ライフサイエンスコーパス: ER-alpha

1 ER alpha activation of mGluR1a is dependent on CAV1, whe

2 ER alpha and ER beta agonists PPT and DPN inhibited and

3 ER alpha binds to a potential Stat5a ERE.

4 ER alpha mRNA was expressed more abundantly on EPCs comp

5 ER alpha plays a more prominent role in this process.

6 ER alpha signals through multiple pathways, which can be

7 ER alpha t(1/2) was reduced in ER alpha-negative cell li

8 ER alpha-negative primary breast cancers and cell lines

9 ER-alpha did not repress transcription of an HBV replico

10 ER-alpha expression may be regulated in melanoma via hyp

11 ER-alpha methylation status in tumor (n = 107) and sera

12 ER-alpha was methylated more frequently in metastatic th

13 ion of pERK1/2 MAPK, phosphorylated Ser(118)-ER-alpha, and cyclin D1.

14 lar cross-talks and side-talks among IGF-1R, ER-alpha, and phosphatidylinositol 3-kinase (PI3K)/Akt s

15 able and overlapping ESR1 mRNA levels in 200 ER alpha-negative and 50 ER alpha-positive primary breas

16 mRNA levels in 200 ER alpha-negative and 50 ER alpha-positive primary breast cancers examined, which

17 premalignant (EIII8) or tumorigenic (MCF-7), ER-alpha(+) tamoxifen-resistant (EIII8-TAM(R)) or ER-alp

18 s suggest that 3MC and PCB directly activate ER alpha, and this was confirmed in a competitive ER alp

19 ults show that PCB and 3MC directly activate ER alpha-dependent transactivation and extend the number

20 hat Src cooperates with estrogen to activate ER alpha proteolysis.

21 y proliferation, but also estrogen-activated ER alpha loss in a subset of ER alpha-negative breast ca

22 Src siRNA impaired ligand-activated ER alpha loss in BT-20 cells.

23 Inducible Src stimulated ligand-activated ER alpha transcriptional activity and reduced ER alpha t

24 Src inhibition impaired ligand-activated ER alpha ubiquitylation and increased ER alpha levels.

25 Thus, in weanling rats sex affected ER alpha and ER beta neuronal densities in brainstem reg

26 Nuclear receptor estrogen receptor alpha (ER alpha) controls the expression of hundreds of genes r

27 sion correlate with estrogen receptor alpha (ER alpha) expression in breast tumors.

28 ranslocation of the estrogen receptor alpha (ER alpha) have been described, but the mechanisms releva

29 hly correlated with estrogen receptor alpha (ER alpha) in human breast tumors.

30 hly correlated with estrogen receptor alpha (ER alpha) in human breast tumors.

31 ctivity through AhR-estrogen receptor alpha (ER alpha) interactions.

32 Estrogen receptor alpha (ER alpha) mediates breast cancer proliferation through t

33 ally interacts with estrogen receptor alpha (ER alpha), both in vitro and in vivo.

34 interaction between estrogen receptor alpha (ER alpha), caveolin-1 (Cav-1) and c-Src, and increased p

35 3-H1 in influencing estrogen receptor alpha (ER alpha)-mediated gene expression.

36 and proteolysis of estrogen receptor alpha (ER alpha; encoded by ESR1).

37 activator protein-1/estrogen receptor-alpha (ER alpha) complex to the proximal BRCA-1 promoter.

38 membrane-associated estrogen receptor-alpha (ER alpha) led to activation of metabotropic glutamate re

39 ulation by siRNA of estrogen receptor-alpha (ER alpha), but not ER beta, inhibited estrogen-stimulate

40 ever, the roles of estrogen receptors alpha (ER alpha) and beta (ER beta) in EPC biology are largely

41 n receptor (AR) and estrogen receptor alpha (ER-alpha) activity is higher in digit 4 than in digit 2.

42 cotransfected with estrogen receptor alpha (ER-alpha) after 17beta-estradiol stimulation.

