ライフサイエンスコーパス: aromatase

1 ic activity of the estrogen-producing enzyme aromatase.

2 rization of the DAR-forming ketosynthase and aromatase.

3 androgen receptor-mediated up-regulation of aromatase.

4 cellular identities of neurons that express aromatase.

5 tween the peripheral immune system and brain aromatase.

6 in the nucleus of the solitary tract express aromatase.

7 phalic aromatase activity and immunoreactive aromatase (24 hour time point only).

8 CYP19A1, or aromatase, a cytochrome P450 responsible for estrogen bi

9 g matrix compliance induces transcription of aromatase, a rate-limiting enzyme in oestrogen biosynthe

10 via peripheral endotoxin increases neuronal aromatase; a mechanism that may rapidly generate a poten

11 ividual clones of MCF-10A(arom) with various aromatase activities, we found that the CD24 mRNA levels

12 CYP19A1 amplification caused increased aromatase activity and estrogen-independent ERalpha bind

13 romatase was measured, as were telencephalic aromatase activity and immunoreactive aromatase (24 hour

14 Mechanical wounding reduced fibroblast aromatase activity but increased keratinocyte activity,

15 elated with serotonin/prolactin, but posited aromatase activity correlated significantly with prolact

16 Altogether, the data suggest that aromatase activity supports serotonin production and tha

17 R (qRT-PCR) mRNA expression, enzymatic assay aromatase activity, scratch assay cell migration, immuno

18 cts can be mediated via local alterations in aromatase activity, which precisely regulates the tempor

19 uced proliferation of beta-cells depended on aromatase activity.

20 4 mRNA levels were inversely correlated with aromatase activity.

21 psed patients had acquired CYP19A1 (encoding aromatase) amplification (CYP19A1(amp)).

22 lopment, but the causal relationship between aromatase and breast cancer has not been identified.

23 Female rodent lung displays increased aromatase and decreased bone morphogenetic protein recep

24 isplayed elevated inhibitory potency against aromatase and enhanced affinity for estrogen receptors w

25 higher levels of miR-106a and -19b and lower aromatase and hGCM1 expression in placentas from preecla

26 Increased concentrations of aromatase and interleukin 6 in inflamed breast tissue an

27 Migration was blocked by aromatase and steroid sulfatase (STS) inhibitors confirm

28 The affinities of both isomers for aromatase and the estrogen receptors, as well as the pha

29 ylation levels of the genes encoding for the aromatase and the receptor of the follicle stimulating h

30 time that p53 is a key negative regulator of aromatase and, hence, estrogen production in the breast

31 dies were performed with (E)-norendoxifen on aromatase, and the results provide a foundation for stru

32 te circulating androgens and the activity of aromatase; and to then determine behavior and the endoge

33 ere we provide evidence that cytochrome P450 aromatase (AROM), the enzyme converting testosterone to

34 hat overexpresses human CYP19, which encodes aromatase (AROM+ mice), and mice with knockout of Esr1,

35 A ToxCast aromatase assay provided concentration-inhibition relati

36 and evaluated for their abilities to inhibit aromatase, bind to estrogen receptor alpha (ER-alpha) an

37 Aromatase binding to anastrozole is pH-independent, cons

38 Brain aromatase blockade acutely inhibited sexual motivation.

39 Human aromatase catalyzes the synthesis of estrogen from andro

40 Human cytochrome P450 aromatase catalyzes with high specificity the synthesis

41 NAs targeting an estrogen receptor (ER)- and aromatase-centered network identified 46 genes that are

42 Aromatase clusters were also more abundant and tightly p

43 1, and 22 exhibited an inhibitory potency on aromatase comparable to that of letrozole chosen as a re

44 d higher levels of Hsp90 ATPase activity and aromatase compared with wild-type stromal cells.

45 T) domains of the fungal nrPKSs and discrete aromatase/cyclase enzymes in bacteria, regiospecific fir

46 The aromatase/cyclases (ARO/CYCs) are responsible for regios

47 Dual inhibitors of aromatase (CYP19) and aldosterone synthase (CYP11B2) are

48 sulin resistance while exhibiting suppressed aromatase (Cyp19a1) expression and reduced circulating 1

49 yclin A1 expression was also correlated with aromatase (CYP19A1), a key enzyme that directly regulate

50 Aromatase (CYP19A1), the enzyme that converts androgens

51 med to provide baseline information defining aromatase distribution in healthy men and women, against

52 In the bone marrow, cyclin A1 and aromatase enhanced local bone marrow-releasing factors,

53 ty but also for estradiol production via the aromatase enzyme and estradiol action via the alpha isof

54 by prostaglandin E2 (PGE2) activation of the aromatase enzyme, as we reported previously and confirm

55 on of the proliferation marker Ki-67 and the aromatase enzyme.

