ライフサイエンスコーパス: estrogen-dependent

1 investigated whether ethanol hypotension is estrogen dependent.

2 s, even in cell lines where PR expression is estrogen dependent.

3 timal proliferation after vascular injury is estrogen dependent.

4 Copulation in continuers appears estrogen dependent.

5 invasive mammary tumor formation is strictly estrogen dependent.

6 at in vivo T cell trafficking is gender- and estrogen-dependent.

7 was discontinued, indicating that they were estrogen-dependent.

8 R) action by blocking the interactions of an estrogen-dependent activation function (AF-2) with p160

9 independent activation function 1 (AF-1) and estrogen-dependent activation function 2 (AF-2) of ERalp

10 Estrogen-dependent activation of PAK1 required the phosp

11 Finally, our studies reveal that the estrogen-dependent activation of preloaded Pol II facili

12 -beta; it also transduces membrane-initiated estrogen-dependent activation of the mitogen-activated p

13 lement within this enhancer region abolishes estrogen-dependent activity, and chromosome conformation

14 44 to alanines in helix 12 (AF2ER) minimized estrogen-dependent AF-2 transcriptional activation.

15 Proliferation of MCF-7 cells is estrogen dependent and antiestrogen sensitive.

16 Tumor growth is estrogen dependent and required for intratumoral lymphan

17 ER-positive breast cancer cells, it promotes estrogen-dependent and -independent ER transcriptional a

18 ells, and the effect may be mediated by both estrogen-dependent and -independent mechanisms.

19 Data indicate that estrogen-dependent and -independent pathways are involve

20 addition, COBRA1 was shown to regulate both estrogen-dependent and -independent transcription of the

21 er, has been shown previously to affect both estrogen-dependent and calcium/calmodulin-dependent path

22 ert its oncogenicity through tissue-specific estrogen-dependent and estrogen-independent functions.

23 n and induction of apoptosis are obtained in estrogen-dependent and estrogen-independent human breast

24 ow demonstrate that hER-alpha36 inhibits the estrogen-dependent and estrogen-independent transactivat

25 acts as a dominant-negative effector of both estrogen-dependent and estrogen-independent transactivat

26 sured levels and mRNA expression of EGFRs in estrogen-dependent and independent MXT mouse mammary can

27 In the female cat, this behavior is estrogen dependent, and estrogen induces axonal sproutin

28 ess, transformation by a v-Myb-ER fusion was estrogen dependent, and upon withdrawal of the hormone,

29 on of progesterone receptor (PR) is normally estrogen-dependent, and progesterone is only active in t

30 The MCF-7 cell line is a model of estrogen-dependent, antiestrogen-sensitive human breast

31 The MCF-7 cell line is a model of estrogen-dependent, antiestrogen-sensitive human breast

32 eneralized CNS arousal can foster a specific estrogen-dependent, aroused behavior, sexual behavior.

33 Interestingly, COBRA1 does not affect the estrogen-dependent assembly of transcription regulatory

34 his facilitation bears on CNS mechanisms for estrogen-dependent behaviors, ovariectomized rats were s

35 ated by estrogen and tamoxifen in the ZR75-1 estrogen dependent breast cancer cell line.

36 s required for ER-mediated transcription and estrogen-dependent breast cancer cell growth.

37 n mediating anti-estrogenic effects of RA in estrogen-dependent breast cancer cells and suggest that

38 rations of genistein stimulate the growth of estrogen-dependent breast cancer cells in vivo in a dose

39 In addition, RA treatment of estrogen-dependent breast cancer cells opposes estrogen

40 Treatment of estrogen-dependent breast cancer cells with Protac-B ind

41 tor might be involved in Cyr61 expression in estrogen-dependent breast cancer cells.

42 induced cell growth and G(1)/S transition in estrogen-dependent breast cancer cells.

43 on pathways that are present in ER-positive, estrogen-dependent breast cancer cells.

44 n and enhanced the tumorigenic properties of estrogen-dependent breast cancer cells.

45 ed uterine estrogen responses, and inhibited estrogen-dependent breast cancer growth in vitro and in

46 e found that tamoxifen, a drug used to treat estrogen-dependent breast cancer, caused remarkable impr

47 xifen, the major adjuvant drug treatment for estrogen-dependent breast cancer, has been shown previou

48 Using a model of postmenopausal, estrogen-dependent breast cancer, we investigated the an

49 research for the prevention and treatment of estrogen-dependent breast cancer.

