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1 nd binding domain of estrogen receptor beta (ER-beta).
2 ctivation of estrogen receptor subtype beta (ER-beta).
3 at ADA3 directly interacts with ER alpha and ER beta.
4 nscriptional activities of both ER alpha and ER beta.
5 s containing the consensus ERE sequence than ER beta.
6 activity on ER alpha while being inactive on ER beta.
7 for one of the two ER subtypes, ER alpha or ER beta.
8 njury is totally preserved in the absence of ER beta.
9 cates the involvement of another ER, perhaps ER beta.
10 vity by hPMC2 is enhanced in the presence of ER beta.
11 R alpha, either alone or in combination with ER beta.
12 will require antagonism of ER alpha but not ER beta.
13 ressed more abundantly on EPCs compared with ER beta.
14 on through the two ER subtypes, ER alpha and ER beta.
15 ge (T-H) are mediated via estrogen receptor (ER)beta.
16 xpress both estrogen receptor (ER)-alpha and ER-beta.
17 ranslated exon 0N and the promoter region of ER-beta.
18 CGIs, led to transcriptional inactivation of ER-beta.
19 oximately 7.5% of oxytocin (OT) MNCs express ER-beta.
20 ptor (ER) alpha and the more recently cloned ER-beta.
21 and anticancer effects that are mediated by ER-beta.
22 contained cells that were immunostained for ER-beta.
23 es and subjected to binding experiments with ER-beta.
24 GGTCAnnnTGACC, which bind both ER-alpha and ER-beta.
25 780 blocks activation by ER-alpha but not by ER-beta.
26 oprotection occurs through the activation of ER-beta.
27 ibit robust expression of estrogen receptor (ER)-beta.
29 udy, we evaluated the effect of ER-alpha vs. ER-beta activation on ECM production, deposition, and un
30 We hypothesize that estrogen protects by ER-beta activation, which leads to S-nitrosylation (SNO)
32 s of the highly selective estrogen receptor (ER) beta agonist indazole chloride (Ind-Cl) on functiona
33 etabolite and a selective estrogen receptor (ER) beta agonist, is approximately 400x more potent than
34 agonist [propylpyrazoletriol (PPT)], and an ER-beta agonist [WAY-200070 (WAY)] with TNF-alpha or pla
37 alpha agonist), or diarylpropionitrile (DPN, ER-beta agonist) before allergen challenge to determine
38 or an estrogen receptor (ER)-alpha (but not ER-beta) agonist into the dorsal hippocampus rapidly imp
40 which were developed as nuclear ER-alpha and ER-beta agonists/antagonists, have previously been impli
41 eric ER(alpha/beta) (AF-1alpha/AF-2beta) and ER(beta/alpha) (AF-1beta/AF-2alpha) proteins that resemb
42 scriptional activation studies with chimeric ER(beta/alpha) and ER(alpha/beta) showed that only ER(al
46 l human CD34(+) stem cells contained RNA for ER beta and AR, which increased with cell differentiatio
47 The AD-like effect of estradiol involved ER beta and G-protein coupled receptor 30, whereas its b
48 pression of mRNA for both estrogen receptor (ER) beta and transforming growth factor beta1 was determ
53 s of PR and pS2, DU145 expressed messages of ER-beta and PR, and PC-3 cells exhibited ER-alpha, ER-be
54 tions requiring the ligand binding domain of ER-beta and through abrogation of the ability of PGC-1 t
56 ncreases in estrogen receptors (ER-alpha and ER-beta) and a decrease in progesterone receptor levels,
60 alpha (ER-alpha) and estrogen receptor beta (ER-beta), and antagonize the activity of beta-estradiol
61 fter the raloxifene treatment, PC3 (ER-alpha/ER-beta+) and DU145 (ER-beta+ only) cells were selected
63 ng the biological roles of both ER alpha and ER beta, and they might form the basis for the developme
64 osphorylation of the corresponding region of ER beta, and this correlates with the lack of forskolin/
65 replacement and the number of cortical GABA, ER-beta, and ER-beta/GABA double-labeled neurons was exa
67 X is functionally distinct from ER-alpha and ER-beta, and that, like ER-alpha, it is re-expressed in
68 contrast, in DU145 cells, which express only ER-beta, antiestrogens, but not estrogens, are growth in
69 versed by cotreatment of DU145 cells with an ER-beta antisense oligonucleotide, hence lending additio
70 expression plasmid pCI-ER alpha, but not pCI-ER beta, aromatase activity was elevated by 17beta-estra
71 avourable disease outcome, the usefulness of ER beta as a clinical prognostic marker remains to be de
72 constitutive activity of estrogen receptor (ER) beta as an important regulator of metabolic diseases
73 e results lend further support to a role for ER-beta as a poor prognostic factor in breast cancer.
