFR is required stromally, and that local AREG administration can rescue Adam17(-/-) transplants.

25 Exogenous AREG alone stimulated prostate epithelial cell growth, a

26 tumors that have high expression of EREG or AREG also have significantly longer progression-free sur

27 ], TGFB1 [transforming growth factor-beta1], AREG [amphiregulin], and HGF [hepatocyte growth factor])

28 Moreover, amphiregulin (Areg), an EGFR ligand, is critical for the amplification

29 Amphiregulin (AREG), an epidermal growth factor receptor ligand, is im

30 YAP1 and its proproliferative target genes (AREG and CCND1), suggesting these were proliferative FLC

31 ty cells displayed increased transcripts for Areg and Ebi3, suggesting distinct functional profiles.

32 d mutations in Adam17 (which is required for AREG and EREG processing) and in Egfr both produce a str

33 We found that AREG and EREG were required for autocrine EGFR signaling

34 athway is required to maintain expression of AREG and EREG, as blocking DNA repair molecules, TET1 GA

35 driven by overexpression of the EGFR ligands AREG and EREG.

36 er elements within the proximal promoters of AREG and EREG.

37 Additionally, ectoine reduces production of AREG and interleukin-8 by CF primary bronchial epithelia

38 er, these results raise the possibility that AREG and other low- or high-affinity binders of EGFR mig

39 Both AREG and prostaglandin E2 converge to activate signaling

40 ated in AREG-knockout mice recognized murine AREG and reproducibly prolonged animal survival in the s

41 d by BRCA1, we have identified amphiregulin (AREG) and early growth response-1 (EGR1).

42 factor receptor (EGFR) ligands amphiregulin (AREG) and epiregulin (EREG), and systemic lipopolysaccha

43 factor receptor (EGFR) ligands amphiregulin (AREG) and epiregulin (EREG).

44 factor receptor (EGFR)-ligand amphiregulin (AREG) and sensitize epithelial cells for enhanced regene

45 n shedding of the EGFR ligands amphiregulin (AREG) and TGF-alpha, which rely upon the cell surface pr

46 Interactions among IL-33, amphiregulin (AREG), and Tregs highlighted a mechanism reinforcing imm

47 ed genes in this list include GSTM2, HSD11B, AREG, and C8B.

48 epidermal growth factor (EGF) family (Ereg, Areg, and Epgn) showed increased expression that was ass

49 rom tumour of ADAM17 substrates TNFR1-alpha, AREG, and TGF-alpha (4-15-fold reductions, p<0.0001 for

50 Consequently, anti-AREG antibody treatment dose-dependently ameliorated GN.

51 we generated a neutralizing monoclonal anti-AREG antibody.

52 Then sudden decreases in Areg appear at the 0.18-0.26 range of cholesterol mole f

53 GFalpha are biased agonists, whereas BTC and AREG are balanced agonists with respect to selectivity o

54 uctal development occur only when ADAM17 and AREG are expressed on mammary epithelial cells, whereas

55 ated the diagnostic utility of amphiregulin (AREG) as a pancreatic cyst fluid biomarker to differenti

56 the EGF receptor (EGFR) ligand amphiregulin (AREG) as an important mediator of inflammatory diseases.

57 tibodies and small interfering RNA targeting AREG attenuated, but did not completely abrogate the gro

58 and IL-17A administration activates the YAP-AREG axis in mice epidermis.

59 ing miR-200 targets, including amphiregulin (AREG), betacellulin (BTC), and the transcription factor

60 eversed the growth inhibition in response to AREG-blocking antibodies but not to shRNA-mediated AREG

61 tion was sufficient to attenuate DCA-induced AREG, but not TGF-alpha shedding.

62 TACE and AREG, but not TGF-alpha, were overexpressed in both colo

63 Conversely, inhibition of AREG by an anti-AREG-neutralizing antibody or deletion o

64 mples also confirmed increased expression of Areg by intragraft Tregs also during rejection.

65 factor receptor (EGFR) ligand Amphiregulin (AREG) by co-activating the transcription factor CREB, an

66 Production of amphiregulin (Areg) by regulatory T (Treg) cells promotes repair after

67 uencing; and epiregulin (EREG)/amphiregulin (AREG) by RNAseq.