43 aromatase, bind to estrogen receptor alpha (ER-alpha) and estrogen receptor beta (ER-beta), and anta

44 tradiol (E2)-bound oestrogen receptor alpha (ER-alpha) causes a global increase in eRNA transcription

45 The role of estrogen receptor alpha (ER-alpha) in melanoma is unknown.

46 Estrogen receptor alpha (ER-alpha) is a nuclear hormone receptor that controls se

47 E2 treatment of the estrogen receptor alpha (ER-alpha) negative MCF-10F cell line on the in vitro exp

48 breast cancers are estrogen receptor alpha (ER-alpha) positive, and although women typically initial

49 The estrogen receptor alpha (ER-alpha) regulates expression of target genes implicate

50 re mediated via the estrogen receptor alpha (ER-alpha), the existence of another novel ER, G protein-

51 uced recruitment to estrogen receptor alpha (ER-alpha)-bound eRNA(+) active enhancers in interphase b

52 variable levels of estrogen receptor-alpha (ER-alpha) and androgen receptors.

53 Estrogen receptor-alpha (ER-alpha) and ER-beta exhibit fine differences in their

54 eatly overexpressed estrogen receptor-alpha (ER-alpha) and pS2, an estrogen-regulated gene.

55 in the function of estrogen receptor-alpha (ER-alpha) as assessed by serine 305 (S305) activation an

56 In rat hippocampus, estrogen receptor-alpha (ER-alpha) can initiate nongenomic signaling mechanisms t

57 ting in the loss of Estrogen Receptor-alpha (ER-alpha) expression and other luminal markers.

58 involvement of the estrogen receptor-alpha (ER-alpha) in locomotor recovery, is still a subject of m

59 through decreasing estrogen receptor-alpha (ER-alpha) level when cultured with luminal BrCA cell lin

60 Estrogen receptor-alpha (ER-alpha) plays a crucial role in normal breast developm

61 nd to interact with estrogen receptor-alpha (ER-alpha), and HE4 overexpression resulted in ER-alpha d

62 ck of expression of estrogen receptor-alpha (ER-alpha), progesterone receptor (PR), and human epiderm

63 xifen resistance in estrogen receptor-alpha (ER-alpha)-positive breast cancers.

64 markers, including estrogen receptor-alpha (ER-alpha, encoded by ESR1).

65 ds of cases express estrogen receptor-alpha (ER-alpha, encoded by ESR1).

66 recruited to the ERE of BRCA1 promoter in an ER alpha-dependent manner.

67 (<2 nm) to lower affinity complexes with an ER alpha monomer at higher SRC-RID concentrations (appro

68 A Notch mimetic peptide could activate an ER-alpha promoter reporter in a BRCA1-dependent manner,

69 nsylcadaverine, and proteolysis of BSA in an ER-alpha dependent manner, and increased resistance to 4

70 ion in the developing hippocampus through an ER-alpha-dependent mechanism.

71 ause functional recovery was blocked with an ER-alpha antagonist.

72 ts for the robust coexpression of GATA-3 and ER alpha in human breast cancers.

73 Moreover, GATA-3 and ER alpha regulate their own expression in breast cancer

74 o be a novel link between Src activation and ER alpha proteolysis and support a model whereby crossta

75 number of ligands that activate both AhR and ER alpha.

76 Src and ER alpha levels were inversely correlated in primary bre

77 educed sensitivity to U0126 or LY294002, and ER-alpha hyperphosphorylation in the activation function

78 Characteristically, NSP cells are ER-alpha positive and epithelial type with little tumori

79 rs of reduced risk of NSCLC characterized as ER-alpha and/or ER-beta positive.

80 ins in cerebrovascular mitochondria, such as ER-alpha, cytochrome c, subunit IV of complex IV, and ma

81 We assessed ER-alpha hypermethylation in primary and metastatic mela

82 itation assays showed an interaction between ER-alpha and HNF-4alpha; this interaction prevented HNF-

83 Both ER alpha and ER beta contribute to E2-mediated EPC activ

84 In both ER alpha-positive and -negative cell lines, both proteas

85 Estradiol increased the density of both ER-alpha and ER-beta protein clusters along dendrites.

86 Based on these findings, a partial BRCA1 : ER-alpha three-dimensional structure is proposed.

87 ucture/function relationship for the BRCA1 : ER-alpha interaction.

