ライフサイエンスコーパス: ERalpha

1 ERalpha and ERbeta form heterodimers binding DNA at spec

2 ERalpha and ERbeta regulation of gene transcription is f

3 ERalpha and PR can be quantitatively assayed noninvasive

4 ERalpha binding was evident at the promoters of these ge

5 ERalpha expression is used to determine whether patients

6 ERalpha protein levels, subcellular localization, and tr

7 ERalpha therefore functions as a transcriptional effecto

8 ERalpha was found at active enhancers in endometrial can

9 fen, a selective ER modulator that acts as a ERalpha-AF1 agonist/ERalpha-AF2 antagonist.

10 hanism that contributes to the low or absent ERalpha expression in BLBC.

11 n that mTORC1 can phosphorylate and activate ERalpha on S167 via its effector-the 40S ribosomal S6 ki

12 m targets of PI3K and these kinases activate ERalpha.

13 rst histone acetyltransferase that activates ERalpha expression which may be potentially targeted to

14 s a histone acetyltransferase that activates ERalpha promoter.

15 pplied therapy in breast cancer that affects ERalpha interactions with coregulators and shifts the DN

16 modulator that acts as a ERalpha-AF1 agonist/ERalpha-AF2 antagonist.

17 Notably, almost all ERalpha-immunoreactive cells of the OV/MEPO also express

18 n co-localizes with estrogen receptor alpha (ERalpha) and activates its nuclear translocation in mESC

19 ast cancers express estrogen receptor alpha (ERalpha) and depend on estrogen signals for continued gr

20 Estrogen receptor alpha (ERalpha) and progesterone receptor (PR) are important st

21 eight by repressing estrogen receptor alpha (ERalpha) expression.

22 ic mutations in the estrogen receptor alpha (ERalpha) gene (ESR1), especially Y537S and D538G, have b

23 receptors (GRs) and estrogen receptor alpha (ERalpha) in breast cancer development remain poorly unde

24 es that depend upon estrogen receptor alpha (ERalpha) in HSCs.

25 Estrogen receptor alpha (ERalpha) is a critical prognostic and predictive biomark

26 Estrogen receptor alpha (ERalpha) is a key regulator of breast growth and breast

27 Estrogen receptor alpha (ERalpha) is a major regulator of metabolic processes in

28 Estrogen receptor alpha (ERalpha) is a master driver of a vast majority of breast

29 Estrogen receptor alpha (ERalpha) is an important target for the design of drugs

30 The estrogen receptor alpha (ERalpha) is highly expressed in both endometrial and bre

31 Estrogen receptor alpha (ERalpha) is highly expressed in renal tissue.

32 were high affinity estrogen receptor alpha (ERalpha) ligands but displayed a range of efficacies and

33 docrine therapy for estrogen receptor alpha (ERalpha) positive breast cancer.

34 breast cancers are estrogen receptor alpha (ERalpha) positive.

35 Estrogen receptor alpha (ERalpha) regulates gene transcription through two activa

36 NA-binding sites of estrogen receptor alpha (ERalpha) show great plasticity under the control of horm

37 resses a functional estrogen receptor alpha (ERalpha) signaling pathway.

38 function mutants of estrogen receptor alpha (ERalpha) to define two distinct phases of ligand-depende

39 ranscription factor estrogen receptor alpha (ERalpha) used to treat breast cancer, increases risks of

40 cinogenesis via the estrogen receptor alpha (ERalpha), androgens play a critical role as prohormones

41 s with antisense to estrogen receptor alpha (ERalpha), but not beta (ERbeta), mRNA, prevented the ind

42 Estrogen, via estrogen receptor alpha (ERalpha), exerts several beneficial effects on metabolis

43 and mediated by the estrogen receptor alpha (ERalpha), was found to upregulate the proteasome and the

44 pression through its nuclear receptor alpha (ERalpha), which requires co-activators, such as steroid

45 Estradiol acts via estrogen receptor alpha (ERalpha)-expressing afferents of GnRH neurons, including

46 Many estrogen receptor alpha (ERalpha)-positive breast cancers develop resistance to e

47 Many estrogen receptor alpha (ERalpha)-positive breast cancers initially respond to ar

48 es, particularly in estrogen receptor alpha (ERalpha)-positive breast cancers.

