ライフサイエンスコーパス: ERalpha

1 ERalpha exhibits nuclear expression in all three striata

2 ERalpha knockout in MCF7 and MCF7-Cd cells significantly

3 ERalpha phosphorylation may integrate CAR into estrogen

4 ERalpha requires co-activators to mediate transcription

5 ERalpha(+) reactive astrocytes were found at early and l

6 ERalpha-coregulator peptide binding in vitro and RIME (r

7 ERalpha-expressing neuron-ablation also reduced pruritog

8 ERalpha-positive breast cancers are successfully treated

9 ERalpha-positive patients are frequently treated with ta

10 on and is required for the induction of E(2)/ERalpha target genes and E(2)-induced oncogenic cell gro

11 orthosteric stabilizers that increase 14-3-3/ERalpha affinity up to 40-fold and propose the mechanism

12 damage similar to that of E2 treatment in a ERalpha-dependent manner.

13 0 and forms a ternary complex to co-activate ERalpha transcriptional activity and concomitantly enhan

14 proteasome-mediated degradation of activated ERalpha, resulting in loss of ERalpha-driven gene expres

15 to this risk and how these mechanisms affect ERalpha signaling have yet to be elucidated.

16 a caused enhanced growth, particularly after ERalpha inhibition, in hypoxia, or when glutamine levels

17 f selective estrogen receptor (ER) agonists (ERalpha /PPT or ERbeta: DPN); or non-selective sex hormo

18 receptor (CAR) KO, estrogen receptor alpha (ERalpha KO, phosphorylation-blocked ERalpha S216A KI mic

19 Estrogen receptor alpha (ERalpha) activity is associated with increased cancer ce

20 RH) neurons express estrogen receptor alpha (ERalpha) and androgen receptor (AR), suggesting changing

21 t that can activate estrogen receptor alpha (ERalpha) and contribute to the development and progressi

22 ast cancers express estrogen receptor alpha (ERalpha) and depend on this key transcriptional regulato

23 l horn that express estrogen receptor alpha (ERalpha) and explored the behavioral consequences of the

24 tional enhancers of estrogen receptor alpha (ERalpha) and that this association is up-regulated by tr

25 ifen and subsequent estrogen receptor alpha (ERalpha) antagonists represents a tremendous therapeutic

26 h the expression of estrogen receptor alpha (ERalpha) in breast cancer and is linked to a good progno

27 Here, we ablate estrogen receptor alpha (ERalpha) in the medial basal hypothalamus and find a rob

28 Estrogen receptor alpha (ERalpha) is a key transcriptional regulator in the major

29 Estrogen receptor alpha (ERalpha) is a ligand-dependent transcription regulator,

30 Global estrogen receptor alpha (ERalpha) knockout (KO) mice exhibit a disruption of the

31 dies indicated that estrogen receptor alpha (ERalpha) might impact the progression of hepatocellular

32 Estrogen receptor alpha (ERalpha) modulates gene expression by interacting with c

33 endocrine action of estrogen receptor alpha (ERalpha) on the skeleton.

34 breast cancers are estrogen receptor alpha (ERalpha) positive (ER+), and resistance to current hormo

35 ependent and retain estrogen receptor alpha (ERalpha) reactivity, but have decreased levels of proges

36 activation through estrogen receptor alpha (ERalpha) to that of 17beta-estradiol.

37 e gene encoding the estrogen receptor alpha (ERalpha) was previously identified in a female patient w

38 eptide derived from Estrogen Receptor alpha (ERalpha), an important breast cancer target that is nega

39 The classical estrogen receptor alpha (ERalpha), but not ERbeta, in the liver plays a critical

40 r, estrogen (E2), through E2 receptor alpha (ERalpha), increases uterine Igf1 mRNA levels.

41 (TNBC), which lacks estrogen receptor alpha (ERalpha), progesterone receptor, and human epidermal gro

42 we investigated the estrogen receptor alpha (ERalpha)-mediated EA of six newly synthesized bisguaiaco

43 for postmenopausal estrogen receptor alpha (ERalpha)-positive (ER(+)) breast cancer.