88 involves selective trimming of N-glycans by ER alpha-mannosidase I and subsequent recognition by the

89 gen to enhance transcriptional activation by ER-alpha of endogenous estrogen-responsive genes.

90 Gene expression controlled by ER-alpha is modulated by Ca(2+) via calmodulin (CaM).

91 cific enhancer-promoter looping initiated by ER-alpha binding.

92 he lesion cavity, an effect also mediated by ER-alpha.

93 A model of the complete CaM.ER-alpha complex was constructed by combining these two

94 experiment in which PCB and 3MC induced CFP-ER alpha/YFP-ER alpha interactions.

95 pha, and this was confirmed in a competitive ER alpha binding assay and in a fluorescence resonance e

96 I8-Tam(R) cells correlated with constitutive ER-alpha hyperphosphorylation that was unaffected by the

97 owever, the mean size of synapses containing ER-alpha was larger than that of unlabeled excitatory sy

98 percentage of excitatory synapses containing ER-alpha, nor were there any group differences in distri

99 e differentially associated with cytoplasmic ER-alpha and/or nuclear ER-beta expression-defined NSCLC

100 er (SERD) that both antagonizes and degrades ER-alpha and is active in patients who have progressed o

101 Tumors were poorly differentiated ER-alpha and progesterone receptor-negative adenocarcino

102 regulation involving AP1 motifs that direct ER alpha-DNA interaction is required to increase Igf1 tr

103 Thus, distinct ER alpha signaling pathways can differentially regulate

104 act within the same neuron through divergent ER alpha signaling pathways to regulate different neurot

105 alk between liganded ER alpha and Src drives ER alpha transcriptional activity and targets ER alpha f

106 tivation, at least in part by stabilizing E2/ER-alpha/eRNA-induced enhancer-promoter looping.

107 Depletion of endogenous ER alpha, not ERbeta, by siRNA attenuated resveratrol- a

108 unoprecipitation assay, PCB and 3MC enhanced ER alpha (but not AhR) association with the estrogen-res

109 crystal structures of the main ERQC enzyme, ER alpha-glucosidase II (alpha-GluII; from mouse), alone

110 Upon the addition of estradiol, ER alpha binds directly to this distal enhancer in vivo,

111 munolabeling for androgen (AR) and estrogen (ER alpha) receptors revealed no colocalization of hcrt/o

112 to triple-negative ones that do not express ER-alpha- and Her-2 and are highly tumorigenic in xenogr

113 with AR and few hcrt/orx neurons expressing ER alpha, suggesting that hormonal regulation of hcrt/or

114 postnatal days (PNDs) 0, 2, 4, 7, and 19 for ER alpha (ERalpha; Esr1), beta (ERbeta; Esr2), and Kiss1

115 Counts and densities for ER alpha were greater in females than males in almost al

116 ndent on CAV1, whereas CAV3 is necessary for ER alpha and ER beta activation of mGluR2/3.

117 e transfection of a small inhibitory RNA for ER alpha but were not affected by the small inhibitory R

118 e deacetylase activity were not required for ER-alpha-mediated repression of HBV genes.

119 were severely impaired in EPCs obtained from ER alpha-knockout mice (ER alphaKO) and moderately impai

120 enesis when cocultured with fibroblasts from ER-alpha(-)/PgR(-) or ER-alpha(+)/PgR(+) breast tumors;

121 Given this progression from ER-alpha-positive to ER-alpha-negative lesions, we teste

122 Additionally, full ER alpha function is needed to mediate other cellular si

123 on the expression of tumor suppressor genes ER-alpha and CDH1 in MDA-MB-231 breast cancer cells.

