ライフサイエンスコーパス: progesterone

1 n and increase during the luteal phase (high progesterone).

2 ure bound to the other substrate (17alpha-OH-progesterone).

3 and the second and third months of estradiol/progesterone.

4 tely gain or lose binding in the presence of progesterone.

5 onse to binding its cognate steroid hormone, progesterone.

6 uent visits, received treatment with vaginal progesterone.

7 drocortisone inhibited CatSper activation by progesterone.

8 X-aptamers and selected them for binding to progesterone.

9 terferences from estradiol, testosterone and progesterone.

10 al gain of the aptasensor after binding with progesterone.

11 uprolide plus estradiol; and leuprolide plus progesterone.

12 PG-2) exhibited exceptional selectivity for progesterone.

13 en 3 months of continuous combined estradiol/progesterone.

14 g/ml, p=0.01), despite comparable mean serum progesterone.

15 nth, or second and third months of estradiol/progesterone.

16 domised, placebo-controlled trial of vaginal progesterone, 200 mg daily taken from 22-24 to 34 weeks

17 women in both groups were prescribed vaginal progesterone, 200 mg/d, until 36 weeks 6 days of gestati

18 regnanolone (10 mg/kg, IP) and attenuated by progesterone (30 mg/kg, IP) in SD-subjected, but not con

19 er oral 17beta-estradiol (1 mg per day, plus progesterone [45 mg] vaginal gel administered sequential

20 he environmental fate and bioavailability of progesterone, a steroid hormone known to cause endocrine

21 the promoter of GLI1, a critical mediator of progesterone action in the Indian Hedgehog pathway, by C

22 This study reveals that progesterone-activated endocannabinoid depletion by ABHD

23 The steroid hormone progesterone activates CatSper of human sperm via bindin

24 Even at postmenopausal concentrations, progesterone activates PR-A, inducing invasiveness by co

25 Progesterone administration has been shown to reduce the

26 Progesterone administration resulted in a significant pr

27 In conclusion, progesterone ameliorated TMJ inflammation through inhibi

28 ivated or inhibited by synthetic estrogen or progesterone analogs that do not bind to ER or PR.

29 on models) but was associated with increased progesterone and a reduced risk of anovulation (highest

30 he 5alphaR inhibitor finasteride, as well as progesterone and allopregnanolone.

31 esult is a hyperactive pathway, initiated by progesterone and amplified by DNA damage-induced NF-kapp

32 Levels of progesterone and C-reactive protein (CRP) in plasma were

33 ESC were treated in vitro for 1-8 days with progesterone and cAMP (decidualized) in the presence or

34 Postpartum progesterone and CRP declined sharply from 90.85 +/- 42.

35 ostpartum, there was a dramatic reduction in progesterone and CRP, together with an improvement in BO

36 n be calibrated for accurate measurements of progesterone and demonstrated successful measurements wi

37 an neutrophils exposed to pregnancy hormones progesterone and estriol promote the establishment of ma

38 sence of uterine glands and dysregulation of progesterone and estrogen signaling by a Recombination S

39 he body, mediated by the female sex hormones progesterone and estrogen.

40 dicated lag phases for Andro production from progesterone and for DHEA from pregnenolone, indicating

41 rm of breast cancer that lacks the estrogen, progesterone and HER2 receptors and is resistant to targ

42 a structure of WT human P450 21A2 with bound progesterone and now present a structure bound to the ot

43 P450 (P450) 17A1 catalyzes the oxidations of progesterone and pregnenolone and is the major source of

44 Interestingly, both compounds competed with progesterone and pregnenolone sulfate and significantly

45 ccur in the presence of elevated circulating progesterone and suggests non-metabolizable progestogen

46 he 17alpha-hydroxylation of pregnenolone and progesterone and the subsequent 17alpha,20-lyase reactio

47 D2 is highly expressed in spermatozoa, binds progesterone, and acts as a progesterone-dependent lipid

48 (nanomolar) affinities for glucocorticoids, progesterone, and androgens.

49 cation of 3 steroid molecules, epitiostanol, progesterone, and mifepristone, which decrease ferroport

50 We found that the 17alpha-OH-progesterone- and progesterone-bound complex structures

51 n-only contraceptive use and high endogenous progesterone are both associated with increased frequenc

52 In rodents, estrogens and progesterone are critical for reproduction, including pr

53 that (i) pregnenolone sulfate together with progesterone are the main steroids that activate CatSper

54 Indeed, SC increased the levels of progesterone, as well as its derivatives 5alpha-dihydrop

55 In contrast, fish exposed to progesterone associated with the silty loam sediment did

56 d the prolonged cycle length and rescued the progesterone blockade LH surge, while RU486 into the ARC

57 found that the 17alpha-OH-progesterone- and progesterone-bound complex structures are highly similar

58 d in physiological conditions in which serum progesterone, but not E2, is elevated (e.g., lactating r

59 The discovery of chemosensors that recognize progesterone by alteration of self-aggregation state is

60 rticularly when cells are hypersensitized to progesterone by PR-A overexpression.