68 Key regulators are suggested to be AREG, CCL2, WNT4, and cAMP-responsive element modulator.

69 es promoting keratinocyte migration, such as AREG, CD24, EPHB2, ITGAX, PTGS, SCT1, SERPINB2, SERPINE1

70 urprisingly uncovered that Treg secretion of Areg contributed to CR.

71 BRCA1-related BC, cancer-associated AhR and AREG control tumor growth and production of chemokines t

72 These results demonstrate that AREG controls G2/M progression and cytokinesis in kerati

73 analysis of OvCa patients revealed that high AREG correlates with poor prognosis of patients expressi

74 AREG cytoplasmic and extracellular domains (AREG-CTD and AREG-ECD), as well as full-length AREG prec

75 and is significantly restored by proAREG and AREG-CTD but not by AREG-ECD.

76 ur findings uncover an important role of the AREG-CTD in regulating cell division, which may be relev

77 Moreover, the AREG-CTD was sufficient to normalize cell cycle distribu

78 xpressing silencing-proof, membrane-tethered AREG cytoplasmic and extracellular domains (AREG-CTD and

79 AREG deficiency impairs parietal cell regeneration but i

80 AREG deficiency in knockout mice significantly diminishe

81 brosis, but not if the donor cells were made AREG deficient prior to transfer.

82 ally, heart transplants from recipients with Areg-deficient Tregs showed less fibrosis, vasculopathy,

83 and TACE to the cell membrane, resulting in AREG-dependent activation of EGFR, mitogen-activated pro

84 meliorated intestinal disease severity in an AREG-dependent manner.

85 gs protected KDOs from hypoxia in a ST2- and AREG-dependent manner.

86 ion, and myofibroblast differentiation in an AREG-dependent manner.

87 Together, our findings define an AREG-dependent signaling pathway that mediates the oncog

88 Because AREG depletion retarded growth of xenografted ovarian tu

89 Furthermore, AREG directly skewed M/M to a proinflammatory M1 phenoty

90 Exosomal AREG displayed significantly greater membrane stability

91 xplore the functional importance of specific AREG domains, we stably transduced keratinocytes express

92 impaired in Areg(-/-) mice, and recombinant AREG down-regulated Cyp7a1 mRNA in hepatocytes.

93 mesenchymal cells (LMC) qualitatively alters Areg downstream signaling.

94 d the role of the EGFR ligand, amphiregulin (AREG), during cholestatic liver injury and regulation of

95 smic and extracellular domains (AREG-CTD and AREG-ECD), as well as full-length AREG precursor (proARE

96 restored by proAREG and AREG-CTD but not by AREG-ECD.

97 recent advances in our understanding of the AREG-EGF receptor pathway and its involvement in infecti

98 e CRTC1-MAML2 fusion gene and its downstream AREG-EGFR signaling in human MEC cancer cell growth and

99 Furthermore, our data show that Areg-EGFR signaling induces HIF1a, which binds and trans

100 our study revealed that aberrantly activated AREG-EGFR signaling is required for CRTC1-MAML2-positive

101 Conclusion: AREG-EGFR signaling protects from cholestatic injury and

102 The AREG/EGFR axis is a potential therapeutic target for acu

103 Our study reveals a previously unidentified AREG/EGFR-mediated T(reg)/CAF coupling that controls the

104 mitant decrease in signaling as reflected by AREG, EGR1, and FOS expression.

105 actor (EGF)-like growth factor amphiregulin (AREG) engages EGFR on Treg cells and, in different disea

106 AREG enhanced myeloid cell responses via inducing chemok

107 ury and genetic disruption of the endogenous AREG-epidermal growth factor receptor (EGFR) pathway exa

108 ptor (EGFR) pathway, including amphiregulin (AREG), epiregulin (EREG), and ectodomain cleavage protea

109 e found dendritic cell (CLEC7A, amphiregulin/AREG, EREG) and macrophage products (CCL13) among the to

110 that the average expression of EGFR ligands (AREG, EREG, HBEGF, TGFA, and EPGN) is associated with os

111 Expression of AREG/EREG and RAS and BRAF mutations were assessed in ar

112 ant correlation between overall survival and AREG/EREG expression level.