56 Like aromatase, ERbeta1 label colocalized with glial fibrilla

57 Elevated expression of aromatase (estrogen synthase) in breast tissues increase

58 differences in the cellular distribution of aromatase (estrogen synthase) in several species suggest

59 w in rats that systemic administration of an aromatase (estrogen synthase) inhibitor after seizure on

60 to exhibit strong expression of ERalpha and aromatase (estrogen synthetase, CYP19) in midshipman.

61 unocytochemistry revealed greater numbers of aromatase-expressing neurons in LPS birds.

62 cytoarchitecture and cellular identities of aromatase-expressing neurons in the auditory and sensori

63 Ablation of the oxytocin receptor in aromatase-expressing neurons of the medial amygdala (MeA

64 Notably, aromatase-expressing neurons were found in dense somato-

65 However, conceptus aromatase expression and estrogen secretion were decreas

66 We did not find sex differences in aromatase expression and neither the pattern nor the num

67 glandin E2 (PGE2), stimulates adipose tissue aromatase expression and subsequent estrogen production,

68 is was correlated with enhanced preadipocyte aromatase expression following incubation in conditioned

69 activity, levels of PKM2 and HIF-1alpha, and aromatase expression in LFS stromal cells.

70 lencing either HIF-1alpha or PKM2 suppressed aromatase expression in LFS stromal cells.

71 Increased aromatase expression was also detected in female human p

72 ctivated glucocorticoid receptor, decreasing aromatase expression, induces Leydig tumor regression bo

73 Although p53 down-regulates aromatase expression, the underlying mechanisms are inco

74 Inhibition of Hsp90 ATPase suppressed aromatase expression.

75 ibition of Hsp90 ATPase activity and reduced aromatase expression.

76 ated glucocorticoid receptor to regulate the aromatase gene transcriptional activity through the recr

77 For the past 40 years, aromatase has been a target of intense inhibitor discove

78 leated syncytiotrophoblast with induction of aromatase (hCYP19A1) and chorionic gonadotropin (hCGbeta

79 e and female zebra finches, a combination of aromatase immunohistochemistry and conventional tract tr

80 ontrast, calbindin was not co-expressed with aromatase in any region investigated.

81 We established a model by expressing aromatase in ERalpha- MCF-10A human breast epithelial ce

82 erneuron subtypes, and are co-expressed with aromatase in human temporal cortex.

83 M2/HIF-1alpha axis mediates the induction of aromatase in LFS.

84 Our results suggest that overexpression of aromatase in MCF-10A cells causes malignant transformati

85 ve morphs for ERbeta1, ERbeta2, ERalpha, and aromatase in the forebrain and saccule.

86 he effects of sex on pulmonary expression of aromatase in these models and in lungs from patients wit

87 decreased Th1 and Th17 differentiation in an aromatase-independent fashion, but also exacerbated cell

88 campal estrogen synthesis, intra-hippocampal aromatase inhibition also suppressed seizures.

89 urons in rodent BLA responded differently to aromatase inhibition both in vivo and in vitro, our find

90 itutitary-gonadal axis in female FHMs, where aromatase inhibition decreases the conversion of testost

91 The resulting total aromatase inhibition was input to a mathematical model o

92 Further, chronic aromatase inhibition within the dentate gyrus blocked th

93 en patients with good or poor outcomes after aromatase inhibition.

94 protective activities, probably unrelated to aromatase inhibition.

95 n suppression (OFS), in combination with the aromatase inhibitor (AI) exemestane.

96 Purpose Adherence to aromatase inhibitor (AI) therapy for early-stage breast

97 ESR1 mutations are selected by prior aromatase inhibitor (AI) therapy in advanced breast canc

98 ESR1 have been associated with resistance to aromatase inhibitor (AI) therapy in patients with ER+ me

99 tive study assessed the impact of 2 years of aromatase inhibitor (AI) therapy on the incidence of ova

100 ng recurrence/progression after nonsteroidal aromatase inhibitor (AI) therapy.

101 was > 10% after 2 to 4 weeks of neoadjuvant aromatase inhibitor (AI) therapy.