49 by an antagonist of estrogen receptor alpha (ERalpha).

50 on of the biomarker estrogen receptor alpha (ERalpha).

51 etic aberrations in estrogen receptor-alpha (ERalpha) leading to enhanced anti-hormone therapeutic ef

52 D5), WNT2, Sp1, and estrogen receptor-alpha (ERalpha) mRNA, were markedly up-regulated during SynT di

53 lective deletion of estrogen receptor-alpha (ERalpha) or selective inhibition of RANKL in hematopoiet

54 Estrogen receptor-alpha (ERalpha) plays an important role in normal and abnormal

55 breast cancers are estrogen receptor-alpha (ERalpha) positive, underscoring the dependence of cancer

56 between Hippo and oestrogen receptor-alpha (ERalpha) signalling.

57 erentially affected estrogen receptor-alpha (ERalpha)-binding genes.

58 a major problem in estrogen receptor-alpha (ERalpha)-positive breast cancer.

59 eeded for feedback (estrogen receptor alpha [ERalpha]); kisspeptin neurons in the arcuate and anterov

60 Treatment with the alternative ERalpha ligand 27-hydroxycholesterol (27HC) induced ERal

61 An ERalpha-specific agonist enhanced IL-4-induced M2 gene e

62 cular mechanism by which G9a functions as an ERalpha coactivator.

63 ncreased mEPSC frequency, was mimicked by an ERalpha agonist in males, whereas in females, an ERbeta

64 horylation of S305 by IKKbeta establishes an ERalpha cistrome that substantially overlaps with the es

65 This transgenic mouse model expressing an ERalpha folding-biosensor is useful in evaluation of est

66 ts of a new estrogen signaling network in an ERalpha-negative cell line and in an original patient-de

67 th WT/KO males or heterozygous males with an ERalpha DNA-binding domain mutation knocked in (WT/KI) t

68 gh two activation functions (ERalpha-AF1 and ERalpha-AF2).

69 acies and potencies as antiproliferative and ERalpha-downregulating agents.

70 tructural changes, but antiproliferative and ERalpha-downregulating efficacies generally paralleled o

71 ects were abolished in ERalpha-deficient and ERalpha-AF1-deficient mice, revealing the specific role

72 hat demonstrated both altered expression and ERalpha binding had decreased methylation.

73 egative interference between dietary FAs and ERalpha-signaling during anti-microbial defence.

74 umor specimens showed that lack of FOXA1 and ERalpha expression was associated with a longer interval

75 es for a genomic interplay between FOXA1 and ERalpha in breast cancer and tamoxifen-associated endome

76 e uncovered a direct link between mTORC1 and ERalpha.

77 the feed-forward regulation between SGK3 and ERalpha in breast cancer.

78 Ex vivo culture of human breast tissue and ERalpha(+) tumors provided evidence for upregulation of

79 t AE responses were compound, cell-type, and ERalpha-mutant dependent.

80 d browning of SAT in 1-year-old obese WT and ERalpha(-/-) female mice.

81 gnetic particles heavily decorated with anti-ERalpha antibody and horseradish peroxidase (MP-Ab-HRP)

82 strogen receptor partial agonist (ShERPA) at ERalpha would provide such an agent.

83 and increases histone H3K9 trimethylation at ERalpha promoters.

84 endometrial cancers with publicly available ERalpha ChIP-seq data in breast tumors and found a strik

85 MOF complex, G9a links the crosstalk between ERalpha methylation and histone acetylation that governs

86 enes via modification of the genes that bind ERalpha.

87 istochemistry we investigated 14 biomarkers (ERalpha, ERbeta1, ERbeta2, ERbeta5, PR, AR, Bcl-2, HER2,

88 n which may be potentially targeted to block ERalpha at transcriptional level.