44 timulation in human estrogen receptor alpha (ERalpha)-positive breast cancer cells.

45 hanisms mediated by estrogen-receptor alpha (ERalpha).

46 e the estrogen (E2)-estrogen receptor alpha (ERalpha).

47 e gene that encodes estrogen receptor alpha (ERalpha); as a result, this gene is accumulating changes

48 osteoblasts express estrogen receptor alpha (ERalpha); however, osteosarcomas do not express ERalpha

49 tumors to a benign, Estrogen Receptor-alpha (ERalpha) positive, Rictor-negative phenotype and reduces

50 imarily through the estrogen receptor-alpha (ERalpha), but the respective importance of nuclear ERalp

51 Here we report that estrogen receptor-alpha (ERalpha)-expressing neurons in the ventrolateral subdivi

52 4k bp region of Klk1b21 gene responded as an ERalpha AF-1-dependent estrogen-responsive promoter.

53 ng estrogen receptor binding 1 (GREB1) as an ERalpha target gene in Ishikawa cells, we demonstrate th

54 this, binding sites for both HIF-1alpha and ERalpha overlap in SNAT2's cis-regulatory elements.

55 upporting a synergetic role of AP-2gamma and ERalpha in activation of CA12.

56 hereas tamoxifen acts as an antiestrogen and ERalpha antagonist in breast cancer but also on the memb

57 where its loss increases the activity AR and ERalpha, respectively.

58 l processes that occur after SE assembly and ERalpha binding are needed for gene responses.

59 ant suppression of cell-cycle-associated and ERalpha target genes, phenotypes that were not observed

60 t through microRNA regulation of ERalpha and ERalpha-activated profibrotic pathways.Methods: ER expre

61 irect and indirect regulation of ERalpha and ERalpha-associated genes, GATA3, FOXA1, EGFR, CDH1, DSP,

62 possible recruitment mechanisms of FoxA1 and ERalpha, thus demonstrating that ChExMix can effectively

63 one formation in female mice; both GPR30 and ERalpha are potential therapeutic targets for cholestero

64 ion reduced tumor growth and metastasis, and ERalpha knockout prevented the effects of DAC in vivo.

65 s positively correlated with ERalpha/Src and ERalpha/PI3K expression, hallmarks of nongenomic estroge

66 ates of gallstones were 80% in wild-type and ERalpha(-/-) mice treated with G-1 compared to 10% in wi

67 contrast to other steroid receptors, such as ERalpha, the activation function of androgen receptor (A

68 non-canonical function of YAP1 and TEAD4 as ERalpha cofactors in regulating cancer growth, highlight

69 h its two nuclear receptors, alpha and beta (ERalpha, ERbeta), is an important mechanism of transcrip

70 letion decreases long-range contacts between ERalpha enhancers and their target promoters.

71 a switch in the regulation of SNAT2 between ERalpha and HIF-1alpha, leading to endocrine resistance

72 el FEN1 inhibitor, which effectively blocked ERalpha function and inhibited proliferation of tamoxife

73 r alpha (ERalpha KO, phosphorylation-blocked ERalpha S216A KI mice, it is now demonstrated that, afte

74 moxifen-treated patients, effectively blocks ERalpha function and inhibits proliferation of tamoxifen

75 ession could enhance the translation of both ERalpha and FOXM1, it also led to enhanced transcription

76 ism conferring tamoxifen resistance via both ERalpha dependent and independent pathways.

77 Specifically, estrogen-bound ERalpha represses transcription of the EIF3F gene, while

78 expression of eIF3f is tightly controlled by ERalpha at the transcriptional (genomic pathway) and tra

79 ould promote cellular activities mediated by ERalpha and FOXM1 signalling pathways.

80 d effects of estrogen are mostly mediated by ERalpha and unique to the phase of mammary involution.

81 nduction in MCF7 cells was also regulated by ERalpha, but it became predominantly a hypoxia-inducible

82 In conclusion, we demonstrate that central ERalpha-signaling limits longitudinal bone growth and ra

83 ERalpha-regulated genes, while non-classical ERalpha-regulated genes were less impacted by the loss o

84 ficantly reduced the expression of classical ERalpha-regulated genes, while non-classical ERalpha-reg

85 Consistently, ERalpha regulates levels of U34-modifying enzymes and th

86 Elucidating the mechanisms that control ERalpha function may further our understanding of breast

87 stant cell lines as well as ex vivo-cultured ERalpha-positive breast tumors.

