ライフサイエンスコーパス: estrogen

1 I or MeDS in postmenopausal women not taking estrogen.

2 s associated with these SEs are regulated by estrogen.

3 5alpha-reductase (5alpha-R) or to the active estrogen 17beta-estradiol (E2) via the aromatase enzyme.

4 Elevations in estrogen (17beta-estradiol, E2) are associated with incr

5 lysis of brain microsomal enzymes shows that estrogen 4-hydroxylation is the main metabolic pathway i

6 Pre-treating VK2 E6/E7 cells with estrogen (4 nM) and challenging with 1L-17A & F (12 h) s

7 Thus, direct estrogen action in GHRH/Kiss1 dual-phenotype neurons mod

8 is long-standing finding dominates models of estrogen action in striatal regions.

9 Sex-specific estrogen action is an integral component for generating

10 hus limiting treatment duration or demanding estrogen add-back approaches.

11 eptibility or immunopathology, regardless of estrogen administration.

12 les and underlying the protective effects of estrogen against metabolic disease.

13 logy of E(4) and BMI-135 as less-potent full-estrogen agonists as well as their molecular mechanisms

14 The MPA is estrogen-sensitive and estrogens also have potent effects on both temperature a

15 lecular structure, when used in concert with estrogen and androgen machine learning models, allow for

16 rch is needed to better define the role both estrogen and metabolic comorbidities have in the COVID-1

17 thelial breast cancer cells characterized by estrogen and progesterone receptor expression (ER+/PR+),

18 ally exclusive with mutations in the nuclear estrogen and progesterone receptors, suggesting a role i

19 h the transcriptional programs controlled by estrogen and progesterone receptors, without fully abrog

20 HR = 0.80; 95% CI = 0.73-0.87), and combined estrogen and progestogen (HR = 0.78; 95% CI = 0.70-0.87)

21 (HR = 0.89; 95% CI = 0.84-0.95), or combined estrogen and progestogen (HR = 0.82; 95% CI = 0.76-0.88)

22 rogen sulfotransferase (SULT1E1) inactivates estrogen and regulates its metabolic homeostats.

23 ) response was dependent on both circulating estrogen and translation regulation signaling in the spi

24 e of substituted triphenylethylene synthetic estrogens and diethylstilbestrol were used.

25 rapy), treatment with oral conjugated equine estrogens and medroxyprogesterone acetate (CEE+MPA) resu

26 Estrogens and progesterone control breast development an

27 associated with contraception are synthetic estrogens and progestins.

28 ure to increased steroid hormones, including estrogens, androgens or glucocorticoids during pregnancy

29 not the immediate precursor pregnenolone or estrogen, another major mammalian steroid hormone.

30 endent transcription can be activated by the estrogen-antagonists, fulvestrant (ICI) and 4OHT.

31 ll signalling is augmented following topical estrogen application.

32 Estrogens are presumed to underlie, at least in part, th

33 Estrogens are synthesized from androgens by the enzyme a

34 menopausal process characterised by reduced estrogen, associates with an increased risk of recurrent

35 To decipher the molecular mechanism of estrogens at the estrogen receptor (ER) complex by diffe

36 homeostasis by sulfonating and deactivating estrogens, but studies on the role of SULT1E1 in AKI are

37 e in subjects aged less than 50 years, where estrogen can play a role in attenuating the autosomal ge

38 It is now known that low doses of estrogens can cause apoptosis in long-term estrogen depr

39 t on circulating sex hormones in mice, where estrogen caused an extension of sensitivity and testoste

40 d to receive 0.625 mg/d of conjugated equine estrogen (CEE) plus 2.5 mg/d of medroxyprogesterone acet

41 hormone therapy trials of conjugated equine estrogens (CEE) among posthysterectomy participants and

42 isease (CHD), whereas oral conjugated equine estrogens (CEE) did not.