89 tor of ERalpha that can be targeted to block ERalpha gene expression is a critical topic of endocrine

90 ndocrine therapy, which is designed to block ERalpha signaling.

91 luminal breast cancer cells, and by blocking ERalpha activity with fulvestrant, LRIG1 is decreased th

92 ngly contrasts with the contribution of both ERalpha-AFs in breast cancer proliferation, shedding new

93 ining genome-wide mapping of chromatin-bound ERalpha with estrogen-induced transcript and metabolic p

94 uripotency transcription factors mediated by ERalpha.

95 K3), a kinase transcriptionally regulated by ERalpha in breast cancer, sustains ERalpha signaling and

96 (MP-Ab-HRP) were used to efficiently capture ERalpha from the sample solution.

97 milar to estrogen in the breast, we compared ERalpha sites in tamoxifen-associated endometrial cancer

98 udies demonstrated that these mutants confer ERalpha constitutive activity and antiestrogen resistanc

99 of miR-22 via direct binding to a conserved ERalpha-binding element within the primary miR-22 precur

100 D)-induced obesity using female aP2-Cre(-/+)/ERalpha(fl/fl) mice (atERalphaKO).

101 In addition, TSEC treatment also degraded ERalpha protein in uterine tissue and breast cancer cell

102 y overlaps with the estradiol (E2)-dependent ERalpha cistrome.

103 r ERalpha KIKO females lacking ERE-dependent ERalpha signaling.

104 iting excessive EnR stress and also depletes ERalpha expression/function, we propose SGK3 inhibition

105 Two different ERalpha ligands, estradiol and 27HC, work together to pr

106 G9a dimethylates ERalpha at K235 both in vitro and in cells.

107 photransferase CHPT1, identified as a direct ERalpha-regulated gene, was required for estrogen-induce

108 GDC-0810 induces a distinct ERalpha conformation, relative to that induced by curren

109 wn to be antiproliferative and downregulated ERalpha and ERbeta expression in MCF-7 breast cancer cel

110 TLK2-high breast cancer cells, downregulates ERalpha, BCL2 and SKP2, impairs G1/S cell cycle progress

111 f the ERalpha gene and thereby downregulates ERalpha expression and consequently its transcriptional

112 sensitive to fulvestrant, despite effective ERalpha downregulation.

113 Blimp1(-) progeny that are invariably Elf5(+)ERalpha(-)PR(-).

114 uctural organization of the pre-existing ERE/ERalpha/SRC-3/p300 complex.

115 reased arcuate expression of Kiss1 and Esr1 (ERalpha) and liver expression of G6pc and Pepck in WT an

116 Outgrowth of metastases expressing ERalpha mutations Y537S and D538G is common after endocr

117 chronic graft-versus-host disease in female ERalpha-knockout mice.

118 hieving significant FLuc complementation for ERalpha (p < 0.01), p53 (p < 0.005), FKBP12 (p < 0.03),

119 hese genes was highest in cases positive for ERalpha.

120 tracer for ER with relative selectivity for ERalpha.

121 ing different cell-signaling mechanisms from ERalpha, ERbeta, or 17beta-estradiol.

122 nscription through two activation functions (ERalpha-AF1 and ERalpha-AF2).

123 Series I acrylic acid ligands were generally ERalpha selective.

124 oxifen-resistant model and those that harbor ERalpha mutations.

125 To address this question, heterozygous ERalpha knockout (WT/KO) dams were fed a control breeder

126 Here, we report how ERalpha impacts these processes by reprogramming metabol

127 In ERalpha+ MBC, only AR had prognostic significance, sugge

128 These effects were abolished in ERalpha-deficient and ERalpha-AF1-deficient mice, reveal

129 amoxifen in wild-type mice were abrogated in ERalpha-AF1-deficient mice.

130 and chromatin immunoprecipitation assays in ERalpha- and HER2-positive human BT-474 breast cancer ce

131 ied and translocated to other chromosomes in ERalpha-positive breast cancer cells.