88 ced mammary tumor development with deficient ERalpha expression that confers tamoxifen resistance in

89 ble to fulvestrant in its ability to degrade ERalpha in both MCF-7 and CAMA-1 cell lines.

90 start site (TSS) with multiple E2-dependent ERalpha-binding regions.

91 We utilized CRISPR-Cas9 to disrupt ERalpha in adulthood.

92 or 6 (NCOA6) is essential for estradiol (E2)/ERalpha-activated GREB1 transcription.

93 In the presence of E2, ERalpha bound the GREB1 enhancer and also associated wit

94 To explore the role of CXXC5 in E2-ERalpha mediated cellular events, we verified by generat

95 d subtler, but pronounced, impacts on either ERalpha binding or MCF-7 cell proliferation.

96 pressing short hairpin RNAs targeting either ERalpha or ERbeta into the VTA and found that knockdown

97 cated that subordinate females have elevated ERalpha, ERbeta and OTR mRNA compared to dominant female

98 3' untranslated region of the gene encoding ERalpha (ESR1) with and without miRNA let-7 mimics or in

99 e the first in vivo evidence that endogenous ERalpha AF-1 dominant estrogenic-genes exist in estrogen

100 zed by active chromatin states, and enhanced ERalpha binding but decreased transcription factor CCCTC

101 iptional activity and concomitantly enhances ERalpha acetylation.

102 esults underscore the importance of estrogen-ERalpha-mediated control of eIF3f expression for the pro

103 Estrogen/ERalpha signaling is critical for breast cancer progress

104 , which are positively regulated by estrogen/ERalpha signaling but negatively regulated by BRCA1.

105 c, receptor-mediated effects (estrogenicity, ERalpha); and (iv) adaptive response to oxidative stress

106 lpha); however, osteosarcomas do not express ERalpha due to promoter DNA methylation.

107 ng in hormonal dysregulation in which female ERalpha KO mice have elevated levels of serum estradiol

108 polysome association, are reduced following ERalpha depletion lack features which limit translation

109 TEAD as possible actionable drug targets for ERalpha(+) breast cancer.

110 ChIP-seq analyses confirm that Foxa1, ERalpha, and AR occupy distal enhancers in sperm.

111 t endogenous promoters containing functional ERalpha responsive elements.

112 Furthermore, ERalpha overexpression reduced tumor growth and metastas

113 e nucleus of the hypothalamus (mpARH) and GE-ERalpha(vlVMH) neurons preferentially project to the dor

114 via the anoctamin 4 channel, and inhibits GE-ERalpha(vlVMH) neurons through opening the ATP-sensitive

115 alpha(vlVMH)) or glucose-excited neurons (GE-ERalpha(vlVMH)).

116 Hypoglycemia activates GI-ERalpha(vlVMH) neurons via the anoctamin 4 channel, and

117 uations, being glucose-inhibited neurons (GI-ERalpha(vlVMH)) or glucose-excited neurons (GE-ERalpha(v

118 Further, we show that GI-ERalpha(vlVMH) neurons preferentially project to the med

119 the pituitary on the background of a global ERalpha-null (PitERtgKO) mouse.

120 otypes in ovariectomized female GPR30(-/-) , ERalpha(-/-) , and wild-type mice injected intramuscular

121 diverse protein targets: sEH (a hydrolase), ERalpha (a nuclear receptor), and c-KIT (a kinase).

122 ve feedback regulation, whereas hypothalamic ERalpha is necessary for the precise control of LH secre

123 Studies identifying ERalpha-regulated pathways for disease prevention will l

124 that ERRFI1 is selectively downregulated in ERalpha-positive breast cancers and breast cancers drive

125 FEN1 as the strongest determining factor in ERalpha-positive patient prognostication.

126 endocrine therapies with PRMT1 inhibitors in ERalpha-positive tumors.