50 vel anticancer strategy for the treatment of estrogen-dependent breast cancer.

51 rovides a potential therapeutic strategy for estrogen-dependent breast cancer.

52 herapies for the prevention and treatment of estrogen-dependent breast cancer.

53 breast tissues and hence the reduced risk of estrogen-dependent breast cancer.

54 e, are preeminent drugs for the treatment of estrogen-dependent breast cancer.

55 s a potential new target in the treatment of estrogen-dependent breast cancer.

56 and mechanisms underlying the progression of estrogen-dependent breast cancers to estrogen-independen

57 ffective for the prevention and treatment of estrogen-dependent breast cancers, but is associated wit

58 ave been developed to treat individuals with estrogen-dependent breast cancers, some tumors show de n

59 tors may be useful as therapeutic agents for estrogen-dependent breast cancers.

60 ulfatase have potential for the treatment of estrogen-dependent breast cancers.

61 t does not stimulate the proliferation of an estrogen-dependent breast carcinoma cell line.

62 ne kinase 1 (SK1) plays an important role in estrogen-dependent breast tumorigenesis, but its regulat

63 Furthermore, this higher preference is estrogen-dependent, but does not vary across the female

64 This chimeric c-RelER protein causes estrogen-dependent, but otherwise c-Rel-specific, transf

65 stigated in Rat1-A fibroblasts expressing an estrogen-dependent c-myc construct, mycER.

66 the majority of breast cancers and promotes estrogen-dependent cancer progression by regulating the

67 therapy for the prevention and treatment of estrogen-dependent cancer.

68 The role of female hormones in estrogen-dependent cancers has been debated for years.

69 OHE1-16alphaOHE1 ratio, on the prevention of estrogen-dependent cancers remains to be determined.

70 (ERs) are targets for endocrine treatment of estrogen-dependent cancers.

71 n receptor in cancer has been established in estrogen-dependent cancers.

72 Most notably, the estrogen-dependent CD11b(int)Ly6C(-) DC express langerin

73 otency relative to raloxifene in an in vitro estrogen dependent cell proliferation assay (IC50 = 0.05

74 logues were synthesized and shown to inhibit estrogen-dependent cell growth in a mouse uterine growth

75 to an ER-responsive promoter and its role in estrogen-dependent cell proliferation and malignant phen

76 In conclusion, SUSD3 is a novel promoter of estrogen-dependent cell proliferation and regulator of c

77 Cdk4 siRNA also inhibits estrogen-dependent cell proliferation in GH3 cells and c

78 s with estrogen receptor alpha in regulating estrogen-dependent cell proliferation.

79 ns of genistein will stimulate the growth of estrogen-dependent cells in vivo in a dose-dependent man

80 activity and provides a growth advantage to estrogen-dependent cells.

81 ors in estrogen-independent cells but not in estrogen-dependent cells.

82 vely participate in auditory selectivity via estrogen-dependent changes in activity.

83 n any brain region examined, suggesting that estrogen-dependent changes in behavior are mediated by d

84 Several estrogen-dependent changes in the rhesus immune status c

85 pon reduction of endogenous AIB1 expression, estrogen-dependent colony formation in soft agar and tum

86 we identify the product of human MTA3 as an estrogen-dependent component of the Mi-2/NuRD transcript

87 s issue of Cell, demonstrate that MTA3 is an estrogen-dependent component of the NuRD complex and ide

88 Endometriosis is a chronic, estrogen-dependent condition that causes dysmenorrhea an

89 ate the molecular mechanisms involved in the estrogen-dependent control of plasminogen activator inhi

90 eceptor function alone is not sufficient for estrogen-dependent cyclin D1 expression and proliferatio

91 These results may explain the lack of estrogen-dependent cyclin D1 expression and proliferatio

92 Because estrogen-dependent cyclin D1 expression has been linked

93 has been recently correlated with a lack of estrogen-dependent cyclin D1 expression in cells enginee

94 estigated the mechanisms responsible for the estrogen-dependent, cytochrome P450 (CYP)-mediated dilat

95 d tamoxifen inhibited the differentiation of estrogen-dependent DC from bone marrow precursors ex viv

96 ar level, DUSP3 deletion was associated with estrogen-dependent decreased phosphorylation of ERK1/2 a

97 an alternate mechanism that could impact on estrogen-dependent developmental and pathological system

98 ibute to variation in the pathophysiology of estrogen-dependent disease.