43 e myeloid progenitors (HoxB8 progenitors) in estrogen-containing media, followed by differentiation t

44 Consistently, the estrogen conversion into androgens in strain DHT3 cell e

45 This highlights another possibility that estrogen could cause changes in the gut microbiota, ther

46 These findings demonstrate that estrogens decrease osteoclast number by attenuating resp

47 Serum estrogen decreased significantly both in postmenopausal

48 te showed lower expression of RANKL than the estrogen-deficient group (P < 0.05).

49 onstrated stronger staining for OPG than the estrogen-deficient group (P < 0.05).

50 The estrogen-deficient group presented lower BH than all oth

51 mber of TRAP-stained cells was higher in the estrogen-deficient group than in estrogen-sufficient gro

52 of bone markers in tooth-extraction wound in estrogen-deficient rats whereas its benefits in estrogen

53 er (estrogen-sufficient); ovariectomy+water (estrogen-deficient), sham-surgery+strontium ranelate (62

54 +strontium ranelate (625 mg/kg/d) (strontium/estrogen-deficient).

55 here was no evidence for selection in highly estrogen-dependent candidate genes, including those for

56 rogenitors using retroviral expression of an estrogen-dependent fusion protein of the HoxB8 transcrip

57 -related gene signature in the vagina during estrogen-dependent murine VVC.

58 Although blocking estrogen-dependent signaling is a cornerstone of adjuvan

59 Long-term estrogen deprivation (LTED) with tamoxifen (TAM) or arom

60 However, postmenopausal estrogen deprivation during midlife and older age has a

61 dvantage of ER-mutant tumor cells to survive estrogen deprivation, anchorage independence, and invasi

62 cluding AR, CHI3L1, and ISG, arise following estrogen-deprivation, and ER-mutant metastases may respo

63 f estrogens can cause apoptosis in long-term estrogen deprived (LTED) breast cancer cells resistant t

64 rmation of reactive estrogen metabolites and estrogen-DNA adducts in female but not male mice.

65 n is up-regulated by treating the cells with estrogen (E2), displaying a positive correlation with th

66 protein (BMP) signaling as a mediator of the estrogen effects.

67 The naturally occurring estrogen estetrol and Selective Human Estrogen-Receptor

68 WT cells with long-term estrogen exposure only exhibited some of these transcrip

69 ed by overall reproductive stage or by fecal estrogen (fE) and progesterone (fP) concentrations.

70 sive alcohol drinking.SIGNIFICANCE STATEMENT Estrogen has potent effects on the dopamine system and i

71 Physiological levels of estrogen have been shown to stimulate DNA damage in brea

72 Estrogens have been shown to regulate the immune system

73 (SULT1E1, or EST) plays an important role in estrogen homeostasis by sulfonating and deactivating est

74 ith reduced levels of androgens in males and estrogens in females.

75 males were protected irrespective of ovarian estrogen, in this study, we show that males accumulate m

76 Estrogen increases dramatically during pregnancy but qui

77 As estrogen increases susceptibility to vaginal colonizatio

78 nhibition of PI3K suppresses PRR11-mediated, estrogen-independent growth.

79 PRR11 promotes estrogen-independent proliferation and confers endocrine

80 This therapeutic effect is attributed to estrogen-induced apoptosis via the estrogen receptor (ER

81 e (TPE) derivatives and a novel mechanism of estrogen-induced cell death in breast cancer, which is n

82 The data revealed that PAX2 can inhibit estrogen-induced gene transcription and this effect is e

83 induction of stress response, DNA repair, or estrogen-induced genes, and these pathways are novel pot

84 While neutrophils mediate estrogen-induced inflammation and adipocytes repopulatio

85 ed inflammation and adipocytes repopulation, estrogen-induced mammary cell death was via lysosome-med

86 In mixtures containing estrogens, induction of the cyp19b transcript occurred a

87 sis of ERalpha and FOXM1 contributes to anti-estrogen insensitivity in ER(+) breast cancer.