77 try to further characterize the phenotype of ER-beta-bearing cells by double labeling for the GABAerg
80 inhibitory activities and high ER-alpha and ER-beta binding affinities of several of the resulting a
82 P-dependent activation of gene expression by ER beta but not ER alpha, indicating that the former sub
84 he developing brain, is neither ER-alpha nor ER-beta but a novel, plasma membrane-associated, putativ
85 enous gene, this element is nonresponsive to ER-beta but confers estrogen-dependent inhibition of tra
86 s been demonstrated that LNCaP cells express ER-beta but not ER-alpha and that tamoxifene induces apo
87 P was shown to recognize in vitro translated ER beta, but not ER alpha, as well as a 60-kDa protein f
95 se relationship exists between the extent of ER-beta CGI methylation and receptor expression in norma
98 d the major groove of the DNA helix, but the ER beta DBD and hinge region failed to bend ERE-containi
99 R and Western blot analysis for ER-alpha and ER-beta demonstrated that all three cell lines express E
101 (i) ER-beta1 is the obligatory partner of an ER-beta dimer, whereas the other isoforms function as va
103 the loss of expression of estrogen receptor (ER)-beta during the development of prostate cancer (PCa)
104 discernable activity with ER-alpha, but with ER-beta, E(2) was displaced with an IC(50) of 125 microM
106 estrogen receptor-alpha (ER-alpha, Esr1) or ER-beta (Esr2) increased ILC2-mediated airway inflammati
108 lly prepared aglycons bound significantly to ER-beta, except for 27-deoxyactein aglycon, which showed
111 ling and discovered that axons from cortical ER-beta-expressing inhibitory neurons terminate on BDNF-
113 arcinogenesis was characterized by a loss of ER-beta expression at the protein and transcript levels
117 after osmotic manipulation, suggesting that ER-beta expression was not driven by ligand availability
119 promoter CGI, which correlated with loss of ER-beta expression, was detected in microdissected sampl
120 ted with cytoplasmic ER-alpha and/or nuclear ER-beta expression-defined NSCLC in postmenopausal women
122 lin D1, and aromatase], "estrogen metabolism/ER-beta factor" (ER-beta, peroxisome proliferator-activa
123 , and in contrast to the estrogen metabolism/ER-beta factor, higher current body mass index among pre
126 ber of perirhinal neurons double-labeled for ER-beta/GABA was reduced by 28% (P<0.01 compared to vehi
130 gues can activate ER alpha(Glu353-->Ala) and ER beta(Glu305-->Ala) with very large selectivites, demo
133 cloning of a second estrogen receptor (ER), ER beta, has prompted a reevaluation of the role of ERs
134 .8% (intact) and 94.5% +/- 1.4% (ovx) of all ER-beta-immunoreactive cells coexpress parvalbumin, and
138 l animals, but they were virtually devoid of ER-beta-immunoreactivity (IR) in hyper-osmotic animals.
141 and GCSh point towards an important role for ER beta in cellular protection against oxidative stress.