113 >MyD88-->AREG/EREG-->EGFR signaling pathway is represented in non

114 nificant (P<5 x 10(-8)) loci for dense area (AREG, ESR1, ZNF365, LSP1/TNNT3, IGF1, TMEM184B and SGSM3

115 Treg-specific deletion of ST2 or AREG exacerbated kidney injury and fibrosis in the unila

116 Thus AREG exhibits potential clinical utility in the evaluati

117 e packaged within an individual exosome, and AREG exosomes are rapidly internalized by recipient cell

118 R ligands displayed differential activities; AREG exosomes increased invasiveness of recipient breast

119 nd inflammation, the frequency and number of AREG-expressing ILC2s increases following intestinal inj

120 ntative evidence that rs715212 may influence AREG expression (P eQTL = 0.035), although further funct

121 atinocyte cells suggest that IL-17A enhances AREG expression and keratinocyte proliferation by activa

122 c(+) cells suppressed both induction of lung AREG expression and pulmonary fibrosis.

123 g cholestatic liver injury and regulation of AREG expression by BAs.

124 Mechanically, GPR174 regulates AREG expression by inhibiting the nuclear accumulation o

125 Induced AREG expression in adenocarcinoma cells is able to rescu

126 Finally, we evaluated AREG expression in human renal biopsies.

127 Analysis of AREG expression in major lung cell types revealed induct

128 ation at Ser(127), and induction of Ctgf and Areg expression in response to GPCR activation.

129 Finally, strong upregulation of AREG expression was also detected in kidneys of patients

130 phthyl-isothiocyanate (ANIT) gavage, hepatic AREG expression was markedly up-regulated.

131 The results showed that lung AREG expression was significantly induced in bleomycin-i

132 BA administration induced ileal and hepatic Areg expression, and, interestingly, cholestyramine feed

133 -1 phosphorylation as well as YB-1-dependent AREG expression, thus constituting an AREG/YB-1 self-rei

134 ceptor (ER) dependence of exemestane-induced AREG expression.

135 derived IL-33 potently induced amphiregulin (Areg) expression by recipient Tregs.

136 GPR174 deficiency upregulates amphiregulin (AREG) expression in Tregs, thereby enhancing endothelial

137 transmembrane (TM) precursor, but not of the AREG extracellular domain, markedly reversed the shRNA-m

138 sing immunoregulatory factors, such as Il10, Areg, Fgl2, and Itgb8, and Il21(+) effector conventional

139 l role in mammary morphogenesis by releasing AREG from mammary epithelial cells, thereby eliciting pa

140 Areg from Treg cells promoted hepatocyte gluconeogenesis

141 Here, we demonstrated that amphiregulin (AREG) from bone marrow (BM) leptin receptor (LepR+) nich

142 Mechanistically, we show that Treg-secreted Areg functioned to increase fibroblast proliferation.

143 mplementation imaging studies, amphiregulin (AREG) functioned as a partial agonist, inducing only abo

144 ulations, three genome-wide significant loci AREG, GABRR1 and PDE10A also exhibit strong interactions

145 On the other hand, BAs promoted AREG gene expression and protein shedding in hepatocytes

146 REG-neutralizing antibody or deletion of the Areg gene in LepR-Cre;Brca2fl/fl mice rescued HSC defect

147 Here we determined whether AREG has a role in UVB-induced, Treg cell-mediated suppr

148 The EGFR ligand amphiregulin (AREG) has been implicated as an important autocrine grow

149 ival and tissue growth, and its target gene, AREG, has been reported to promote the development of ps

150 alpha, TNFR1-alpha, TGF-alpha, amphiregulin (AREG), HB-EGF and IL-6Ralpha, from IGROV1-Luc cells, (4.

151 like growth factors, including Amphiregulin (AREG), heparin-binding EGF (HB-EGF), and transforming gr

152 ing EGF, TGF-alpha (TGFalpha), amphiregulin (AREG), heparin-binding EGF-like growth factor (HB-EGF),

153 During homeostasis, TPSAB1(high)AREG(high) resident MCs were mainly detected in the lami

154 production of the EGFR ligand amphiregulin (Areg); however, how Treg cells engage with progenitors w

155 recombinant ADM2 elicited tissue-protective AREG(+) ILC2s and limited intestinal inflammation.

156 c treatment of C57BL/6 mice with recombinant AREG impaired repopulation, leading to HSC exhaustion.

157 es exemestane resistance: exemestane induces AREG in an ER-dependent manner.