124 The molecular mechanism governing ER-alpha transcriptional activity and/or silencing is st

125 ent aromatase inhibitory activities and high ER-alpha and ER-beta binding affinities of several of th

126 However, ER-alpha gene expression can change during the course of

127 Hypermethylated ER-alpha is a significant factor in melanoma progression

128 However, the functional role of GATA-3 in ER alpha-positive breast cancers is yet to be establishe

129 4'-nitroflavone; (b) transient expression in ER alpha-negative HeLa cells of ER alpha lacking the pro

130 miR-21 is higher in ER alpha positive than negative tumors, but no one has e

131 ER alpha t(1/2) was reduced in ER alpha-negative cell lines.

132 e was a HIF-1alpha-dependent CSC increase in ER-alpha-positive cancers following hypoxic exposure, wh

133 orm salt bridges with key lysine residues in ER-alpha (Lys(299), Lys(302), and Lys(303)), which are l

134 orm salt bridges with key lysine residues in ER-alpha (Lys-299, Lys-302, and Lys-303), which is likel

135 R-alpha), and HE4 overexpression resulted in ER-alpha downregulation in vitro and in human ovarian ca

136 A contrasting decrease in CSC was seen in ER-alpha-negative cancers.

137 ith poor response to antihormonal therapy in ER-alpha-positive breast cancer.

138 e-specific transcriptional network including ER alpha and FoxA1 that dictates the phenotype of hormon

139 f hormone-dependent breast cancer, including ER-alpha, FOXA1 and GATA-3.

140 ivated ER alpha ubiquitylation and increased ER alpha levels.

141 both proteasome and Src inhibitors increased ER alpha levels.

142 Pretreatment with Src increased ER alpha ubiquitylation and degradation in vitro.

143 n neonatal uteri, prenatal arsenic increased ER-alpha expression and enhanced estrogen-related gene e

144 not in KIKO or alpha ERKO uteri, indicating ER alpha- and ERE-dependent regulation.

145 monstrate that nanomolar resveratrol induces ER alpha-Cav-1-c-SRC interaction, resulting in NO produc

146 ER alpha indicating that the suppression is ER alpha-mediated.

147 cts via the estrogen receptor alpha isoform (ER alpha) to regulate Kiss1 expression.

148 f the human estrogen receptor alpha-isoform (ER alpha) with the receptor interacting domains (RIDs) o

149 t a model whereby crosstalk between liganded ER alpha and Src drives ER alpha transcriptional activit

150 between the unliganded AhR and the liganded ER alpha plays a positive role in E2-dependent activatio

151 Cohesin, present on many ER-alpha-regulated enhancers even before ligand treatmen

152 We confirmed a role for Runx1 in mediating ER alpha genomic recruitment and regulation of tethering

153 cells was suppressed as a result of membrane ER-alpha signaling through several kinases to inhibit ca

154 nly ER-alpha (NOER) mice] or plasma membrane ER-alpha [membrane-only ER-alpha (MOER) mice], we found

155 Methylated ER-alpha was detected in 42% (8 of 19) of stage III and

156 in AJCC stage I, II, III, and IV, methylated ER-alpha was detected in 10% (2 of 20), 15% (3 of 20), 2

157 Serum methylated ER-alpha is an unfavorable prognostic factor.

158 he clinical significance of serum methylated ER-alpha was assessed among AJCC stage IV melanoma patie

159 Serum methylated ER-alpha was detected more frequently in advanced than l

160 Moreover, ER alpha contributes to upregulation of vascular endothe

161 d binding domains (E domains) of human/mouse ER alpha and ER beta, progesterone receptors A and B, an

162 script in a mouse with a DNA-binding mutated ER alpha (KIKO), indicating that both Igf1 regulation an

163 We found that suppression of GPR30 but not ER-alpha prevented E2-BSA- or E2-induced PKA activation

164 the PKA-dependent pathway via GPR30 but not ER-alpha.

165 We concluded that extranuclear and nuclear ER-alpha collaborate to suppress adipocyte development,

166 sis in mature cells does not involve nuclear ER-alpha.

167 Using mice that express only nuclear ER-alpha [nuclear-only ER-alpha (NOER) mice] or plasma m

168 lated variables were associated with nuclear ER-alpha- or ER-beta-negative NSCLC.

169 Nuclear Smad co-localized with nuclear ER-alpha.

170 The complementary abilities of ER alpha and NM23-H1 together to influence gene expressi

171 of carcinogenesis will require antagonism of ER alpha but not ER beta.