102 nformation exists on the long-term effect of aromatase inhibitor (AI) use on CVD risk in breast cance

103 Aromatase inhibitor (AI) use results in low estrogen lev

104 henotypes evolving in lines resistant to the aromatase inhibitor (AI).

105 The long-range goal has been to create dual aromatase inhibitor (AI)/selective estrogen receptor mod

106 matase inhibitor or tamoxifen followed by an aromatase inhibitor (in sequence).

107 s during which progression occurred included aromatase inhibitor (n = 36), fulvestrant (n = 21), and

108 led before and after 4 months of neoadjuvant aromatase inhibitor (NAI) treatment.

109 variables among three patient groups (no ET, aromatase inhibitor [AI], or tamoxifen) were compared by

110 tablished that a strategy of switching to an aromatase inhibitor after 2 to 3 years of tamoxifen can

111 RATIONALE: The aromatase inhibitor anastrozole blocks the conversion of

112 We assessed the efficacy and safety of the aromatase inhibitor anastrozole for prevention of breast

113 We analysed patients according to which aromatase inhibitor and T-score groups they were allocat

114 lthough s.c. treatment with testosterone and aromatase inhibitor applied beginning on the day of immu

115 eliminated or reduced by the addition of an aromatase inhibitor during CM generation.

116 The Society includes the aromatase inhibitor exemestane in addition to tamoxifen

117 receptor-positive early breast cancer to the aromatase inhibitor exemestane plus ovarian suppression

118 study evaluated entinostat combined with the aromatase inhibitor exemestane versus exemestane alone.

119 ased on experiments with FHMs exposed to the aromatase inhibitor fadrozole, we also show how a toxic

120 gyrus was assessed by local infusion of the aromatase inhibitor fadrozole, whose efficacy was confir

121 e of continuing tamoxifen or switching to an aromatase inhibitor for 10 years total adjuvant endocrin

122 Treatment with an aromatase inhibitor for 5 years as up-front monotherapy

123 e cyclooxygenase inhibitor nimesulide or the aromatase inhibitor formestane.

124 d adjuvant therapy with tamoxifen or with an aromatase inhibitor improved disease-free survival and i

125 Adjuvant therapy with an aromatase inhibitor improves outcomes, as compared with

126 breast cancer resistant to treatment with an aromatase inhibitor in the adjuvant or metastatic settin

127 sitive disease, antiestrogen therapy with an aromatase inhibitor is a reasonable alternative to obser

128 ighly proliferative after treatment with the aromatase inhibitor letrozole and identified a D189Y mut

129 R(+) breast cancers after treatment with the aromatase inhibitor letrozole.

130 ter pretreatment with a clinical dose of the aromatase inhibitor letrozole.

131 nimum of 5 years of adjuvant therapy with an aromatase inhibitor or tamoxifen followed by an aromatas

132 eutic target to combat or delay the onset of aromatase inhibitor resistance in breast cancer.

133 substantial improvements in patient outcome, aromatase inhibitor resistance remains a major clinical

134 nce of PIK3CA mutation, primary or secondary aromatase inhibitor resistance, and measurable or non-me

135 ated RET signaling is enhanced in a model of aromatase inhibitor resistance.

136 of overall survival was not higher with the aromatase inhibitor than with placebo.

137 Extending treatment with an aromatase inhibitor to 10 years may further reduce the r

138 The extension of treatment with an adjuvant aromatase inhibitor to 10 years resulted in significantl

139 ree thermal regimes; some eggs were given an aromatase inhibitor to produce sons at temperatures that

140 as E2 release, and (3) direct infusion of an aromatase inhibitor to the S-ME suppressed spontaneous G

141 cer whose disease had progressed on or after aromatase inhibitor treatment and had received up to one

142 n part 2, we stratified patients by previous aromatase inhibitor treatment for advanced or metastatic

143 e or relapse during or within 6 months of an aromatase inhibitor treatment in the adjuvant setting an

144 more importantly, predicted poor response to aromatase inhibitor treatment with the development of re

145 W embryonic gonads that were masculinized by aromatase inhibitor treatment.

146 act of GDNF-RET signaling in the response to aromatase inhibitor treatment.

147 responding rapidly to temperature shifts and aromatase inhibitor treatment.