99 Endometriosis is considered an estrogen-dependent disease.

100 ations among exposure to these compounds and estrogen-dependent diseases (such as endometriosis) have

101 A promising approach for the treatment of estrogen-dependent diseases is the reduction of intracel

102 are attractive targets for the treatment of estrogen-dependent diseases like endometriosis and breas

103 -HSD1 is a novel target for the treatment of estrogen-dependent diseases, as it catalyzes intracellul

104 ogen hypersensitivity and the development of estrogen-dependent ductal carcinoma in situ lesions.

105 ) mice developed endometrial hyperplasia and estrogen-dependent endometrial cancer, exhibiting increa

106 ER-negative line of melanoma lineage and the estrogen-dependent, ER-positive MCF-7 line, this study p

107 TPSF noncompetitively inhibits estrogen-dependent ERalpha-mediated gene expression with

108 Although estrogen-dependent experimental rodent models of C. albi

109 ted estrogen receptor 1 and was required for estrogen-dependent expression of genes that encode antio

110 oding the catabolic enzyme CYP7B1) decreased estrogen-dependent expression of vascular nitric oxide s

111 (ER(+)) human mammary epithelial cells in an estrogen-dependent fashion.

112 itical role in the involvement of the LHb in estrogen-dependent female reproductive behaviors.

113 has been strongly connected to androgen and estrogen dependent gene expression, it serves as a promi

114 lpha and ERK2 and enables ERK2 modulation of estrogen-dependent gene expression and proliferation pro

115 ic estrogen 17alpha-ethynylestradiol (EE) on estrogen-dependent gene expression and receptor binding

116 The abundance of cyclin D1 determines estrogen-dependent gene expression in the mammary gland

117 n a neural circuit that controls aggression, estrogen-dependent gene expression is increased in long

118 hat estrogens decrease aggression by driving estrogen-dependent gene expression.

119 for evaluation of cellular proliferation and estrogen-dependent gene expression.

120 e mechanism for inactivating CARM1-regulated estrogen-dependent gene expression.

121 ct ERE binding is required for most of (75%) estrogen-dependent gene regulation and 90% of hormone-de

122 a new MED1-interacting protein required for estrogen-dependent gene transcription and breast cancer

123 ng activity of ER and subsequent blockade of estrogen-dependent gene transcription.

124 ERalpha levels controls the transcription of estrogen-dependent genes linked to breast cancer cell pr

125 e ER binding may be a required factor of the estrogen dependent growth response in MCF-7 cells, parti

126 iphering the cellular events associated with estrogen-dependent growth and the subsequent outgrowth o

127 In addition, bortezomib inhibited estrogen-dependent growth in soft agar.

128 polymerase II to target gene promoters, and estrogen-dependent growth of breast cancer cells.

129 nhibits ERalpha-mediated gene expression and estrogen-dependent growth of cancer cells.

130 the effects of Raf-1 kinase activity on the estrogen-dependent growth of human breast cancer cells,

131 ve human breast tumor cells and required for estrogen-dependent growth of MCF7 tumor xenografts.

132 ith up-regulated DLC1 were hypersensitive to estrogen-dependent growth stimulation and that DLC1 had

133 ere estrogen receptor-positive and exhibited estrogen-dependent growth.

134 isoflavone, genistein, stimulates growth of estrogen-dependent human breast cancer (MCF-7) cells in

135 that genistein enhanced the proliferation of estrogen-dependent human breast cancer (MCF-7) cells in

136 profiled the expression of 800 miRNAs in the estrogen-dependent human breast cancer cell line MCF7 an

137 er cells (MDA-MB-231); and (b) the growth of estrogen-dependent human breast cancer cells (MCF-7).

138 Estrogen-dependent human breast cancer cells stably tran

139 In estrogen-dependent human breast cancer cells, chromatin

140 Evidence has been accumulating that some estrogen-dependent human breast cancers require estrogen

141 xifen cooperate to inhibit the growth of the estrogen-dependent human MCF-7 breast cancer cell line m

142 These findings suggest a link between the estrogen-dependent hypotensive effect of chronically adm

143 strogen/c-jun interaction is involved in the estrogen-dependent hypotensive effect of ethanol.