142 elped to delineate the roles of ER alpha and ER beta in modulating transcription of genes containing
145 g through the AP1 element, overexpression of ER beta in tumors expressing both ER subtypes may explai
150 ditional support to a central role played by ER-beta in mediating growth-inhibitory action of antiest
152 state cancer cells in vitro, the presence of ER-beta in metastatic cells may have important implicati
156 both estrogen receptor-alpha (ER-alpha) and ER-beta in ovarian, breast and endometrial cancer cell l
158 entage of oxytocin (OXY) neurons coexpressed ER-beta in the PVN (84.39% +/- 2.99%), there was very li
161 estrogen receptor-alpha (ER alpha), but not ER beta, inhibited estrogen-stimulated telomerase functi
162 t binds to both receptors, but enhances only ER beta interaction with SRC1 and SRC3 while exhibiting
163 pin-releasing hormone neurons also expressed ER-beta ir in the PVN (12.57% +/- 1.99%), but there was
165 ta expression was selective for MNCs because ER-beta-IR remained unaltered in PVN parvocellular neuro
166 FOS-IR in parvocellular neurons that retain ER-beta-IR suggest a role for neuronal activation in the
167 Expression of FOS-IR in MNCs with attenuated ER-beta-IR, and the absence of FOS-IR in parvocellular n
168 A critical step in understanding the role of ER beta is demonstrating that the mRNA is translated int
171 these studies indicate that ligand-activated ER-beta is a potential therapeutic target to combat obes
172 first evidence that epigenetic regulation of ER-beta is a reversible and tumor stage-specific process
176 abundant cortical nuclear estrogen receptor, ER-beta, is present in GABAergic neurons, prompting us t
179 GnRH-1 neurons expresses estrogen receptor (ER) beta, it is unclear whether E2 acts directly on GnRH
180 n functions signaled through hER-alpha66 and ER-beta; it also transduces membrane-initiated estrogen-
181 we used ER alpha-knockout (ER alpha KO) and ER beta-knockout (ER beta KO) mice in an animal model of
183 cardioprotective effect of DPN was found in ER-beta-knockout mice, indicating that the DPN-induced c
188 In addition to higher estrogen receptor (ER) beta levels, enhanced ERbeta activity was detected i
189 discriminate between different ER alpha and ER beta ligand complexes suggests that the biological ef
192 litis (EAE) mice with the estrogen receptor (ER) beta ligand diarylpropionitrile (DPN) has been shown
194 s studies have shown that estrogen receptor (ER) beta ligands could inhibit experimental autoimmune e
197 xpression of ADA3 enhances the ER alpha- and ER beta-mediated sequence-specific transactivation.
198 Based on our recent finding of anti-estrogen/ER-beta-mediated growth inhibition of prostate cancer ce
200 C/ in situ hybridization study revealed that ER beta mRNA and immunoreactivity were colocalized in ne
201 of these studies have demonstrated that (1) ER beta mRNA is translated into immunoreactive protein t
202 studies that a variety of estrogen receptor (ER) beta mRNA transcripts are expressed in human breast
203 prostate cancer cell lines, LNCaP expressed ER-beta mRNA along with transcripts of PR and pS2, DU145
205 ol and testosterone were not correlated with ER-beta mRNA expression after osmotic manipulation, sugg
208 transcription-PCR revealed no difference in ER-beta mRNA levels between normal and malignant colon t
209 ell lines, in which it was demonstrated that ER-beta mRNA was significantly up-regulated in the resis
211 ochemistry demonstrated that the decrease in ER-beta mRNA was translated into depletion of receptor p
212 lines (LNCaP and DU145), that express little ER-beta mRNA, with a demethylating agent increased level
214 , in weanling rats sex affected ER alpha and ER beta neuronal densities in brainstem regions associat
215 d characterized a genuine estrogen receptor (ER) beta-null mouse line (named ERbeta(ST)(L-/L-)) and s
216 sion of the estrogen receptors (ER alpha and ER beta) on the globoid cells, activated astrocytes and
218 reatment, PC3 (ER-alpha/ER-beta+) and DU145 (ER-beta+ only) cells were selected to further characteri
219 ting the first 18 amino acids of the longest ER-beta open reading frame reported to date, and polyclo
221 tide oxytocin (OT) or the estrogen receptor (ER)-beta or ER-alpha had been selectively "knocked out"
225 tase], "estrogen metabolism/ER-beta factor" (ER-beta, peroxisome proliferator-activated receptor-gamm
226 mediated ischemic protection suggesting that ER-beta plays a key role in mediating the beneficial eff
227 at the activation of estrogen receptor-beta (ER-beta) plays an important cardioprotective role agains
228 vasopressin-immunoreactive neurons were also ER-beta positive in the PVN (66.14% +/- 2.47%) and SON (
231 antitate areas and densities of ER alpha and ER beta-positive neurons within medullary regions associ
233 or alpha (ER alpha), estrogen receptor beta (ER beta), progesterone receptor (PR), and androgen recep
234 ains (E domains) of human/mouse ER alpha and ER beta, progesterone receptors A and B, and the androge
235 Immunofluorescence microscopy showed that ER beta protein was present in glycoprotein (GP) IIb(+)
237 ER-beta-specific antibodies to characterize ER-beta protein expression in breast cancer cell lines a
238 nant colon tissue showed a selective loss of ER-beta protein expression when compared to normal colon
239 on is associated with a marked diminution of ER-beta protein expression, possibly through a posttrans
241 pressed estrogen receptor (ER)alpha, but not ER-beta protein levels, and abrogated downstream estroge
249 reated ovariectomized C57BL/6J mice with the ER-beta selective agonist 2,2-bis(4-hydroxyphenyl)-propr
250 ligand 16alpha-iodo-17beta-estradiol and the ER-beta selective ligand genistein failed to elicit ERK
253 We evaluated the pharmacological effect of ER-beta-selective ligands (beta-LGNDs) in animal models
254 ther with the inability of the ER-alpha- and ER-beta-selective ligands to elicit ERK phosphorylation,
257 2-mediated responses were due to ER alpha or ER beta signaling, ER alpha-knockout (alphaERKO) or ERbe
258 viously unrecognized directions for studying ER-beta signaling and design of ER-beta-based therapies.