127 BRCA1 knockdown in ERalpha+ luminal breast cancer cells increases intensity

128 e USP11 may represent a prognostic marker in ERalpha(+) breast cancer.

129 was blocked by tamoxifen and not observed in ERalpha-negative cells.

130 ng ligand, is significantly overexpressed in ERalpha(+) luminal breast cancer.

131 expression correlates with poor prognosis in ERalpha(+) luminal breast cancer, but not in other subty

132 rough a distal estrogen-responsive region in ERalpha-positive cell lines by upregulation of ERalpha.

133 d patients, and FEN1 played a causal role in ERalpha-driven cell growth.

134 indicate that NCOA6 has an essential role in ERalpha-mediated transcription by increasing enhancer-pr

135 gnificantly associated with poor survival in ERalpha-positive (ERalpha(+)) patients.

136 A newly identified role for USP11 in ERalpha transcriptional activity represents a novel mech

137 nding to estrogen receptors (ERs), including ERalpha and GPER1, and through differential production v

138 overexpressing breast cancer, the increased ERalpha protein expression in turn enhances FOXM1 transc

139 was significantly associated with increased ERalpha and FOXM1, and significantly associated with tam

140 er, these results provide a new insight into ERalpha and IGF-1R interference, and open novel perspect

141 mice indicate that this BPA effect involves ERalpha and phosphoinositide 3-kinase.

142 sion of ERalpha and converts TNBC to luminal ERalpha-positive, rendering TNBC cells targetable by tam

143 e with tamoxifen-inducible Thy1-Cre mediated ERalpha inactivation during late puberty specifically in

144 tance of nuclear ERalpha (NOER) and membrane ERalpha (MOER) pools to glucose homeostasis are unknown.

145 endothelial healing is mediated by membrane ERalpha in endothelial cells, while the effect of tamoxi

146 st in breast cancer but also on the membrane ERalpha of endothelial cells, it accelerates endothelial

147 The 150 bp minimum ERalpha binding element (EBE) consists of three direct r

148 relationship (SAR) studies of small-molecule ERalpha degraders based on the proteolysis targeting chi

149 disrupted estradiol (E2)-insensitive mutant ERalpha, but AF-1-dependent transcription can be activat

150 ts in gene regulatory activity of the mutant ERalpha proteins.

151 red transcriptional response of this mutant (ERalpha-Q375H) and four other missense mutations at this

152 Inactivation of neuronal ERalpha did not alter the body weight in males, whereas

153 In contrast, inactivation of neuronal ERalpha had no major effect on bone growth in males.

154 onsiderations, we hypothesized that neuronal ERalpha-signaling may contribute to the skeletal growth

155 h this thought in mind, we developed a novel ERalpha antagonist that exhibits enhanced potency due to

156 In conclusion, nuclear ERalpha signaling is predominant in maintaining glucose

157 a), but the respective importance of nuclear ERalpha (NOER) and membrane ERalpha (MOER) pools to gluc

158 Lack of nuclear ERalpha alters the central control of insulin sensitivit

159 helial healing through activation of nuclear ERalpha in smooth muscle cells, inviting to revisit the

160 Approximately 30% of ERalpha breast cancer patients relapse with metastatic d

161 Despite the ability of ERalpha antagonists to increase survival rates, resistan

162 ucing ERbeta, consistent with the ability of ERalpha to alter ethanol sensitivity of VTA neurons.

163 In addition, we show that the ablation of ERalpha completely attenuates the beneficial metabolic e

164 oxifen is mediated by the nuclear actions of ERalpha in smooth muscle cells.