132 nhanced anti-hormone therapeutic efficacy in ERalpha-negative breast cancer.

133 enetic reactivation of ERalpha expression in ERalpha-negative breast cancer cells.

134 gnificantly inhibited breast tumor growth in ERalpha-negative mouse xenografts, especially when combi

135 P and HRG produced a synergistic increase in ERalpha recruitment to the c-Myc gene.

136 erapeutic approaches targeting Src or MEK in ERalpha-36-positive patients.

137 s with pro-inflammatory cytokines results in ERalpha-dependent activation of gene expression and prol

138 sion and that restoration of ERE-independent ERalpha signaling partially reestablishes susceptibility

139 aromatase activity and estrogen-independent ERalpha binding to target genes, resulting in CYP19A1(am

140 ligand 27-hydroxycholesterol (27HC) induced ERalpha-dependent HSC mobilization and EMH but not HSC d

141 s and BSp are highly effective in inhibiting ERalpha-negative breast cancer due at least in part to e

142 eased knowledge regarding membrane initiated ERalpha actions may provide means to develop new selecti

143 Interestingly, ERalpha-ERE-DNA pull-down assays also revealed that, upo

144 ream to IGFBP5, which overlaps an intergenic ERalpha-bound enhancer that loops to the IGFBP5 promoter

145 rated a functional genomic network involving ERalpha and FOXA1 together with the enhancer-enriched tr

146 The ER consists of 2 isoforms, ERalpha and ERbeta, which have distinct biologic functio

147 refore, we hypothesized that females lacking ERalpha would be more susceptible to maternal HFD.

148 cancer cells, liganded GR represses a large ERalpha-activated transcriptional program by binding, in

149 In the presence of LATS, ERalpha was targeted for ubiquitination and Ddb1-cullin4

150 female mice lacking the ability to localize ERalpha to the membrane due to a point mutation in the p

151 tumors in SCID mice, we also observed lower ERalpha protein levels and a reduced tumor mass, implyin

152 7 cells overexpressing the AhRR showed lower ERalpha protein levels, reduced responsiveness to estrad

153 ted and also elicited an increase in mammary ERalpha and ERbeta expression.

154 ids may adversely affect patients with mixed ERalpha+/CK5+ breast cancer.

155 In cell line models, ERalpha, AR, and the transcription factor FOXA1 cooperat

156 The enCNV is correlated with modified ERalpha binding and monoallelic-repression of IGFBP5 fol

157 er wild-type (WT; 231 WT ER) or G521R mutant ERalpha (231 G521R ER), which is defective in estradiol

158 with recursive partitioning in node-negative ERalpha-positive breast cancer using quantitative CK5 an

159 of estrogen receptor beta (ERbeta), but not ERalpha, abolished the effect of E2 on apoptosis.

160 ulin resistance requires ERalpha-AF2 but not ERalpha-AF1.

161 ffects on the vagina are mediated by nuclear ERalpha activation.

162 ate that the selective activation of nuclear ERalpha is both necessary and sufficient to elicit funct

163 Absence of ERalpha protects female mice from developing nephritis,

164 rthermore, we showed that, in the absence of ERalpha, G93A-SOD1 failed to activate OMI and the protea

165 Cytokine activation of ERalpha and endocrine resistance is dependent on phospho

166 with sustained transcriptional activation of ERalpha and ERbeta.

167 Whereas activation of ERalpha stimulates cell proliferation and cell survival,

168 uggest that ligand-independent activation of ERalpha through PRL/PAK1 may impart resistance to anti-e

169 Thus identifying the epigenetic activator of ERalpha that can be targeted to block ERalpha gene expre

170 n that hormone-binding domain alterations of ERalpha in breast cancer contribute to acquired resistan

171 rt a role for hormone-binding alterations of ERalpha in primary endometrial cancer, with potentially

172 eveal an ordered and cooperative assembly of ERalpha enhancers requiring functional interplay among p

173 Of note, the direct binding of ERalpha-36 to ERK2 prevents its dephosphorylation by MKP

174 gen and that macrophage-specific deletion of ERalpha impaired this M2 polarization.