88 This highlights a molecular mechanism for estrogen insensitivity syndrome involving mutations that

89 eviously identified in a female patient with estrogen insensitivity syndrome.

90 Estrogen is an important risk factor for cholesterol gal

91 Conversion of C(19) androgens into C(18) estrogens is thought to be an irreversible reaction.

92 ne-resistance, whereby physiologic levels of estrogen kill breast cancer (BC).

93 does not support the hypothesis that higher estrogen levels decrease LC risk.

94 r development in infants exposed to abnormal estrogen levels or estrogenic compounds during pregnancy

95 Studies have suggested that estrogens may protect mice from AKI.

96 In particular, the biphasic effects of estrogens mediate the skeletal sexual dimorphism.

97 ectively, our findings identify a pathway of estrogen-mediated immune regulation in the intestine, wh

98 Genes associated with these SEs affected key estrogen-mediated uterine functions, including transform

99 monstrates a strong link between UVA-induced estrogen metabolism and increased susceptibility of fema

100 the protective effect of various endogenous estrogen metabolites against oxidative neurotoxicity in

101 zing enzyme CYP1B1 and formation of reactive estrogen metabolites and estrogen-DNA adducts in female

102 oxidative neurotoxicity among 25 endogenous estrogen metabolites tested, and its protective effect i

103 Estrogen metabolites were measured in blood and urine sa

104 ry or sulfated bile acids, and benzoate) and estrogen metabolites, as well as decreased levels of pho

105 ffect of UVA was driven by the activation of estrogen-metabolizing enzyme CYP1B1 and formation of rea

106 Steroid estrogens modulate physiology and development of vertebr

107 nd 54.3%, respectively) and much less by the estrogen module (20.2% and 2.7%, respectively).

108 RS had strong negative correlation with its estrogen module (rho = -0.79) and moderate positive corr

109 chanisms underlying the lithogenic effect of estrogen on gallstone formation have become more complic

110 The divergent impact of estrogen on hepatobiliary fate was confirmed in a human

111 that switch the normally positive effects of estrogen on SF1 neuronal activity and glucose balance co

112 use of any (HR = 0.79; 95% CI = 0.74-0.85), estrogen-only (HR = 0.80; 95% CI = 0.73-0.87), and combi

113 use of any (HR = 0.83; 95% CI = 0.76-0.88), estrogen-only (HR = 0.89; 95% CI = 0.84-0.95), or combin

114 soma sp. strain DHT3 capable of catabolizing estrogens or androgens anaerobically.

115 ieved by administering progestins, synthetic estrogens, or a combined treatment.

116 also essential for ovulation, our results of estrogen pathway activation in miR-200-expressing OSE ce

117 on be considered in addition to androgen and estrogen pathway interference.

118 receptor (ER) complex by different types of estrogens-planar [17beta-estradiol (E(2))] and angular t

119 thysterectomy participants and of these same estrogens plus medroxyprogesterone acetate (MPA) among p

120 l populations, but there is no clear link to estrogen pollution.

121 d similar magnitude inverse associations for estrogen positive (ER(+ve)) breast cancer and for colon

122 cancer comprises interventions that suppress estrogen production and/or target the ER directly (overa

123 Estrogen, proliferation, invasion, and HER2 module score

124 istochemical data in BALB/c mice showed that estrogen promotes involution by exacerbating inflammatio

125 Immunohistochemistry on 134 estrogen receptor (ER(+)) primary breast cancer samples

126 ions in the presence or absence of selective estrogen receptor (ER) agonists (ERalpha /PPT or ERbeta:

127 the molecular mechanism of estrogens at the estrogen receptor (ER) complex by different types of est

128 Tamoxifen is the most prescribed selective estrogen receptor (ER) modulator in patients with ER-pos

129 Estrogen receptor (ER) positive breast cancer is frequen

130 same interactions, but for invasive cancer, estrogen receptor (ER) positive cancer and with broader

131 nts were selected by the following criteria: estrogen receptor (ER) status, lymph node invasion, recu

132 etween parity and breast cancer according to estrogen receptor (ER) status, with an increased risk of

133 ction was assessed among treatment, BMI, and estrogen receptor (ER) status.