172 xpression in ER alpha-negative HeLa cells of ER alpha lacking the protein-binding domain for the AhR;

173 le rats to quantitate areas and densities of ER alpha and ER beta-positive neurons within medullary r

174 timulated breast cancer growth downstream of ER alpha and AIB1 and upstream of the cell cycle regulat

175 emonstrating the physiological importance of ER alpha-to-mGluR1a signaling.

176 The interactions of ER alpha with all three SRC-RIDs, measured throughout th

177 siRNA knockdown of ER alpha blocked the E(2)-induced increase in Pdcd4, PTE

178 a process that parallels the recruitment of ER alpha.

179 transferase CARM1 is a positive regulator of ER alpha-mediated transcriptional activation.

180 e crucial role of GATA-3 for the response of ER alpha-positive breast cancers to estradiol.

181 ods also showed that only a subpopulation of ER alpha was available to form complexes with the SRC-RI

182 rogen-activated ER alpha loss in a subset of ER alpha-negative breast cancers, altering prognosis and

183 oss age and treatment, synaptic abundance of ER-alpha is correlated with individual performance in tw

184 ion of MEK5 included increased activation of ER-alpha independent growth signaling pathways and promo

185 Activation of ER-alpha is one mechanism by which PRL may contribute to

186 downregulation of expression and activity of ER-alpha and the progesterone receptor (PR), MEL-18 over

187 Direct DNA binding of ER-alpha and histone deacetylase activity were not requi

188 methylation led to an increase in binding of ER-alpha to the Hoxa10 ERE both in vitro as and in vivo

189 ChIP assay demonstrated that the binding of ER-alpha to the SNAT2 promoter gradually increased in th

190 sistance through IL-6-induced degradation of ER-alpha in luminal BrCAs.Oncogene advance online public

191 on at these sites and inhibit degradation of ER-alpha.

192 on at these sites and inhibit degradation of ER-alpha.

193 hich are potent antagonists and degraders of ER-alpha and in which the ER-alpha degrading properties

194 CaM facilitates dimerization of ER-alpha in the absence of estrogen, and stimulation of

195 ata suggest that CaM-induced dimerization of ER-alpha is required for estrogen-stimulated transcripti

196 ere any group differences in distribution of ER-alpha within the synapse.

197 The distributions of ER-alpha immunoreactivity (ir) and ER-beta ir were nonov

198 is region, overcame the repressive effect of ER-alpha.

199 higher 2D:4D ratio, whereas inactivation of ER-alpha increases growth of digit 4, which leads to a l

200 that selectively disrupt the interaction of ER-alpha with CaM may be useful in the therapy of breast

201 his binding competes with the interaction of ER-alpha with its consensus ERE.

202 rin (Lf) efficiently downregulates levels of ER-alpha, PR, and HER-2 in a proteasome-dependent manner

203 ture of Ca(2+)-CaM bound to two molecules of ER-alpha (residues 287-305).

204 hich explains why CaM binds two molecules of ER-alpha in a 1:2 complex and stabilizes ER-alpha dimeri

205 s why full-length CaM binds two molecules of ER-alpha in a 1:2 complex and stabilizes ER-alpha dimeri

206 Mutants of ER-alpha at the CaM-binding site (W292A and K299A) weake

207 aintaining a specific methylation pattern of ER-alpha gene.

208 for understanding how the complex pattern of ER-alpha methylation and transcriptional silencing is ge

209 cells with PRL increased phosphorylation of ER-alpha at residues implicated in unliganded ER-alpha a

210 Rates of ER-alpha methylation in AJCC stage I, II, and III primar

211 s of CaM each bound to a localized region of ER-alpha (residues 287-305).

212 ermeable) or E2 induced the up-regulation of ER-alpha and GPR30 and attenuated hepatic injury.

213 Calcium-dependent regulation of ER-alpha is critical for activating gene expression and

214 In HepG2 cells, up-regulation of ER-alpha reduced HBV transcription, which required a spe

215 thway- specific, and the local remodeling of ER-alpha chromatin structure by pRb2/p130 multimolecular

216 gative cells rescues the BRCA1 repression of ER-alpha activity and that the E7 and E6 oncoproteins in

217 xposures are associated with reduced risk of ER-alpha- and ER-beta-expressing NSCLC.

