ライフサイエンスコーパス: estrogen-dependent

1 investigated whether ethanol hypotension is estrogen dependent.

2 timal proliferation after vascular injury is estrogen dependent.

3 Copulation in continuers appears estrogen dependent.

4 s, even in cell lines where PR expression is 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 The cancer and metastatic lung nodules are estrogen dependent and retain estrogen receptor alpha (E

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

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

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

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

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

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

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

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

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

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

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

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

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

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 ht isolated flavonoids were screened against estrogen-dependent breast cancer cell lines besides norm

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

77 was upregulated by estrogen/ER and regulated estrogen-dependent cell growth.

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

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

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

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

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

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

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

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

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

87 reased DA activity during estrus and reveals estrogen-dependent changes in neuronal function.

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

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

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

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

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

93 the putative roles of KP(LS) neurons in the estrogen-dependent control of GnRH neurons and/or variou

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

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

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

97 Because estrogen-dependent cyclin D1 expression has been linked

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

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

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

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

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

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

104 Endometriosis is considered an estrogen-dependent disease.

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

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

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

108 Treating estrogen-dependent diseases like endometriosis with drug

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

110 rovides an opportunity for future studies in estrogen-dependent diseases, such as endometriosis.

111 for the treatment of endometriosis and other estrogen-dependent diseases.

112 Endometriosis is a common estrogen-dependent disorder wherein uterine lining tissu

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

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

115 at suppress estrogen biosynthesis to inhibit estrogen-dependent ER activity.

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

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

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

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

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

121 Mechanistically, in an estrogen-dependent fashion, SIRT7 mediates PTEN deacetyl

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

146 ds were formed and in vivo in the context of estrogen-dependent growth.

147 Endometriosis is a chronic, estrogen-dependent gynecological condition affecting app

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

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

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

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

152 Estrogen-dependent human breast cancer cells stably tran

153 In estrogen-dependent human breast cancer cells, chromatin

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

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

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

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

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

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

160 Estrogen-dependent increases in arousal, measured by hom

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

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

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

164 Endometriosis is an estrogen-dependent inflammatory disorder characterized b

165 Endometriosis is a chronic, estrogen-dependent, inflammatory disease defined by endo

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

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

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

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

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

171 Comprehensive characterization of the estrogen-dependent kisspeptin neuron transcriptome sheds

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

191 12310A attained tumor regression in the ER+, estrogen-dependent MCF-7 breast cancer xenograft model w

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

221 e facilitate establishment of therapy-naive, estrogen-dependent PDX tumors that progress to lethal me

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

223 ol replacement revealed a critical window of estrogen-dependent plasticity between 3 and 6 wk, which

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

249 ) neurons play well-established roles in the estrogen-dependent regulation of reproduction, little is

250 .0 to 9.0 months induces a high frequency of estrogen-dependent renal cancers.

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

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

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

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

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

256 The estrogen-dependent role of TNFR1-mediated supraspinal ne

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

290 to prevent bone deterioration, and to reduce estrogen-dependent tumor growth.

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

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

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

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

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

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

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

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

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

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