134 amined separately, and further classified by estrogen receptor (ER) status.

135 alcium are associated with decreased risk of estrogen receptor (ER)+ and ER- breast cancer, and of tr

136 cused on a subclass of EDCs that impacts the estrogen receptor (ER), a pivotal transcriptional regula

137 NBC) in which the three major receptors i.e. estrogen receptor (ER), progesterone receptor (PR) and h

138 Estrogen receptor (ER), progesterone receptor (PR), and

139 an aggressive breast cancer subtype lacking estrogen receptor (ER), progesterone receptor, and human

140 TRPM8 mRNA predict poor clinical outcome in estrogen receptor (ER)-negative breast cancer patients,

141 Responses to immunotherapy are uncommon in estrogen receptor (ER)-positive breast cancer and to dat

142 , is the most frequently mutated oncogene in estrogen receptor (ER)-positive breast cancer.

143 surable radiographic and biologic changes in estrogen receptor (ER)-positive DCIS.

144 How different estrogen receptor (ER)-targeting therapies, including th

145 ibuted to estrogen-induced apoptosis via the estrogen receptor (ER).

146 Tamoxifen is an antagonist of estrogen receptor (ERalpha), a transcription factor expr

147 OVSAHO and COV362 express moderate levels of estrogen receptor (ERalpha), which translated into impro

148 al blockade of estrogen synthesis or nuclear estrogen receptor (ESR) signaling enhanced liver size an

149 eously promoted expression and activation of estrogen receptor (ESR1/ER) and its target genes (PGR, K

150 Estrogen receptor -alpha signaling increased IL-33 relea

151 shows how alternative 'supergene' alleles of Estrogen Receptor 1 are differentially expressed in spec

152 f the amygdalohippocampal area (AHiPM), onto estrogen receptor 1-expressing (Esr1(+)) neurons in the

153 hibition and morpholino knockdown of nuclear estrogen receptor 2b (esr2b) increased hepatocyte gene e

154 Mutations in ESR1 that confer constitutive estrogen receptor alpha (ER) activity in the absence of

155 ast cancer patients with tumors that express estrogen receptor alpha (ER) generally respond well to h

156 been thought to be functionally connected to estrogen receptor alpha (ER) in breast cancer.

157 Estrogen signaling through estrogen receptor alpha (ER) plays a major role in endom

158 Approximately 70% of breast cancers express estrogen receptor alpha (ERalpha) and depend on this key

159 associates with transcriptional enhancers of estrogen receptor alpha (ERalpha) and that this associat

160 (CA12) is associated with the expression of estrogen receptor alpha (ERalpha) in breast cancer and i

161 Estrogen receptor alpha (ERalpha) is a key transcription

162 Estrogen receptor alpha (ERalpha) is a ligand-dependent

163 Early studies indicated that estrogen receptor alpha (ERalpha) might impact the progr

164 t there is possible neuroendocrine action of estrogen receptor alpha (ERalpha) on the skeleton.

165 More than 75% of breast cancers are estrogen receptor alpha (ERalpha) positive (ER+), and re

166 nding and transcriptional activation through estrogen receptor alpha (ERalpha) to that of 17beta-estr

167 s missense mutation in the gene encoding the estrogen receptor alpha (ERalpha) was previously identif

168 Herein, we investigated the estrogen receptor alpha (ERalpha)-mediated EA of six new

169 ene has captured ESR1, the gene that encodes estrogen receptor alpha (ERalpha); as a result, this gen

170 Here we identify estrogen receptor alpha (Esr1)-expressing cells in the p

171 egulation of gene expression (SATB1) and the estrogen receptor alpha (ESR1).