144 independent in the ERKO, although it remains estrogen dependent in a wild type.

145 synthesis, and sildenafil efficacy were not estrogen dependent in male hearts.

146 Estrogen-dependent increases in arousal, measured by hom

147 tromedial nucleus of the hypothalamus (VMH), estrogen-dependent induction of oxytocin receptors requi

148 The estrogen-dependent induction of PR mRNA expression in th

149 Endometriosis is considered to be an estrogen-dependent inflammatory disease, but its etiolog

150 Endometriosis is an estrogen-dependent inflammatory disorder characterized b

151 Estrogen-dependent inhibition of binge-like eating was b

152 ment is nonresponsive to ER-beta but confers estrogen-dependent inhibition of transcription with ER-a

153 of MCF-7 cells to estrogen, stabilizing the estrogen-dependent interaction between p300 and ERalpha.

154 brinolysis and bradykinin generation that is estrogen dependent is suggested.

155 in-coupled receptor superfamily and mediates estrogen-dependent kinase activation as well as transcri

156 amic alpha(1)-adrenoceptors also facilitates estrogen-dependent lordosis.

157 mimetic that may promote the development of estrogen-dependent malignancies, such as breast cancer.

158 nique among human Ads by causing exclusively estrogen-dependent mammary tumors in experimental animal

159 roup D human adenovirus type 9 (Ad9) induces estrogen-dependent mammary tumors in female rats and req

160 e 9 (Ad9) is unique in eliciting exclusively estrogen-dependent mammary tumors in rats and in not req

161 adenovirus type 9 (Ad9) elicits exclusively estrogen-dependent mammary tumors in rats, and an essent

162 novirus type 9 (Ad9), which uniquely elicits estrogen-dependent mammary tumors in rats, is encoded by

163 omal TGF-alpha promoter in MCF-7 cells in an estrogen-dependent manner but not to the pS2 promoter.

164 CITED1 bound directly to ERalpha in an estrogen-dependent manner through its transactivating do

165 REL-dependent transactivation in trans in an estrogen-dependent manner, and ERalpha can interact with

166 en receptor-alpha (ERalpha) and ERbeta in an estrogen-dependent manner, but it affected transcription

167 imera (v-RelER) which transforms cells in an estrogen-dependent manner, we constructed subtraction cD

168 ed the activation of the IL-2 promoter in an estrogen-dependent manner.

169 arget protein c-MYC binds its promoter in an estrogen-dependent manner.

170 ainst an estrogen independent MDA-MB-435 and estrogen dependent MCF-7 breast cancer cell lines and on

171 ncer, regulate the level of IRS-1 protein in estrogen-dependent MCF-7 and ZR75 breast cancer cells.

172 vascular endothelial growth factor (VEGF) by estrogen-dependent MCF-7 breast cancer cells could aboli

173 In ERalpha+/progesterone receptor-positive, estrogen-dependent MCF-7 breast cancer cells, we stably

174 ivating MAP kinase, is growth-inhibitory for estrogen-dependent MCF-7 breast cancer cells.

175 t and metabolite compounds did not stimulate estrogen-dependent MCF-7 cell proliferation above solven

176 Estrogen-dependent MCF-7 cells exhibited a relatively hi

177 d antagonist effects on the proliferation of estrogen-dependent MCF-7 cells in a dose-dependent manne

178 ed as an antiestrogen and potently inhibited estrogen-dependent MCF-7 proliferation with IC(50) value

179 was observed as low as 0.5 mg/kg dose in the estrogen-dependent MCF-7 xenograft model, where this eff

180 For estrogen-dependent MCF-7/BUS breast cancer cells, overex

181 ogen-independent (MDA-MB-231 and BT 549) and estrogen-dependent (MCF-7 and ZR-75-1) human breast canc

182 Transient transfection of BCAR3 in estrogen-dependent MCF7 cells induced activation of luci

183 identified 46 genes that are dispensable in estrogen-dependent MCF7 cells, but are selectively requi

184 nt breast cancer cell line 578-T, but not in estrogen-dependent MCF7 or ZR-75-1 cells.