158 embrane metalloproteinase ADAM17 can process AREG in culture and Adam17(-/-) mice tend to phenocopy E

159 nctions have been described, but the role of AREG in GN remains unknown.

160 es and associated with reduced expression of AREG in ILC2s.

161 were to evaluate the importance and role of AREG in pulmonary fibrosis, identify the cellular source

162 eration by inducing the tissue growth factor Areg in T cells.

163 d tumors as "high expressor" (either EREG or AREG in top tertile for messenger RNA level) or "low exp

164 level) or "low expressor" (neither EREG nor AREG in top tertile).

165 Deletion of Areg in Treg cells protected mice from NASH-dependent gl

166 Deletion of Areg in Treg cells, but not in myeloid cells, reduced NA

167 Lack of ST2 or AREG in Tregs worsened kidney injury.

168 e body of literature regarding amphiregulin (AREG) in human cancer, most knowledge focuses on its cel

169 In this study, we hypothesize that AREG induced in bone marrow-derived CD11c(+) cells is es

170 Furthermore, recombinant AREG induced telomerase reverse transcriptase, which app

171 AREG induces ongoing YB-1 phosphorylation as well as YB-

172 ry fibrosis, identify the cellular source of AREG induction, and analyze its regulation of fibroblast

173 A interference-mediated silencing of TGR5 or AREG inhibited DCA-induced EGFR, MAPK, and STAT3 signali

174 Small interference RNA targeting AREG inhibited ExeR proliferation, confirming that AREG

175 AREG is a low affinity EGFR ligand, which is upregulated

176 AREG is a proinflammatory mediator of GN via (1) enhanci

177 Expression of EREG/AREG is a useful biomarker for anti-EGFR therapy; optimi

178 Recent studies revealed that AREG is also present in the tumor microenvironment (TME)

179 Areg is an EGF secreted by multiple immune cells to shap

180 models, it was shown that mast cell-derived AREG is essential for optimal Treg cell function in vivo

181 Our data show that AREG is essential for UVB-induced CHS suppression.

182 AREG is highly abundant in abdominal fluids of patients

183 periments demonstrate that AGR2 induction of AREG is mediated by activation of the Hippo signaling pa

184 icant amelioration of disease indicates that AREG is pathogenic in GN.

185 In particular, Areg is proposed to play a major role in Treg-mediated m

186 nhibited ExeR proliferation, confirming that AREG is truly functioning as a growth factor of ExeR cel

187 xpression of the growth factor amphiregulin (AREG) is a dominant functional signature of gut-associat

188 Amphiregulin (AREG) is an important regulator of cellular growth in ke

189 , and we provide evidence that amphiregulin (AREG) is important for activating this signaling axis in

190 n of the ordered (i.e., superlattice) phase (Areg) is slightly and continuously decreasing at every c

191 cancer patients and found that amphiregulin (AREG) is the most abundant and generalized ligand secret

192 Constitutive expression of FoxM1 in AREG knockdown cells normalized cell proliferation, redu

193 locking antibodies but not to shRNA-mediated AREG knockdown.

194 A new antibody we generated in AREG-knockout mice recognized murine AREG and reproducib

195 h a mutant KRAS allele exhibited both higher AREG levels and greater invasive potential than exosomes

196 Cyst fluid AREG levels are significantly higher in cancerous and hi

197 ong the cyst fluid samples, the median (IQR) AREG levels for non-mucinous (n = 6), benign mucinous (n

198 AREG levels greater than 300 pg/ml possessed a diagnosti

199 First, we demonstrated increased AREG levels in livers from patients with primary biliary

200 ingle-center retrospective study to evaluate AREG levels in pancreatic cyst fluid by ELISA from 33 pa

201 ate of CD142(-) ASPCs into a non-adipogenic, Areg-like state.

202 Administration of exogenous AREG limited intestinal inflammation and decreased disea

203 o independent BRCA1 response elements on the AREG located at positions -202/-182 and +19/+122.

204 Moreover, AREG mAbs and IL-33 concertedly inhibited tumor growth.

205 cing of the EGF-related factor amphiregulin (AREG) markedly inhibits the expansion of human keratinoc

206 as outside this interval sudden increases in Areg may appear.