172 Estrogen receptor alpha gene (ESR1) mutations occur freq

173 /progenitor activity, elevated expression of estrogen receptor alpha, and increased DNA damage in cel

174 resistance to competition are seen with the estrogen receptor and its DNA response elements.

175 d small effects on cAMP levels but G protein estrogen receptor antagonists had little effect on respo

176 Disagreements about the phenotype of estrogen receptor beta (ERbeta) knockout mouse, created

177 and its receptor, oxytocin and its receptor, estrogen receptor beta, serotonin receptors (Htr1a, Htr2

178 n to lineage-specific transcription factors, estrogen receptor binding sites were also found to have

179 C/inositol trisphosphate receptor (IP3R) and estrogen receptor co-regulation in spinal cord yielded C

180 Fulvestrant is a potent selective estrogen receptor degrader (SERD), which degrades the ER

181 s, where soft microenvironments downregulate estrogen receptor expression and upregulate autophagy, t

182 ceptor signaling despite the conservation of estrogen receptor expression.

183 human epidermal growth factor receptor 2 and estrogen receptor had an impact on preoperative SLN visu

184 The selective estrogen receptor modulator (SERM) toremifene was previo

185 east cancer cells were more resistant to the estrogen receptor modulator tamoxifen as a result of inc

186 The selective estrogen receptor modulators (SERMs), including 4-hydrox

187 biological parameters such as polyploidy and estrogen receptor negative status.

188 ne therapy resistance frequently develops in estrogen receptor positive (ER+) breast cancer, but the

189 lbociclib is a new challenge to treatment of estrogen receptor positive (ER+) breast cancer.

190 A set of predominantly estrogen receptor positive tumors (ER + 85%) and their n

191 l phenotypes such as breast tumor status and estrogen receptor status (AUC = 0.999, 0.94 respectively

192 For newly diagnosed breast cancer, estrogen receptor status (ERS) is a key molecular marker

193 androgen receptor (AR) or indirectly via the estrogen receptor through aromatase conversion to estrad

194 groups, induce various conformations of the estrogen receptor's ligand-binding domain, which in turn

195 one receptors, such as androgen receptor and estrogen receptor(1-4), but mechanisms regulating its bi

196 Reduced ESR1 (estrogen receptor, ERalpha) expression is observed in mu

197 ccount for underlying tumor heterogeneity by estrogen receptor, progesterone receptor and human epide

198 ed age; nodal status; tumor size; grade; and estrogen receptor, progesterone receptor, and Ki-67 labe

199 otein expression as markers of recurrence in estrogen receptor- positive (ER+) breast cancer tissue.

200 ally required for response to two classes of estrogen receptor-alpha (ER) antagonists.

201 -GAP (GTPase-activating protein), is also an estrogen receptor-alpha (ER) transcriptional co-represso

202 reased autophagy and decreased expression of estrogen receptor-alpha.

203 We investigated the effect of BP-3 and PP on estrogen receptor-dependent transactivation and DNA dama

204 ugh previous studies revealed populations of estrogen receptor-expressing neurons in primary afferent

205 s match existing subtypes of amplified-HER2, estrogen receptor-negative human tumors by molecular exp

206 Estrogen receptor-positive (ER(+)) breast cancer is the

207 transcription factor FOXA1 are a hallmark of estrogen receptor-positive (ER(+)) breast cancers.

208 y is prognostic among women with early-stage estrogen receptor-positive (ER+) and human epidermal gro

209 expression levels are elevated in metastatic estrogen receptor-positive (ER+) and TNBC clinical tissu

210 ly and has been shown to be overexpressed in estrogen receptor-positive (ER+) breast cancers.