175 Deletion of ERalpha in kisspeptin cells decreased glutamate transmis

176 94.7-108% were achieved for the detection of ERalpha in MCF-7 cell lysate.

177 this issue of expression and distribution of ERalpha in AD brain using a specific ERalpha antibody.

178 inked bridge with the C-terminal F domain of ERalpha that enables inter-domain communication and cons

179 and Helix 12 in the ligand-binding domain of ERalpha, which leads to a stabilized agonist state and a

180 nd selective antagonist and downregulator of ERalpha in vitro and in vivo in ER-positive models of br

181 as retinol metabolism, occurs downstream of ERalpha activation and is essential for the progression

182 This article reviews the current evidence of ERalpha and PR PET imaging as predictive and early-respo

183 We investigated the influence of ERalpha on molecular pathways during nephritis by microa

184 get genes, and it leads to the inhibition of ERalpha-dependent binding of components of the MegaTrans

185 , a nonsteroidal small-molecule inhibitor of ERalpha, which is a potent and selective antagonist and

186 ulators are eliminated by siRNA knockdown of ERalpha in mESCs.

187 ficiency in mice is mainly caused by lack of ERalpha-mediated suppression of RANKL expression in bone

188 hypothesis, these data suggest that loss of ERalpha signaling blocks the influence of maternal HFD o

189 However, no parallels of ERalpha transcriptional action in breast and endometrial

190 PET of ERalpha and ERbeta levels could provide more insight in

191 esistance is dependent on phosphorylation of ERalpha at S305 in the hinge domain.

192 by mosaic presence of a minor population of ERalpha-negative cancer cells expressing the basal cytok

193 Individual quantification of ERalpha and ERbeta expression, rather than total ER leve

194 at least in part, epigenetic reactivation of ERalpha expression in ERalpha-negative breast cancer cel

195 least in part to epigenetic reactivation of ERalpha, which in turn increases TAM-dependent anti-estr

196 and E2 treatment enhances the recruitment of ERalpha and SRC-1 to the estrogen response element at th

197 down MYST3 resulted in profound reduction of ERalpha expression, while ectopic expression of MYST3 ha

198 ST3 binds to the proximal promoter region of ERalpha gene, and inactivating mutations in its HAT doma

199 Our study reveals regulation of ERalpha expression mediated by the EnR stress response a

200 ations have been identified as regulators of ERalpha signaling in breast cancer.

201 contrasting with the specific requirement of ERalpha-AF2 in the metabolic actions of 17beta-estradiol

202 The potential role of ERalpha in AD pathogenesis has been explored by several

203 ts demonstrate a profound regulatory role of ERalpha in ryanodine receptor-dependent transition to ch

204 ficient mice, revealing the specific role of ERalpha-AF1 activation.

205 e asked whether the DNA-binding signature of ERalpha differs between endometrial tumors that arise in

206 tors and shifts the DNA-binding signature of ERalpha upon prolonged exposure in breast cancer.

207 However, previous studies of ERalpha regulation have focused on luminal and HER2-posi

208 A subgroup of ERalpha-positive breast cancer is characterized by mosai

209 and 3-ketosteroid receptors for a subset of ERalpha-positive breast cancers.

210 h was identified by prospectively optimizing ERalpha degradation, antagonism and pharmacokinetic prop

211 o this end, wild-type, ERalpha-deficient, or ERalpha-AF1-deficient ovariectomized female mice were fe

212 ked in (WT/KI) to produce WT, ERalpha KO, or ERalpha KIKO females lacking ERE-dependent ERalpha signa

213 ified mTOR as the kinase that phosphorylates ERalpha on S104/106 and activates transcription of ER ta

214 quinoline 40 has been identified as a potent ERalpha antagonist and selective estrogen receptor degra

215 ecific estrogen receptor (ER) agonist), PPT (ERalpha-specific agonist) and DPN (ERbeta-specific agoni

216 Cases were predominantly ERalpha (84%, 82%) and PR positive (74%, 71%), respectiv

217 eased Ca(2+) currents via oestrogen receptor ERalpha.