185 eased PAI-1 promoter activity in BAECs by an estrogen-dependent mechanism, whereas ERbeta suppressed

186 d reperfusion (RSL+I/R) than are males by an estrogen-dependent mechanism.

187 nd afferent arteriolar responsiveness via an estrogen-dependent mechanism.

188 an unexpected divergence in androgen- versus estrogen-dependent mechanisms in, respectively, type II

189 n dendritic morphology are driven in part by estrogen-dependent mechanisms, as evidenced by decreased

190 dent cell-cycle gene expression program, and estrogen-dependent mitogenic growth.

191 erexpression may represent one way to confer estrogen-dependent mitogenic stimulation to breast cance

192 Hyperalgesic priming, an estrogen dependent model of the transition to chronic pa

193 However, studies using an estrogen-dependent murine model of vaginal candidiasis h

194 Studies with an estrogen-dependent murine model of vaginal candidiasis s

195 In the estrogen-dependent MXT tumors, the concentration of EGF

196 An expression of MMP-26 in the estrogen-dependent neoplasms is likely to contribute to

197 erplay between Ser and metalloproteinases in estrogen-dependent neoplasms.

198 ding novel evidence that endometriosis is an estrogen-dependent neuroinflammatory disorder.

199 Heightened expression of the estrogen-dependent oncogene, Myb, in tumors suggests a b

200 dogenous CTMP decreased the proliferation of estrogen-dependent or estrogen-independent breast cancer

201 lative roles each plays in the sex-specific, estrogen-dependent organization of gonadotropin signalin

202 that MTA3 constitutes a key component of an estrogen-dependent pathway regulating growth and differe

203 o critical components for maintenance of the estrogen-dependent phenotype.

204 e approved in the U.S. in the late 1990s for estrogen-dependent postmenopausal breast cancer.

205 more, resveratrol inhibited the formation of estrogen-dependent preneoplastic ductal lesions induced

206 llular and physiological actions of GPR30 in estrogen-dependent processes and discuss the relationshi

207 BARX2 also influences estrogen-dependent processes such as anchorage-independe

208 -mediated and the non-transcription-mediated estrogen-dependent production of nitric oxide by vascula

209 Endometriosis is a debilitating, estrogen-dependent, progesterone-resistant, inflammatory

210 EC on ERalpha inhibition also suppressed the estrogen-dependent progression of endometriosis.

211 Additionally, RUNX3 inhibits the estrogen-dependent proliferation and transformation pote

212 terminal differentiation, and inhibition of estrogen-dependent proliferation in breast cancer cells.

213 gen-responsive target gene promoters and for estrogen-dependent proliferation of breast cancer cells.

214 knockdown to show that Ada3 is critical for estrogen-dependent proliferation of ER-positive breast c

215 liferation of mouse embryonic fibroblasts or estrogen-dependent proliferation of mammary carcinoma MC

216 , and its depletion significantly attenuated estrogen-dependent proliferation of MCF-7 cells.

217 g a well characterized cell culture model of estrogen-dependent proliferation of MCF7 human breast ca

218 stigate the role of cyclin D1, a mediator of estrogen-dependent proliferation, in growth of tamoxifen

219 of estrogen receptor (ER) and inhibition of estrogen-dependent proliferative events.

220 bit increased invasion without affecting the estrogen-dependent proliferative response, which suggest

221 The estrogen-dependent pS2 gene was used as a positive contr

222 The induction of estrogen-dependent rat mammary tumors by human adenoviru

223 mpromised female NCr mice bearing human MCF7 estrogen-dependent, receptor-positive xenografts.

224 n breast cancer cells reduces the endogenous estrogen-dependent recruitment of p300 to the promoters

225 ChIP-PCR demonstrated estrogen-dependent recruitment of the coactivator SRC3 t

226 repair that occur during menstruation before estrogen-dependent regeneration.

227 ggesting that the VMH may play a role in the estrogen-dependent regulation of aggression in this spec

228 To examine estrogen-dependent regulation of IGF-I expression at the

229 .0 to 9.0 months induces a high frequency of estrogen-dependent renal cancers.

