ライフサイエンスコーパス: AREG

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

2 production of the EGFR ligand amphiregulin (AREG).

3 -fold over equivalent amounts of recombinant AREG.

4 g is mitigated by systemic administration of AREG.

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

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

7 ere selectively blocked by neutralization of AREG.

8 xemestane strongly induced the expression of AREG.

9 imilar to the treatment of recombinant human AREG.

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

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

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

13 Exogenous AREG alone stimulated prostate epithelial cell growth, a

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

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

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

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

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

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

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

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

22 Both AREG and prostaglandin E2 converge to activate signaling

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

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

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

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

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

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

29 we generated a neutralizing monoclonal anti-AREG antibody.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

47 AREG deficiency in knockout mice significantly diminishe

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

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

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

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

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

53 Because AREG depletion retarded growth of xenografted ovarian tu

54 Exosomal AREG displayed significantly greater membrane stability

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

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

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

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

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

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

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

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

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

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

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

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

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

68 Thus AREG exhibits potential clinical utility in the evaluati

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

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

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

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

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

74 Induced AREG expression in adenocarcinoma cells is able to rescu

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

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

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

78 -1 phosphorylation as well as YB-1-dependent AREG expression, thus constituting an AREG/YB-1 self-rei

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

120 Administration of exogenous AREG limited intestinal inflammation and decreased disea

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

139 BRCA1 depletion leads to induction of the AREG protein.

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

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

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

143 grin alpha6beta4 signaling were required for AREG secretion.

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

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

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

147 Finally, AREG significantly enhanced fibroblast motility, which w

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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