218 er surgery, patients with estrogen receptor (ERalpha)-positive breast cancer are treated with adjuvan

219 e demonstrate that in the estrogen receptor (ERalpha)-positive LBC cells Twist1 silences Foxa1 expres

220 estrogen receptor, namely estrogen receptor (ERalpha-36), associated with a poor prognosis in breast

221 acts like the classical estrogen receptors, ERalpha and ERbeta, to facilitate hippocampal memory in

222 scription by binding to 2 nuclear receptors, ERalpha and ERbeta, which differentially regulate gene t

223 HAT domain abolished its ability to regulate ERalpha, suggesting MYST3 functioning as a histone acety

224 ound that EnR stress response down-regulates ERalpha expression through the protein kinase RNA-like E

225 ERbeta represses ERalpha-mediated activation of the ERE and the RET promo

226 inst obesity and insulin resistance requires ERalpha-AF2 but not ERalpha-AF1.

227 titutively active and antiestrogen-resistant ERalpha.

228 Results ERalpha transcriptional function was abolished in the mu

229 like EnR kinase (PERK) arm, and SGK3 retains ERalpha expression and signaling by preventing excessive

230 Furthermore, S305-ERalpha activation led to enhanced phosphorylation of Se

231 nic approaches thus indicates that selective ERalpha-AF1 activation by tamoxifen is sufficient to eli

232 t this combinatorial treatment re-sensitized ERalpha-dependent cellular inhibitory responses to an es

233 on led to enhanced phosphorylation of Ser118-ERalpha and promoted cell proliferation and tumor growth

234 Network analysis showed ERalpha, AR and FOXA1 significantly correlated.

235 ug, but it partially rescued Twist1-silenced ERalpha and cytokeratin 8 expression and reduced Twist1-

236 tion of ERalpha in AD brain using a specific ERalpha antibody.

237 vo and the metabolic influence of a specific ERalpha-AF1 action remains to be explored.

238 e profile experiments on kisspeptin-specific ERalpha knock-out mice demonstrate that ERalpha in kissp

239 Absence of LATS stabilized ERalpha and the Hippo effectors YAP and TAZ (hereafter Y

240 ctivation and perhaps reduced ICI-stimulated ERalpha degradation likely contribute to antiestrogen re

241 This study suggests a new paradigm to study ERalpha regulation during breast cancer progression and

242 novel FOXC1-driven mechanism that suppresses ERalpha expression in breast cancer.

243 ulated by ERalpha in breast cancer, sustains ERalpha signaling and drives acquired AI resistance.

244 gy with breast cancer pharmacological target ERalpha (ESR1) raised hopes for improved endocrine thera

245 ific ERalpha knock-out mice demonstrate that ERalpha in kisspeptin cells is required for appropriate

246 and metabolic profiling, to demonstrate that ERalpha reprograms metabolism upon estrogen stimulation,

247 MMTV-HER2/neu transgenic mice, we found that ERalpha and ERbeta expression, mammary tumorigenesis, an

248 We found that ERalpha binds to regulatory-associated protein of mTOR (

249 These observations indicate that ERalpha in kisspeptin cells is required for appropriate

250 different hormonal conditions and shows that ERalpha enhancer use in human cancer differs in the pres

251 These data suggest that ERalpha-dependent expression of LRIG1 dampens ErbB3 sign

252 The ERalpha-binding sites in tamoxifen-associated endometria

253 The ERalpha-MP-Ab-HRP bioconjugate formed was injected into

254 on of priming by low dose ryanodine, and the ERalpha agonist, PPT, induced ryanodine receptor-depende

255 As the ERalpha is most active in females, we postulated that a

256 Counteracting the action of GATA3 at the ERalpha promoter region, overexpression of FOXC1 hinders

257 hat estrogen activated PAK1 through both the ERalpha and GPER1 membrane receptors.