211 HDACIs) may overcome endocrine resistance in estrogen receptor-positive (ER+) metastatic breast cance

212 ene transcript was increased in both luminal estrogen receptor-positive breast cancer and basal tripl

213 Seventy-six percent had estrogen receptor-positive HER2-negative disease.

214 t with a tumor-suppressive role for PADI4 in estrogen receptor-positive tumors.

215 ger and were less likely to have stage I and estrogen receptor-positive tumors.

216 Estrogen receptor-positive/human epidermal growth factor

217 3), prostaglandin-E2 and interaction between estrogen receptor-related alpha, flightless-1 (FLII) and

218 of G protein-coupled receptor 30 (GPR30), an estrogen receptor.

219 me 6 (rs6557168) near ESR1, which encodes an estrogen receptor.

220 oic acid receptor, farnesoid X receptor, and estrogen receptor.

221 TiPARP promotes the degradation of c-Myc and estrogen receptor.

222 patients had triple-negative breast cancer (estrogen receptor/progesterone receptor < 10%), and five

223 has detected pharmaceuticals, hormones, and estrogen-receptor (ER)-, glucocorticoid receptor (GR)-,

224 noma (LSCC) responds to 17beta-estradiol via estrogen-receptor (ER, transcribed from ESR1) dependent

225 thelial cells through mechanisms mediated by estrogen-receptor alpha (ERalpha).

226 urring estrogen estetrol and Selective Human Estrogen-Receptor Partial Agonists are being evaluated i

227 ; OS and PFS were also analyzed according to estrogen-receptor status.

228 common alterations of the SWI/SNF complex in estrogen-receptor-positive (ER(+)) breast cancer.

229 M1-mediated resistance to PI3K inhibition in estrogen-receptor-positive breast cancer.

230 Estrogen receptors (ER) are activated by the steroid hor

231 ol) regulate neuronal function by binding to estrogen receptors (ERs), including ERalpha and GPER1, a

232 upted functional interactions of mGluR5 with estrogen receptors that switch the normally positive eff

233 Finally, we describe how ERs (estrogen receptors) and RAGE (receptor for advanced glyc

234 ent candidate genes, including those for the estrogen receptors, aromatases, and vitellogenins.

235 the rate-limiting enzyme aromatase, but not estrogen receptors, measured by qPCR changes across the

236 Meningiomas often express estrogen receptors, which were linked to higher prolifer

237 dihydrotestosterone significantly inhibited estrogen-regulated gene expression, EMT, and distant met

238 tively in female mice as in males because of estrogen regulation of G protein receptor kinase (GRK);

239 ference in PACAP effects due to differential estrogen regulation of this pathway.

240 (R625H) mutation causes aberrant splicing of estrogen related receptor gamma (ESRRG), which results i

241 tanding, RSs are determined more strongly by estrogen-related features and only weakly by proliferati

242 Here we show that the Drosophila estrogen-related receptor (dERR) directs a transcription

243 nic mice identified the transcription factor estrogen-related receptor alpha (ERRalpha) as a potentia

244 can identify the interactive nuances between estrogen-related receptor alpha, a potential drug target

245 Estrogen-related receptor beta (ERRbeta) is a nuclear re

246 We hypothesized that ERR (estrogen-related receptor) alpha and gamma, known transc

247 in uterine tissue and optimal development of estrogen responses in this tissue.

248 gene responded as an ERalpha AF-1-dependent estrogen-responsive promoter.

249 r cell lines and indirectly through a distal estrogen-responsive region in ERalpha-positive cell line

250 t work suggests that this postpartum drop in estrogen results in an estrogen withdrawal state that is

251 The MPA is estrogen-sensitive and estrogens also have potent effect

252 By describing successful establishment of estrogen-sensitive HGSC xenograft models, OVSAHO and COV

253 Finally, whereas selective ablation of estrogen-sensitive MPA neurons demonstrated that these n

254 Together, these findings suggest a role for estrogen-sensitive MPA neurons in directing the thermore

255 Selectively activating estrogen-sensitive MPA neurons was sufficient to drive a

256 Here, we demonstrate that estrogen-sensitive neurons in the MPA can coordinate hyp

257 l effects, ultimately blocking proliferative estrogen signaling (i.e., oral contraceptives/antagoniza

258 ositive breast cancer patients by repressing estrogen signaling and inducing cell death related pathw

259 rt a model where the developmental timing of estrogen signaling has the potential to permanently alte

260 ts show that ETV4 plays an important role in estrogen signaling in endometrial cancer cells.