218 In light of the critical role of ER-alpha in breast carcinoma, our data suggest that smal

219 ses to estradiol and IGF1 via scaffolding of ER-alpha/PELP1/IGF1R-containing complexes.

220 ishing and maintaining the silenced state of ER-alpha gene can be locus- or pathway- specific, and th

221 the absence of estrogen, and stimulation of ER-alpha by either Ca(2+) and/or estrogen may serve to r

222 eviously, our laboratory cloned a variant of ER-alpha, ER-alpha36, and found that ER-alpha36 mediated

223 or (ER)-alpha36, a membrane-based variant of ER-alpha.

224 both compete for binding at the same site on ER-alpha (residues 292, 296, 299, 302, and 303), which e

225 ] or plasma membrane ER-alpha [membrane-only ER-alpha (MOER) mice], we found that 10-wk-old mice that

226 express only nuclear ER-alpha [nuclear-only ER-alpha (NOER) mice] or plasma membrane ER-alpha [membr

227 ovariectomized wild-type mice received E2 or ER-alpha agonist propyl pyrazole triol (50 microg/25 g)

228 trauma-hemorrhage are mediated via GPR30- or ER-alpha-regulated activation of PKA-dependent signaling

229 with fibroblasts from ER-alpha(-)/PgR(-) or ER-alpha(+)/PgR(+) breast tumors; however, EIII8 cells c

230 pha(+) tamoxifen-resistant (EIII8-TAM(R)) or ER-alpha(-) MDA-MB-231 breast cancer cells to interact a

231 Ds demonstrated selectivity for ER-beta over ER-alpha.

232 reduction of P-MAPK, P-Akt, P-S6, and S118 P-ER alpha in hormone receptor-positive cancers.

233 FR, P-HER-2, P-MAPK, P-Akt, P-S6, and S118 P-ER alpha.

234 ed with the ability of PAK1 to phosphorylate ER-alpha on serine 305 and subsequent secondary activati

235 which suggests important posttranscriptional ER alpha regulation.

236 zed monkeys without E treatment, presynaptic ER-alpha correlated with DR accuracy across memory delay

237 PR30 versus the classical estrogen receptors ER alpha/beta and functional responses associated with l

238 Reciprocally, ER alpha directly stimulates the transcription of the GA

239 R alpha transcriptional activity and reduced ER alpha t(1/2).

240 transcription of HBV genes by up-regulating ER-alpha, which interacts with and alters binding of HNF

241 n sharp contrast, the more distantly related ER-alpha dimerizes so strongly that energetics can only

242 Overexpression of MKP3 rendered ER-alpha-positive breast cancer cells resistant to the g

243 eceptor (PR), MEL-18 overexpression restored ER-alpha expression in TNBC.

244 omatin immunoprecipitation analysis revealed ER alpha binding to these EREs in wild type but not KIKO

245 sion of CCN5 in SP results in EMT reversion, ER-alpha upregulation and delays in tumor growth in xeno

246 The same ER-alpha-dependent contrasting hypoxic-CSC response was

247 of CaM bind to the same site on two separate ER-alpha molecules (residues 292, 296, 299, 302, and 303

248 inhibition of estrogen induction of several ER alpha-associated genes, including TFF1, by HMGN1 corr

249 s were due to ER alpha or ER beta signaling, ER alpha-knockout (alphaERKO) or ERbeta-knockout (betaER

250 n (4-OHT), ICI 182 780 (Faslodex), and siRNA ER alpha indicating that the suppression is ER alpha-med

251 estern blot analysis revealed that the SNAT2 ER-alpha-ERE complex contained poly(ADP-ribose) polymera

252 of ER-alpha in a 1:2 complex and stabilizes ER-alpha dimerization.

253 of ER-alpha in a 1:2 complex and stabilizes ER-alpha dimerization.

254 f transcription through the two ER subtypes, ER alpha and ER beta.