258 ChIP sequencing (ChIP-seq), we compared the ERalpha profiles of 10 endometrial tumors from tamoxifen

259 ivate OMI and the proteasome, confirming the ERalpha dependence of the response.

260 mors and found a striking resemblance in the ERalpha patterns of the two tissue types.

261 ges of transcriptional factor complex in the ERalpha promoter thereby contributing to ERalpha reactiv

262 to endocrine therapy via restoration of the ERalpha activity through survival pathways.

263 be linked to differential activation of the ERalpha axis of the IMS-UPRmt.

264 Mutation of the ERalpha binding site within the pri-miR-22 in vivo elimi

265 the cis-regulatory elements upstream of the ERalpha gene and thereby downregulates ERalpha expressio

266 involved in TSEC-mediated degradation of the ERalpha protein in endometrial and breast cells.

267 alpha and FBXO45-mediated degradation of the ERalpha protein.

268 nce via ligand-independent activation of the ERalpha-cofactor CARM1.

269 We found that the ERalpha adjusts its own activity by preventing processin

270 ed to define the relevance of adipose tissue ERalpha during high-fat diet (HFD)-induced obesity using

271 dynamics and potency of ligands that bind to ERalpha.

272 analogous or dissimilar to E2, also bind to ERalpha.

273 ligand-binding pocket and that FES binds to ERalpha with high specificity.

274 F histone acetyltransferase (HAT) complex to ERalpha target gene promoters to deposit histone H4K16 a

275 the ERalpha promoter thereby contributing to ERalpha reactivation and re-sensitized chemotherapeutic

276 first phase (0-20 min), p300 is recruited to ERalpha by Mediator as well as p300's acetylhistone-bind

277 cond phase (20-45 min), p300 is recruited to ERalpha by steroid receptor coregulators (SRCs) for enha

278 recruitment of transcriptional repressors to ERalpha and FBXO45-mediated degradation of the ERalpha p

279 scriptional program by binding, in trans, to ERalpha-occupied enhancers.

280 After estrogen treatment, ERalpha-36 rapidly associates with Src at the level of t

281 ays also revealed that, upon TSEC treatment, ERalpha interacted with the F-box protein 45 (FBXO45) E3

282 However, the interplay between the two ERalpha-AFs is poorly understood in vivo and the metabol

283 This redundancy in the ability of the two ERalpha-AFs to separately mediate metabolic prevention s

284 The effect of replacing wild type ERalpha in breast cancer cells with these mutations was

285 r ERalphaD538G replace one or both wild-type ERalpha genes.

286 To this end, wild-type, ERalpha-deficient, or ERalpha-AF1-deficient ovariectomiz

287 wed that ESR2 c.948delT results in unopposed ERalpha mediated increased cellular proliferation, activ

288 ne (MCF-7:WS8), in 2D and 3D cultures, using ERalpha in-cell westerns, ERE-luciferase, and cell viabi

289 reast cancer cell proliferation in vitro via ERalpha, suggesting that parabens might be active at exp

290 ant human breast carcinoma cells (VM7Luc4E2, ERalpha-positive).

291 estrogen response elements (DNA-ERE), where ERalpha binds specifically.

292 female mice were greatly increased, whereas ERalpha and beta expression was not altered.

293 We asked whether ERalpha expression contributes to the development of imm

294 an basal-like breast cancer (BLBC), in which ERalpha is underexpressed.

295 etabolism in wild-type females compared with ERalpha-knockout females.

296 ted well with ERbeta expression but not with ERalpha, confirming that Ki is a suitable parameter to q

297 these, only LRIG1 correlated positively with ERalpha, but inversely with ErbB3 in clinical breast can

298 bcutaneously inoculated in the shoulder with ERalpha/ERbeta-expressing SKOV3 human ovarian cancer cel

299 enes, including FOXL2, RSPO1, CYP19A1, WNT4, ERalpha and ERbeta, after one postnatal year in the ovot

300 n mutation knocked in (WT/KI) to produce WT, ERalpha KO, or ERalpha KIKO females lacking ERE-dependen