165 AV1 activity also leads to the activation of ERalpha and impaired regulation of the lymphatic system

166 Activation of ERalpha(vlVMH) to mpARH circuit and inhibition of ERalph

167 t Ajuba functions as a novel co-activator of ERalpha and that Ajuba/DBC1/CBP/p300 ternary complex may

168 EN1 impacted the transcriptional activity of ERalpha by facilitating coactivator recruitment to the E

169 s, which was accompanied by amplification of ERalpha and specific increases in MMP9 and MMP13 express

170 Antagonist and inhibition assay of ERalpha, EGFR and mTOR respectively has been performed u

171 Proteasomal degradation of ERalpha was induced by B-SERDs that achieved the objecti

172 We generated mice with deletion of ERalpha in GHRH cells (GHRH(DeltaERalpha)), which displa

173 Stereotaxic guided deletion of ERalpha in the arcuate nucleus increases bone mass in in

174 ational perturbations caused by depletion of ERalpha largely manifest as "translational offsetting" o

175 ot mutations in the ligand-binding domain of ERalpha, remain dependent on ERalpha signaling, indicati

176 tion of CDK2 or EZH2 allows re-expression of ERalpha and converts TNBC to luminal ERalpha-positive, r

177 address this, we modulated the expression of ERalpha and found that while the loss of ERalpha signifi

178 -Aza-2'-deoxycytidine) induces expression of ERalpha and leads to decreased proliferation and concurr

179 e induce DNA damage mediated by formation of ERalpha-dependent R-loops at concentrations 10-fold lowe

180 Herein, we highlight the important impact of ERalpha on mitochondrial form and function and present h

181 lithogenic actions, working independently of ERalpha, to increase susceptible to gallstone formation

182 ha(vlVMH) to mpARH circuit and inhibition of ERalpha(vlVMH) to DRN circuit both increase blood glucos

183 eoblast differentiation, whereas knockout of ERalpha by CRISPR/Cas9 prevented the effects of DAC.

184 Lack of ERalpha in GHRH neurons disrupts growth in both sexes an

185 h correlates with mRNA and protein levels of ERalpha, associates with poor prognosis in ER-positive b

186 issue staining also confirmed the linkage of ERalpha/miR-141-3p/GSN signaling to the HCC progression.

187 Loss of ERalpha in kisspeptin (Kiss1)-expressing cells is suffic

188 ated genes were less impacted by the loss of ERalpha in MCF7-Cd cells.

189 of ERalpha and found that while the loss of ERalpha significantly impaired cancer cell growth, migra

190 n of activated ERalpha, resulting in loss of ERalpha-driven gene expression and eradicated tumor cell

191 sion, and partially circumvented the loss of ERalpha.

192 nal activity represents a novel mechanism of ERalpha regulation and a pathway to be exploited for the

193 nravel a hitherto unprecedented mechanism of ERalpha-dependent orchestration of transcriptional and t

194 s will aid in understanding the mechanism of ERalpha-dependent tissue-selective activity of SERMs.

195 hanisms of action of selective modulation of ERalpha.

196 D2) do not influence the clinical outcome of ERalpha(+) patients.

197 Overexpression of ERalpha inhibited proliferation and induced osteoblast d

198 cription was contingent upon the presence of ERalpha, and it was the high levels of FOXM1 that confer

199 stitutively binds the DBD and AF2 regions of ERalpha, and these interactions can be markedly enhanced

200 a novel role for USP11 in the regulation of ERalpha activity, where USP11 may represent a prognostic

201 iated in part through microRNA regulation of ERalpha and ERalpha-activated profibrotic pathways.Metho

202 pe through direct and indirect regulation of ERalpha and ERalpha-associated genes, GATA3, FOXA1, EGFR

203 Regulation of ERalpha signaling via its phosphorylation by growth fact

204 all DUBs identified USP11 as a regulator of ERalpha transcriptional activity, which was further vali

205 d YAP1 and TEAD4 protein as co-regulators of ERalpha on enhancers.

206 function as a hormone disrupter, the role of ERalpha in cadmium-induced breast cancer progression rem

207 However, the role of ERalpha in the pituitary is still controversial because

208 We finally identified a set of ERalpha-bound promoter-enhancer looping genes enclosed w

209 The 3D structures of ERalpha, PR, EGFR and mTOR were obtained from the protei

210 expression suggested that a subpopulation of ERalpha neurons in the arcuate nucleus of female mice un

211 amming in governing the protein synthesis of ERalpha and FOXM1 contributes to anti-estrogen insensiti

212 essment of direct transcriptional targets of ERalpha.