148 rding Hologic device for DXA scans, previous aromatase inhibitor use, and baseline bone mineral densi

149 breast cancer progressing on a nonsteroidal aromatase inhibitor were randomly assigned to exemestane

150 We postulated that an aromatase inhibitor would be safer and more effective.

151 de + ATD (androgen antagonist plus steroidal aromatase inhibitor); or (f) dihydrotestosterone (DHT) +

152 ine therapy compared with a third-generation aromatase inhibitor, a standard of care for first-line t

153 nous estrogen in males and females using the aromatase inhibitor, anastrozole, in two models of PH: t

154 ver, pretreatment with fadrozole, a specific aromatase inhibitor, did not block norepinephrine's neur

155 qAOP to predict effects of another, untested aromatase inhibitor, iprodione.

156 mpletely abolished by pre-treatment with the aromatase inhibitor, letrozole.

157 attenuated by systemic administration of the aromatase inhibitor, letrozole.

158 Birds were injected with fadrozole, a potent aromatase inhibitor, or vehicle within 2-5 minutes after

159 Exemestane, a steroidal aromatase inhibitor, reduced invasive breast cancer inci

160 rons under oxidative stress conditions in an aromatase inhibitor-dependent manner.

161 GDNF-RET signaling promoted the survival of aromatase inhibitor-resistant cells and elicited resista

162 has been approved for advanced or metastatic aromatase inhibitor-resistant ER(+) breast cancer.

163 ication of activating ESR1 gene mutations in aromatase inhibitor-resistant metastatic breast cancers.

164 xpression levels in an independent cohort of aromatase inhibitor-resistant patient specimens.

165 r-resistant cells and elicited resistance in aromatase inhibitor-sensitive cells.

166 ESR1 mutations are prevalent in ER-positive aromatase inhibitor-treated MBC.

167 ligand antibody denosumab in postmenopausal, aromatase inhibitor-treated patients with early-stage ho

168 ived from a further independent cohort of 72 aromatase inhibitor-treated patients.

169 be administered with either tamoxifen or an aromatase inhibitor.

170 a diagnosis of MBC and prior exposure to an aromatase inhibitor.

171 r more prescriptions for tamoxifen and/or an aromatase inhibitor.

172 AvodartTM); (d) T + Letrozole (nonsteroidal aromatase inhibitor; FemeraTM); (e) Flutamide + ATD (and

173 ain adverse events were arthralgia and other aromatase-inhibitor related symptoms; no additional toxi

174 otherapy, the interval from the last dose of aromatase-inhibitor therapy, and the duration of treatme

175 a negative association with the efficacy of aromatase-inhibitor treatment.

176 Aromatase inhibitors (AI) are associated with significan

177 Aromatase inhibitors (AI) have become the first-line end

178 Aromatase inhibitors (AI) induce painful musculoskeletal

179 ptoms are the most common adverse effects of aromatase inhibitors (AIs) and can result in decreased q

180 50% of breast cancer survivors treated with aromatase inhibitors (AIs) and is the most common reason

181 For postmenopausal women, aromatase inhibitors (AIs) are the preferred first-line

182 Aromatase inhibitors (AIs) are the standard endocrine th

183 gen receptor-positive (ER+) breast cancer to aromatase inhibitors (AIs) but have been limited to smal

184 reported in randomized clinical trials with aromatase inhibitors (AIs) compared with tamoxifen.

185 Aromatase inhibitors (AIs) have an established role in t

186 mergent symptoms with adjuvant tamoxifen and aromatase inhibitors (AIs) have been associated with sup

187 The so-called third generation aromatase inhibitors (AIs) letrozole, anastrozole, and t

188 Aromatase inhibitors (AIs) prevent estrogen production a

189 that therapy including tamoxifen citrate and aromatase inhibitors (AIs) reduces CBC risk.

190 Adherence to tamoxifen, aromatase inhibitors (AIs), and overall AET (tamoxifen o

191 positive breast cancers initially respond to aromatase inhibitors (AIs), but eventually acquire resis

192 estrogen receptor modulators (SERMs) and/or aromatase inhibitors (AIs).

193 and switching therapy between tamoxifen and aromatase inhibitors (HR, 1.50; 95% CI, 1.23 to 1.83) du

194 rom their first prescription of tamoxifen or aromatase inhibitors (N = 3,395).

195 cancer that has progressed on non-steroidal aromatase inhibitors (NSAIs) is unclear.

196 therapy involves 5 years of the nonsteroidal aromatase inhibitors anastrozole and letrozole.