261 sis we have elucidated that ERalpha-mediated estrogen signaling in osteoclast progenitors decreases "

262 We hypothesize that estrogen signaling increases allergen-induced IL-33 rele

263 ociated with sensitivity to drugs modulating estrogen signaling such as Raloxifene.

264 Estrogen signaling through estrogen receptor alpha (ER)

265 Here, we focused on estrogen stimulation of the well-characterized GREB1 and

266 increased chromatin binding at ER loci upon estrogen stimulation, and an enhanced ER-mediated transc

267 The estrogen-sufficient group and both groups treated with s

268 gher in the estrogen-deficient group than in estrogen-sufficient group at 30 days post-extraction (P

269 The strontium/estrogen-sufficient group demonstrated stronger staining

270 rogen-deficient rats whereas its benefits in estrogen-sufficient rats were modest.

271 +strontium ranelate (625 mg/kg/d) (strontium/estrogen-sufficient); ovariectomy+strontium ranelate (62

272 of the following groups: sham-surgery+water (estrogen-sufficient); ovariectomy+water (estrogen-defici

273 Estrogen sulfotransferase (SULT1E1) inactivates estrogen

274 Estrogen sulfotransferase (SULT1E1, or EST) plays an imp

275 ine SKOV3 could be significantly improved by estrogen supplementation.

276 sociated with a poor response to therapeutic estrogen suppression.

277 Estrogen synthesis and signaling in the brains of verteb

278 Further, while systemic estrogen synthesis blockade suppressed juvenile song pro

279 In contrast, pharmacological blockade of estrogen synthesis or nuclear estrogen receptor (ESR) si

280 Last, serum sex hormone and adipocyte estrogen/testosterone receptor expression profiles provi

281 Estrogen therapy can have unpleasant gynecologic and non

282 Estrogen therapy is effective in treating patients with

283 High-dose synthetic estrogen therapy was the standard treatment of advanced

284 surgery, the potential risks and benefits of estrogen therapy, and the role of the primary care pract

285 Signaling of 17beta-estradiol (estrogen) through its two nuclear receptors, alpha and b

286 els during gestation and then withdrawn from estrogen to simulate postpartum estrogen withdrawal.

287 vity in two neuronal-related cell lines, and estrogen treatment decreased the activity of only the G

288 estigate, in vitro, the effects of a topical estrogen treatment on vaginal epithelial responses follo

289 t underlies breast cancer resistance to anti-estrogen treatments.

290 resulting immunopathology, we asked whether estrogen use in the standard VVC model masks a role for

291 y, current smoking, heavy drinking, and oral estrogen use to assess independent association between m

292 contraception can be achieved with synthetic estrogen, with progestin, and by combining the two hormo

293 ormone-simulated pseudopregnancy followed by estrogen withdrawal in Syrian hamsters, a first for this

294 receptors in the dorsal raphe nucleus during estrogen withdrawal prevented the high-anxiety behaviora

295 is postpartum drop in estrogen results in an estrogen withdrawal state that is related to changes in

296 thdrawn from estrogen to simulate postpartum estrogen withdrawal.

297 d by differentiation toward neutrophils upon estrogen withdrawal.

298 Estrogen-withdrawn females had increased anxiety-like be

299 ted the high-anxiety behavioral phenotype in estrogen-withdrawn females.

300 catalyzes the aromatization of androgens to estrogens within the body.