213 rmed eIF4E could modulate the translation of ERalpha and FOXM1 mRNA.

214 alpha-positive cell lines by upregulation of ERalpha.

215 n phytochemicals which has potent actions on ERalpha, PR, EGFR and mTOR inhibition.

216 ncer cells by decreasing their dependency on ERalpha and increasing the adaptability of the cancer ce

217 nding domain of ERalpha, remain dependent on ERalpha signaling, indicating that either a more potent

218 fects of DNA methyltransferase inhibition on ERalpha and its potential role as a tumor suppressor in

219 uberty, SE-associated genes acquired optimal ERalpha-dependent expression after reproductive maturity

220 r whole ERalpha in a cell-specific manner or ERalpha subfunctions (membrane/extranuclear versus genom

221 ological stages were obtained from patients; ERalpha and ERbeta expression were verified using data f

222 t in birds of the more aggressive phenotype, ERalpha knockdown caused a phenotypic change to that of

223 Thus, this CAR-phosphorylated ERalpha signaling enables these two nuclear receptors to

224 ult1e1 promoter by recruiting phosphorylated ERalpha in the liver as observed with PB-induced livers.

225 Our observations suggest that pituitary ERalpha is involved in the estrogen negative feedback re

226 utcomes in estrogen receptor-alpha-positive (ERalpha(+)) breast cancer.

227 ated with poor survival in ERalpha-positive (ERalpha(+)) patients.

228 irectly interacts with ERalpha to potentiate ERalpha target gene expression, and biologically Ajuba p

229 ggered transcription regulation by promoting ERalpha binding to its enhancers.

230 IGF-1 treatment of MCF-7 cells induced rapid ERalpha methylation by the arginine methyltransferase PR

231 ttranslational modifications of its receptor ERalpha, the best known being phosphorylation.

232 xifen is an antagonist of estrogen receptor (ERalpha), a transcription factor expressed in over 50% o

233 xpress moderate levels of estrogen receptor (ERalpha), which translated into improved growth of xenog

234 Estrogen and its cognate receptor, ERalpha, regulate cell proliferation, differentiation, a

235 Reduced ESR1 (estrogen receptor, ERalpha) expression is observed in muscle from women, me

236 found that the classical estrogen receptors ERalpha and ERbeta were robustly expressed in the adult

237 d in terms of the nuclear estrogen receptors ERalpha and ERbeta.

238 y agonists of the classic estrogen receptors ERalpha/ERbeta, whereas the opposite selectivity was fou

239 eing activated by PB, CAR binds and recruits ERalpha onto the Sulte1 promoter for subsequent phosphor

240 NCOA6 knockout reduced ERalpha recruitment and abolished all of the aforementio

241 ransfections in human myofibroblasts reduced ERalpha expression and associated fibrotic pathways.

242 Reducing ERalpha in the VTA had a more dramatic effect on binge-l

243 role of deubiquitinases (DUB) in regulating ERalpha in breast cancer.

244 ctivation to the hormone receptor, rendering ERalpha modulator drugs such as tamoxifen and aromatase

245 ere conducted.Measurements and Main Results: ERalpha expression increased in IPF lung tissue, myofibr

246 um exposure alters the expression of several ERalpha-responsive genes and increases the malignancy of

247 criptional regulatory responses of these six ERalpha genotypes to a set of ER agonists showed that bo

248 Kisspeptin-specific ERalpha knockout mice exhibit disrupted LH pulses and su

249 ed phenotypes reported in pituitary-specific ERalpha KO mouse models.

250 r viral, caspase-mediated ablation of spinal ERalpha-expressing cells, we observed a significant decr

251 We found that spinal ERalpha-positive neurons are largely excitatory interneu

252 Tumor resistance is still ERalpha-dependent, but mutations usually confer constitu

253 ously showed that upon estrogen stimulation, ERalpha is methylated on residue R260 and forms the mERa

254 agonists to examine the role of ER subtypes (ERalpha and ERbeta) in regulating the ethanol sensitivit

255 Collectively, these studies suggest ERalpha may be a drug target for mitigating chronic dise

256 rials where the impact of agents that target ERalpha and mTOR signaling cross-talk would be tested to