197 tially non-cross-resistant with nonsteroidal aromatase inhibitors and is a mild androgen and could pr

198 Aromatase inhibitors are a standard of care for hormone

199 Purpose Aromatase inhibitors are established breast cancer chemo

200 While anti-estrogens/aromatase inhibitors are initially effective, resistance

201 Third-generation aromatase inhibitors are more effective than tamoxifen f

202 Aromatase inhibitors are the major first-line treatment

203 tment in cancer and other disorders in which aromatase inhibitors are useful.

204 h selective estrogen receptor modulators and aromatase inhibitors are widely used for the treatment o

205 Aromatase inhibitors are widely used in breast cancer an

206 lts demonstrate that adjuvant treatment with aromatase inhibitors can be considered for breast cancer

207 Aromatase inhibitors effectively prevent breast cancer r

208 e CDK4/6 inhibitor palbociclib combined with aromatase inhibitors for the treatment of estrogen recep

209 nation chemotherapy, NET as monotherapy with aromatase inhibitors had a similar clinical response rat

210 Blocking estrogen biosynthesis by aromatase inhibitors has therefore become a first-line e

211 to endocrine therapies such as tamoxifen and aromatase inhibitors is a significant clinical problem.

212 Treatment of breast cancer with aromatase inhibitors is associated with damage to bones.

213 res and suggest that acute administration of aromatase inhibitors may be an effective treatment for S

214 disease pathogenesis in females and suggests aromatase inhibitors may have therapeutic potential.

215 e of potential effects of random mixtures of aromatase inhibitors on the dynamics of women's menstrua

216 ified by type of previous endocrine therapy (aromatase inhibitors only vs selective oestrogen recepto

217 ther by blocking estrogen production through aromatase inhibitors or antiestrogens that compete for h

218 Aromatase inhibitors prevent breast cancer in postmenopa

219 lmethylflavones previously reported by us as aromatase inhibitors proved to be able to interact with

220 son of steroidal and nonsteroidal classes of aromatase inhibitors showed neither to be superior in te

221 estrogen receptor modulator tamoxifen and to aromatase inhibitors that lower circulating estradiol oc

222 carcinogenesis and implicate superiority of aromatase inhibitors to antiestrogens for breast cancer

223 carcinogenesis and implicate superiority of aromatase inhibitors to antiestrogens for breast cancer

224 se of other selective ER modulators or other aromatase inhibitors to lower BC risk is not recommended

225 The application of aromatase inhibitors to postmenopausal breast cancer pat

226 AR, 24.1); however, initiating therapy with aromatase inhibitors was not associated with VTE (HR, 0.

227 compounds library of our earlier synthesized aromatase inhibitors was performed and, according to the

228 Aromatase inhibitors were associated with a significantl

229 itive breast cancer receiving treatment with aromatase inhibitors were randomly assigned in a 1:1 rat

230 enopausal women with breast cancer receiving aromatase inhibitors, and can be administered without ad

231 Mammography, chemotherapy, tamoxifen, aromatase inhibitors, and trastuzumab.

232 evels reported in postmenopausal patients on aromatase inhibitors, but at each time point, at least 1

233 omen with the polycystic ovary syndrome, but aromatase inhibitors, including letrozole, might result

234 ove 10% inhibition of estradiol synthesis by aromatase inhibitors, noticeable (eventually reversible)

235 antihormonal therapies such as tamoxifen and aromatase inhibitors, resistance often emerges.

236 njection of estrogen receptor antagonists or aromatase inhibitors, respectively, decreases sexual mot

237 s and of the side effects of cytochrome P450 aromatase inhibitors, which are frequently used for brea

238 er were assigned to one of two adjuvant oral aromatase inhibitors-exemestane or anastrozole.

239 ers that have progressed on tamoxifen and/or aromatase inhibitors.

240 ET, evenly distributed between tamoxifen or aromatase inhibitors.

241 ed by adjuvant therapy with antiestrogens or aromatase inhibitors.

242 signed and synthesized as nonsteroidal CYP19 aromatase inhibitors.

243 he development of new pyrroloquinoline-based aromatase inhibitors.

244 dicted the treatment outcomes for first-line aromatase inhibitors.

245 ures to millions of potential mixtures of 86 aromatase inhibitors.

246 per se may counteract the intended effect of aromatase inhibitors.