207 ligands epiregulin (EREG) and amphiregulin (AREG) may correlate with EGFR-targeted therapy efficacy

208 fter BDL and ANIT administration compared to Areg(+/+) mice.

209 rotoxic nephritis model of GN was studied in AREG(-/-) mice after bone marrow transplantation, and in

210 Most interestingly, Areg(-/-) mice displayed high hepatic cholesterol 7 alph

211 Importantly, Areg(-/-) mice showed aggravated liver injury after BDL

212 randial repression of Cyp7a1 was impaired in Areg(-/-) mice, and recombinant AREG down-regulated Cyp7

213 wth factor (EGF)-like molecule Amphiregulin (AREG) might be a critical component of type 2-mediated r

214 An average of 24 AREG molecules are packaged within an individual exosome

215 The high levels of AREG mRNA in ExeR cell lines were confirmed by real-time

216 Renal AREG mRNA was strongly upregulated in murine GN.

217 thousand of RPLP0/36B4); however, HB-EGF and AREG mRNAs were strongly induced in human skin organ cul

218 role of epithelial- and mesenchymal-derived AREG, multiple leukocyte populations including mast cell

219 Therapeutic utility of AREG neutralization was assessed.

220 Conversely, inhibition of AREG by an anti-AREG-neutralizing antibody or deletion of the Areg gene

221 In HIV-1 infection, the percentage of AREG(+) NK cells correlated positively with the numbers

222 ts of the novel antibody are warranted; high AREG, normal TP53, and reduced CXCL1 activity might iden

223 Elevated levels of AREG or EREG in gastroesophageal cancer confers sensitiv

224 othesis that high tumor expression of either AREG or EREG would predict panitumumab therapy benefit i

225 rexpression of the EGFR ligand amphiregulin (AREG) or epiregulin (EREG).

226 thout blocking Alt+PNE-stimulated skin IL33, Areg, OSM, CCL11, TSLP or plasma MCPT1.

227 s irreversibly upregulated by suppression of AREG overlapped with genes involved in keratinocyte diff

228 e control with cetuximab (EREG, P = .000015; AREG, P = .000025).

229 d median PFS, 103.5 v 57 days, respectively; AREG: P < .0001, HR = 0.44, and median PFS, 115.5 v 57 d

230 Specifically, we show that AREG participates in DCA-induced EGFR and STAT3 signalin

231 In this study, we show that the YAP-AREG pathway is activated in human psoriatic skin and is

232 Pharmacologically targeting the BMAL1-HIF2A-AREG pathway provides cardioprotection, with maximum eff

233 ough the downstream IGF1 pathway but not the AREG pathway.

234 EG-CTD and AREG-ECD), as well as full-length AREG precursor (proAREG).

235 Areg-producing Treg cells were enriched in the livers of

236 cription factor Blimp-1, which then promotes Areg production and tissue repair.

237 s from both mice and humans, and NMU induced AREG production in mouse and human ILC2s.

238 AREG production was induced by TCF7/WNT, IL-2, and IL-15

239 B1-stimulated WNT antagonist RUNX3 increased AREG production.

240 tive ILC2 responses, defective amphiregulin (AREG) production and increased susceptibility to intesti

241 ranscription directly through binding to the AREG promoter, however, we could not detect BRCA1 on the

242 This revealed that ILC2-derived AREG promotes non-redundant functions in the context of

243 Recombinant AREG protected from ANIT and BDL-induced liver injury an

244 The high levels of AREG protein in ExeR cell lysates and culture media were

245 BRCA1 depletion leads to induction of the AREG protein.

246 To characterize the mechanisms by which AREG regulates autocrine epithelial cell growth, we tran

247 t alters growth factor signaling, influences Areg repair functions is unclear.

248 opulation is a mediator of Treg cell-derived Areg reparative signaling.

249 We point out that the sudden changes in Areg represent first- or second-order concentration-indu

250 tent animals, depletion or overexpression of AREG respectively prolonged or shortened animal survival

251 local interactions between Treg cells and an Areg-responsive population of Col14a1+EGFR+ lung mesench

252 nfluenza A virus (IAV) infection in vivo, an Areg-responsive subset of reparative LMC upregulate glyp

253 ncing of one of these ligands, amphiregulin (AREG), results in keratinocyte growth arrest that cannot

254 Furthermore, AREG's effects on renal cells and monocytes/macrophages

255 m likely involves binding of wildtype p53 to AREG's promoter and autocrine activation of the epiderma

256 Accordingly, depletion of p53 downregulated AREG secretion and conferred tolerance, whereas blocking

257 grin alpha6beta4 signaling were required for AREG secretion.