255 romoting complex 10 activity, which targeted ER-alpha degradation through the ubiquitin-proteasome pa

256 R alpha transcriptional activity and targets ER alpha for ubiquitin-dependent proteolysis.

257 em regions examined were less prevalent than ER alpha neurons.

258 Stat5a transcript through ERE binding; that ER alpha, either alone or together with STAT5, then acts

259 Here we present data that show that ER alpha and mGluR1a directly interact to mediate a rapi

260 electron microscopic data demonstrating that ER-alpha is present within excitatory synapses in dorsol

261 We also observed that ER-alpha was up-regulated after SCI.

262 lly, EMSAs and supershift assays showed that ER-alpha binds to the SNAT2 ERE and that this binding co

263 These data suggest that ER-alpha-positive and negative breast cancer subtypes re

264 ough the lack of group effects suggests that ER-alpha is primarily in synapses that are stable across

265 The ER alpha and beta (ERalpha and ERbeta) were also identif

266 ions associated with the MYC pathway and the ER alpha network to be among the most differential betwe

267 HMGN1 association through recruitment by the ER alpha.

268 of mice bearing targeted alterations in the ER alpha signaling pathways.

269 H1 interacts with ER alpha and increases the ER alpha-estrogen response element (ERE) interaction.

270 On the FOS promoter, which lacks the ER alpha binding sites, constitutively bound serum respo

271 positive regulation of the expression of the ER alpha gene itself by GATA-3.

272 s (XRE, 5'-GCGTG-3') located upstream of the ER alpha-binding region.

273 o cis-regulatory elements located within the ER alpha gene, and this is required for RNA polymerase I

274 10)-tri ene-3,17-diol (ICI 182,780)] and the ER-alpha- and ER-beta-specific agonists [1,3,5-tris(4-hy

275 these protective effects are mediated by the ER-alpha dependent and independent-mechanisms.

276 o significantly delayed tumorigenesis in the ER-alpha-positive high premalignant line PN8a from 100%

277 cates that ER-alpha36 is a new member of the ER-alpha family that mediates membrane-initiated estroge

278 ific pRb2/p130 multimolecular complex on the ER-alpha promoter strongly correlates with the methylati

279 s and degraders of ER-alpha and in which the ER-alpha degrading properties were prospectively optimiz

280 activity mainly by aromatization and through ER alpha.

281 ne whether E2-mediated responses were due to ER alpha or ER beta signaling, ER alpha-knockout (alphaE

282 equired for RNA polymerase II recruitment to ER alpha promoters.

283 vator genes, CAPER and Foxa1, in addition to ER-alpha.

284 n this progression from ER-alpha-positive to ER-alpha-negative lesions, we tested the ability of tamo

285 In aged monkeys that received E treatment, ER-alpha within the postsynaptic density (30-60 nm from

286 alter latency to tumor development or tumor ER-alpha expression.

287 -containing DNA (DBDmut ER) versus wild-type ER alpha.

288 R-alpha at residues implicated in unliganded ER-alpha activity.

289 t CA12 is robustly regulated by estrogen via ER alpha in breast cancer cells, and that this regulatio

290 as its blockade of fluvoxamine's effects was ER alpha-mediated.

291 This effect was ER-alpha mediated, because functional recovery was block

292 The majority of the resultant tumors were ER-alpha-negative.

293 sed Src levels and/or activity compared with ER alpha-positive cancers and cells.

294 hniques, we show that NM23-H1 interacts with ER alpha and increases the ER alpha-estrogen response el

295 inding nucleosomal DNA, still interacts with ER alpha and, strikingly, still represses estrogen-drive

296 sitivity compared with cells cocultured with ER-alpha(+)/PgR(+) tumor fibroblasts.

297 tumors; however, EIII8 cells cocultured with ER-alpha(-)/PgR(-) tumor-derived fibroblasts exhibited d

298 s, exhibiting non-canonical interaction with ER-alpha via its DNA-binding domain (DBD).

299 man mammary epithelial cells with or without ER-alpha transfection.

300 n which PCB and 3MC induced CFP-ER alpha/YFP-ER alpha interactions.