247 The potent aromatase inhibitory activities and high ER-alpha and ER

248 norendoxifen as the first compound with dual aromatase inhibitory and estrogen receptor binding activ

249 Compounds with both aromatase inhibitory and estrogen receptor modulatory ac

250 Aromatase is the cytochrome P450 enzyme that cleaves the

251 Aromatase is the enzyme responsible for synthesis of E2

252 xpression of the critical feminising enzyme, aromatase, is reduced in the presence of over-expressed

253 (Z)-Norendoxifen displayed affinity for aromatase (Ki 442 nM), estrogen receptor-alpha (EC50 17

254 rresponding values for (E)-norendoxifen were aromatase (Ki 48 nM), estrogen receptor-alpha (EC50 58.7

255 and cytokines had returned to baseline, but aromatase mRNA and activity were elevated in both sexes.

256 neurons, and ventromedial to this, an ovoid, aromatase-negative (AR-) nucleus.

257 In total, given their location, these aromatase neurons are poised to engage nociceptive circu

258 from human cortex by identifying a subset of aromatase neurons as putative inhibitory interneurons.

259 A few aromatase neurons express Fos after cheek injection of c

260 f this tracer as a new tool for detection of aromatase-overexpressing primary tumors or metastases in

261 man SynT differentiation, including hCYP19A1/aromatase P450, glial cells missing 1 (GCM1), frizzled 5

262 regulates the expression of cytochrome P450 aromatase (P450arom).

263 n the basal hypothalamus: an oblique band of aromatase-positive (AR+) neurons, and ventromedial to th

264 of HIF-1alpha and PKM2 was recruited to the aromatase promoter II in LFS stromal cells.

265 glucocorticoid responsive element within the aromatase promoter II.

266 o and activates two breast cancer-associated aromatase promoters.

267 Aromatase protein is overexpressed in the breasts of wom

268 the publication of the crystal structure of aromatase purified from human placenta, revealing an and

269 e) is a synthetic steroidal inhibitor of the aromatase reaction that catalyzes the terminal and rate-

270 ron species in the third step of the steroid aromatase reaction.

271 Immunohistochemical staining in an aromatase reporter mouse revealed that many neurons in l

272 steroidogenic enzyme [cytochrome P450(CYP19) aromatase] required for estrogen synthesis in vertebrate

273 lowing it, which together affect function of aromatase SA-I in ER.

274 Aromatase SA-I mediates translocation of a short N-termi

275 To optimize its efficacy and aromatase selectivity versus other cytochrome P450 enzym

276 Overexpression of aromatase significantly increased anchorage-independent

277 .g., Irosustat, as innovative dual-targeting aromatase-steroid sulfatase inhibitors (DASIs) and as mu

278 h) tumor cells expressing elevated levels of aromatase stimulated tumor/host estrogen production and

279 etics were used to study the impact of pH on aromatase structure and androstenedione binding.

280 Here we report that the aromatase substrate androstenedione, unique among severa

281 ge between inhibition of cytochrome P450 19A aromatase (the MIE) and population-level decreases in th

282 Blocking aromatase, the enzyme for the biosynthesis of estrogen,

283 estrogen, here we examined the expression of aromatase, the enzyme that catalyzes the conversion of t

284 Aromatase, the last and obligatory enzyme catalyzing est

285 demonstrating that an important regulator of aromatase, the obesity-associated and tumor-derived fact

286 Recently, elevated levels of aromatase, the rate-limiting enzyme for estrogen biosynt

287 due to actin stress fibre formation dampens aromatase transcription.

288 n contrast, transcript abundance for ERs and aromatase varied significantly between morphs in and aro

289 The selectivity of 10 for aromatase versus other cytochrome P450 enzymes was also

290 Aromatase was co-expressed with parvalbumin in the caudo

291 The central transcription of cytokines and aromatase was measured, as were telencephalic aromatase

292 mory impairment in females, and the level of aromatase was significantly higher in the PFC of females

293 eroidogenic genes and one of these, CYP19A1 (aromatase), was shown to be regulated by the transcripti

294 ockout mouse models for estrogen receptor or aromatase, we observed that perturbation in estrogen tra

295 and antagonists following blockade of brain aromatase, we show here that brain-derived estrogens acu

296 ATPase activity, Aha1, HIF-1alpha, PKM2, and aromatase were increased in the mammary glands of p53 nu

297 tic plasticity in the BLA involving neuronal aromatase, which produces the neurosteroid 17beta-estrad

298 I SAs (SA-Is), we evaluated translocation of aromatase, whose signal anchor follows a hydrophilic reg

299 Complete inhibition of aromatase with ATD, a noncompetitive inhibitor, signific

300 Incubation of purified aromatase with its 19-deutero-19-oxo androgen substrate