260 and cell context-dependent ER(alpha)/Sp1 and ER(beta)/Sp1 action using an E2-responsive construct (pS
261 E2 did not affect or significantly decrease ER(beta)/Sp1 action, and antiestrogens had minimal effec
263 fects were mimicked by an estrogen receptor (ER) beta-specific agonist and were blocked by the classi
264 17-diol (ICI 182,780)] and the ER-alpha- and ER-beta-specific agonists [1,3,5-tris(4-hydroxyphenyl)-4
265 abolish receptor binding, and ER-alpha- and ER-beta-specific antibodies interact with complexes form
266 he RNA expression studies, we have developed ER-beta-specific antibodies to characterize ER-beta prot
267 ice had decreased expression of ER-alpha and ER-beta subtypes and ER transcriptional activity was als
268 pression of estrogen receptor (ER)-alpha and ER-beta subtypes in GS-prone and GS-resistant glomeruli
269 factor requirements, domains of ER alpha and ER beta sufficient for forskolin/IBMX activation, and th
270 s proliferation via oestrogen receptor-beta (ER-beta), the catecholoestradiols mediate P-UAEC prolife
272 Because the prostate contains high levels of ER-beta, the present study investigated the effect of ra
273 ecause the prostate contains a high level of ER-beta, the present study investigated the effect of ra
274 act on the OT system at two levels: through ER-beta, they regulate the production of OT in the hypot
275 , with 22% of samples exclusively expressing ER beta; this was not observed in any of the breast tumo
276 n, we compared the abilities of ER alpha and ER beta to activate transcription and induce distortion
277 The different abilities of ER alpha and ER beta to induce change in DNA structure could foster o
278 a selective modulator of estrogen receptor (ER)beta to suppress inflammatory responses of microglia
282 and BPH-1 cells expressed both ER-alpha and ER-beta transcripts and no PR nor pS2 mRNA in PrEC and o
284 e after trauma-hemorrhage and female 129 Sve ER-beta-/- transgenic mice and ovariectomized wild-type
286 urons with the highest percentage expressing ER-beta was found to be prolactin (PRL) immunoreactive i
287 its specificity for estrogen receptor-beta (ER-beta), was used to immunolocalize the receptor in his
288 lpha (ER-alpha), and estrogen receptor-beta (ER-beta), we found only sparse colocalization between ER
289 in the ligand-binding domain of ER-alpha and ER-beta, we were not surprised to find that SP500263 bin
291 , those tumors that coexpressed ER alpha and ER beta were node positive (P = 0.02; Fisher's exact tes
292 of estrogen receptor (ER)-alpha and those of ER-beta were expressed in our normal PrEC primary cultur
293 A and protein expression of ER-alpha but not ER-beta were suppressed by resveratrol in Ishikawa cells
294 dzein and genistein (compounds known to bind ER-beta) were performed to serve as positive controls.
296 ural estrogen genistein at both ER-alpha and ER-beta, whereas AIB1 had no effect on either the potenc
297 monstrated that all three cell lines express ER-beta, whereas only PC3 and PC3M cells were positive f
298 d increased expression of estrogen receptor (ER)-beta, which upon activation down-regulated ASM proli
299 anslationally modified form of the long-form ER-beta, which has a predicted size of 59 kd based on po
300 d developmentally regulated, and neocortical ER-beta, which is intranuclear and expressed throughout