258 By contrast, BTC and AREG showed a similar affinity for both dimers.

259 However, unlike the other ligands, AREG showed biphasic kinetics for dimer formation, sugge

260 TET-induced expression of AREG shRNA markedly reduced autocrine extracellular sign

261 in psoriasis, namely through activating YAP-AREG signaling.

262 Finally, AREG significantly enhanced fibroblast motility, which w

263 Here we show that growth arrest of AREG-silenced keratinocytes occurs in G2/M and is signif

264 analysis revealed that tetracycline-mediated AREG silencing significantly altered the expression of 2

265 regulated candidate genes including BHLHE40, AREG, SOCS1, CCL5, and DDIT4 were selected and further v

266 These findings suggested that induced AREG specifically in recruited bone marrow-derived CD11c

267 Hyperselection with EREG/AREG status was associated with increased efficacy.

268 xpression of soluble HB-EGF, but not soluble AREG, strongly enhanced KC migration, even in the presen

269 ctivating the transcription factor CREB, and AREG subsequently activated EGFR signaling in an autocri

270 ey organoid viability, which was restored by AREG supplementation.

271 ecipient mice with Treg-specific deletion of Areg surprisingly uncovered that Treg secretion of Areg

272 atinocytes expressing tetracycline-inducible AREG-targeted shRNA with lentiviruses expressing silenci

273 response to TSST-1 and is also necessary for AREG, TGFalpha, and TNFR1 shedding.

274 the closely related ADAM10, is required for AREG, TGFalpha, and TNFR1 shedding.

275 ate directly the expression of amphiregulin (Areg), the progesterone receptor (Pgr) and signal transd

276 AREG then activates the EGFR pathway and leads to the ac

277 e human KC growth is highly dependent on the AREG TM precursor protein and strongly suggest a previou

278 Results indicate that BRCA1 regulates AREG transcription directly through binding to the AREG

279 an attempt to identify the mechanism of the AREG transcriptional repression by BRCA1, we have mapped

280 he ADAM17 proteolytic targets, amphiregulin (AREG), transforming growth factor alpha (TGFalpha), synd

281 virus-mediated expression of the full-length AREG transmembrane (TM) precursor, but not of the AREG e

282 During recovery, AREG treatment promoted repopulation with parietal cells

283 We discuss emerging concepts of AREG tumor biology and highlight their implications for

284 cholestyramine feeding reduced postprandial Areg up-regulation in both tissues.

285 onnection between BRCA1 loss of function and AREG upregulation-a change in gene expression often obse

286 Western blot analysis showed that whereas no AREG was detected in the DMSO control, overnight treatme

287 immune suppression, whereas basophil-derived AREG was essential.

288 mammary organoid growth in culture, but only AREG was expressed abundantly in the developing ductal s

289 Amphiregulin (AREG) was by far the most abundant EGFR ligand in cultur

290 owth factor (EGF)-like protein amphiregulin (AREG) was highly expressed in ExeR cells based on cDNA m

291 hepatocyte growth factor, and amphiregulin (AREG) were elevated in the extracellular environment of

292 six genes (P4HA1, MPZL3, TMC4, PLEKHA6, CA8, AREG) were inversely associated with monoethyl phthalate

293 Genes for reparative factors, such as Areg, were also enriched in ST2(+) Tregs.

294 Cs) is strongly dependent upon amphiregulin (AREG), whereas blockade of heparin-binding EGF-like grow

295 receptor (EGFR) and its ligand amphiregulin (AREG), which generally must be cleaved from its transmem

296 on of the tissue growth factor amphiregulin (Areg), which is strongly reduced in the absence of TIGIT

297 ey enzyme in prostaglandin biosynthesis, and AREG, which codes for the EGFR ligand, amphiregulin.

298 tent DNA damage-associated overexpression of AREG, which exerts similar negative effects on HSC maint

299 her determined that HGF induced secretion of AREG, which is dependent on integrin-growth factor signa

300 endent AREG expression, thus constituting an AREG/YB-1 self-reinforcing loop.