257 n age-matched men and suggest that targeting ERalpha can be a potential approach to modulate glucose

258 ferential estrogen-1 (PaPE-1), which targets ERalpha and mTOR signaling, was able to block changes in

259 We conclude that ERalpha labels a subpopulation of excitatory interneuron

260 Herein, we demonstrate that ERalpha coordinates its transcriptional output with sele

261 microarray analysis we have elucidated that ERalpha-mediated estrogen signaling in osteoclast progen

262 Here we found that ERalpha could decrease HCC cell invasion via suppressing

263 of VTA neurons in female mice and found that ERalpha promotes the enhanced ethanol response of VTA ne

264 We tested the hypothesis that ERalpha, GPER1, and aromatase exhibits sex, region, and

265 Thus, our results indicate that ERalpha(vlVMH) neurons detect glucose fluctuations and p

266 region of its host gene SMG1, We showed that ERalpha-suppressed circ-SMG1.72 could sponge and inhibit

267 Together, our findings suggest that ERalpha can suppress HCC cell invasion via altering the

268 The ERalpha KO females are anovulatory and develop cystic he

269 suppress HCC cell invasion via altering the ERalpha/circRNA-SMG1.72/miR-141-3p/GSN signaling, and ta

270 FFAs activated both the ERalpha and mTOR pathways and rewired metabolism in brea

271 receptor degrader (SERD), which degrades the ERalpha receptor in drug-resistant tumors and has been a

272 e half-site sequences were essential for the ERalpha-dependent transactivation and were differentiall

273 DAC alpha-helical peptides derived from the ERalpha-binding protein SRC2.

274 We found that activation of the ERalpha increased the ethanol-induced excitation of VTA

275 We deleted 430 bp, encompassing one of the ERalpha-binding sites, thereby disrupting interactions o

276 ive transcriptional enhancer upstream of the ERalpha-encoding ESR1 gene.

277 facilitating coactivator recruitment to the ERalpha transcriptional complex.

278 Thus, ERalpha, GPER1, and aromatase cellular immunoreactivity

279 ere, we defined super-enhancers that bind to ERalpha in vivo within hormone-responsive uterine tissue

280 , while maintaining high affinity binding to ERalpha and both potency and efficacy comparable to fulv

281 tructure of one DAC helical peptide bound to ERalpha, which unequivocally corroborated endo stereoche

282 r-promoting function of DLL1 is exclusive to ERalpha(+) luminal breast cancer, as loss of DLL1 inhibi

283 The binding of YAP1/TEAD4 to ERalpha-bound enhancers is augmented upon E(2) stimulati

284 s already display partial selectivity toward ERalpha-like motifs over other representative 14-3-3 cli

285 we wondered whether they could also trigger ERalpha methylation (mERalpha).

286 Unlike ERalpha, AR directly contacts a single SRC-3 and p300.

287 In contrast, mRNAs induced upon ERalpha depletion whose polysome association remains una

288 ormal human breast epithelial cell line when ERalpha was introduced.

289 Therefore, we developed a mouse model where ERalpha is reintroduced to be exclusively expressed in t

290 ansgenic mouse models targeting either whole ERalpha in a cell-specific manner or ERalpha subfunction

291 and hemorrhagic phenotype when compared with ERalpha KO littermates.

292 1R expression was positively correlated with ERalpha/Src and ERalpha/PI3K expression, hallmarks of no

293 eptor, mGluR1, which is known to couple with ERalpha at the plasma membrane.

294 hosphorylation tightens CAR interacting with ERalpha and to activates the promoter.

295 eta) = 0.2-2.7 muM), but no interaction with ERalpha.

296 Moreover, we show that AGO1 interacts with ERalpha and that this interaction is also increased by E

297 ere, we report Ajuba directly interacts with ERalpha to potentiate ERalpha target gene expression, an

298 Mice with ERalpha disruption in AVPV kisspeptin neurons have typic

299 Mice with ERalpha knocked down in arcuate kisspeptin neurons showe

300 ated with extended survival in patients with ERalpha-positive tumors (p = 9.2e-8).