230 pression of RIP140 dose dependently inhibits estrogen-dependent reporter activity in human breast can

231 The habenular complex is involved in several estrogen-dependent reproductive behaviors in female rats

232 Medullary bone (MB), an estrogen-dependent reproductive tissue present in extant

233 Thus, both estrogen-dependent resistance to and androgen-mediated f

234 f estrogen-independent but apparently not to estrogen-dependent rodent mammary and human breast carci

235 , and perhaps hER-alpha36 also may transduce estrogen-dependent signaling in other estrogen target ti

236 re, small interfering RNA to RIP140 enhances estrogen-dependent signaling.

237 wnregulation enhances cell proliferation and estrogen-dependent SK1 activity, mediated by a reduction

238 These cells were grown as strictly estrogen-dependent solid tumors in ovariectomized female

239 o measured in female 129S6/SvEv mice bearing estrogen-dependent SSM3 mouse mammary tumors, male athym

240 mise, but they can only be effective against estrogen-dependent stages of the disease.

241 The method was then applied to the estrogen-dependent T-47D estrogen receptor-positive (ER+

242 gen (ERM)-mediated random mutagenesis in the estrogen-dependent T47D breast cancer cells.

243 enes, and it stimulated the proliferation of estrogen-dependent T47D breast cancer cells.

244 ple mechanisms of recruitment for SWI/SNF in estrogen-dependent target gene expression.

245 st cancer is the conversion of cells from an estrogen-dependent to an estrogen-independent state.

246 tion of the phenotype of breast cancers from estrogen-dependent to estrogen-independent growth often

247 is female-specific system is now known to be estrogen-dependent, to be ontogenetically organized, and

248 mutation made at SFRE significantly reduced estrogen-dependent transcription from the lactoferrin ER

249 gion abolish C1 complex formation and reduce estrogen-dependent transcription from the lactoferrin ER

250 HSF1 complexes participate in repression of estrogen-dependent transcription in breast carcinoma cel

251 that selective dose-dependent antagonism of estrogen-dependent transcription may be possible in targ

252 Repression of estrogen-dependent transcription may contribute to the r

253 -response elements of genes, and it enhances estrogen-dependent transcription more effectively than A

254 PBP in CV-1 cells resulted in enhancement of estrogen-dependent transcription, indicating that PBP se

255 ED1 functions as a selective coactivator for estrogen-dependent transcription.

256 nsfection of AIB1 resulted in enhancement of estrogen-dependent transcription.

257 lanines (L543A, L544A) in helix 12 minimized estrogen-dependent transcriptional activation and revers

258 Despite this, Hsp90 is critical for the estrogen-dependent transcriptional activity of the ERbet

259 possibility that wild-type BRCA1 suppresses estrogen-dependent transcriptional pathways related to m

260 ediated by the nuclear estrogen receptor, as estrogen-dependent transcriptional repression was inhibi

261 roteins in chicken embryo fibroblasts causes estrogen-dependent transformation.

262 Nod1 in MCF-7 cells results in inhibition of estrogen-dependent tumor growth and reduction of estroge

263 rom soy protein will have similar effects on estrogen-dependent tumor growth as pure genistein has no

264 ining varying amounts of genistein increased estrogen-dependent tumor growth in a dose-dependent mann

265 dent MCF-7 breast cancer cells could abolish estrogen-dependent tumor growth in ovariectomized mice.

266 ltaneously with estrogen significantly alter estrogen-dependent tumor growth.

267 MCF-7IL-1 alpha cells formed rapidly growing estrogen-dependent tumors compared to parental cells.

268 ctomized athymic mice, and the growth of the estrogen-dependent tumors was measured weekly.

269 were fed to athymic mice implanted s.c. with estrogen-dependent tumors.

270 s postmenopausal breast cancer patients with estrogen-dependent tumors.

271 ometrial cancers have long been divided into estrogen-dependent type I and the less common clinically

272 ssical ER signaling in vivo by comparing the estrogen-dependent uterine response in mice that express

273 rdiovascular tissue and the role of SRC-3 in estrogen-dependent vasoprotection from vascular injury.

274 sponse element and that TCL1A expression was estrogen dependent, was associated with the variant SNP

275 me (2-96 h) in MCF-7 cell variants that were estrogen-dependent (WS8) or resistant to estrogen depriv

276 antly, when these cells were used to produce estrogen-dependent xenograft tumors in SCID mice, we als