61 Progesterone can block the oestradiol-induced GnRH/LH su

62 rmed by reduced expression of BAT markers in progesterone challenged oophorectomised mice.

63 during the first month of combined estradiol/progesterone compared with the last month of leuprolide

64 ce did not exhibit the same decline in serum progesterone concentrations as younger mice.

65 l interfering RNA (siRNA) completely ablated progesterone conversion in both steroidogenic mouse Leyd

66 In both sediments, progesterone degradation resulted in the production of a

67 ependent on pregnancy hormones (estrogen and progesterone), delta-opioid receptors, and T cells of th

68 ermatozoa, binds progesterone, and acts as a progesterone-dependent lipid hydrolase by depleting the

69 d susceptibility to HIV infection during the progesterone-dominant luteal phase of the menstrual cycl

70 Both receptors rise and fall in response to progesterone during pregnancy.

71 al versus detrimental roles of estrogen plus progesterone (E+P) in breast cancer remains controversia

72 ion by ABHD2 is a general mechanism by which progesterone exerts its genome-independent action and pr

73 e that it is time to explore alternatives to progesterone for preventing preterm birth.

74 incapable of being interviewed) enrolled in Progesterone for the Treatment of Traumatic Brain Injury

75 8 women to the placebo group (n=610) and the progesterone group (n=618).

76 bo group and 59 (10%) of 616 patients in the progesterone group (p=0.27).

77 and childhood outcomes, respectively; in the progesterone group the corresponding numbers were 600, 5

78 r on the childhood outcome (cognitive score, progesterone group vs placebo group, 97.3 [SD 17.9] vs 9

79 oliferated in response to estradiol, whereas progesterone had no effect.

80 After correction for multiple outcomes, progesterone had no significant effect on the primary ob

81 ated in the presence of elevated circulating progesterone has remained an enigma since Csapo first th

82 HR = 1.24; 95% CI = 1.07-1.43 and estrogen + progesterone: HR = 1.23; 95% CI = 1.06-1.42).

83 irst theorized of a functional withdrawal of progesterone in 1965.

84 in ERalphaY537S cells and further induced by progesterone in both cell lines.

85 MC growth in a xenograft assay was driven by progesterone in both uterine leiomyoma subtypes.

86 ral ESC/E(Z) complex genes were increased by progesterone in controls only, and decreased by estradio

87 that contribute to the biological actions of progesterone in the normal breast and in breast cancer.

88 us has forced a reexamination of the role of progesterone in the regulation of the female reproductiv

89 ve of this study was to evaluate the fate of progesterone in two natural sediments and the correspond

90 ove the biotransformation of pregnenolone to progesterone in yeast and to regulate CRISPR activity in

91 an elevation in placental expression of the progesterone inactivating enzyme 20-alpha-hydroxysteroid

92 iants examined for 21-hydroxylation of 21-d3-progesterone, indicating that C-H bond breaking is a rat

93 resulted in a lower uterine level of active progesterone-induced blocking factor 1 (PIBF1), and ther

94 re-neoplastic BRCA1(mut/+) tissue attenuated progesterone-induced proliferation.

95 iven mouse breast cancer model, we show that progesterone-induced signalling triggers migration of ca

96 Here, blastocysts could be recovered from progesterone-induced uterine gland (PUGKO) but not wildt

97 Rather, we find that the pregnancy hormone progesterone induces PDK4 (pyruvate dehydrogenase kinase

98 This study examined the hypothesis that progesterone inhibits LH surge and pulsatile secretion v

99 he rate-limiting enzyme in the conversion of progesterone into the neurosteroid allopregnanolone.

100 Progesterone is a steroid hormone that plays a central r

101 ve protection from arrhythmia induction when progesterone is high.

102 d the mechanisms involved in this decline in progesterone level.

103 g PI-based cART showed a reduction in plasma progesterone levels (P= .026) and an elevation in placen

104 Higher (vs lower) progesterone levels and progesterone to estradiol ratios

105 ngs demonstrate that the change in estradiol/progesterone levels from low to high, and not the steady

106 The measurement of progesterone levels in bodily fluids can assist in early

107 posure resulted in a significant increase in progesterone levels in the 3 and 30 ppb groups.

108 ssue distensibility, hydration, and elevated progesterone levels in the Cox-1 null mice at term.

109 Our data suggest that the decrease in progesterone levels observed in HIV-infected pregnant wo

110 ction of migratory CCR7(hi) CD4 T cells, and progesterone levels predict opportunities for HIV to acc

111 Higher (vs lower) progesterone levels were associated with greater reducti

112 Allopregnanolone levels, but not progesterone levels, were negatively associated with dep

113 reversed PI-based cART-induced decreases in progesterone levels.

114 izing enzyme 20alpha HSD and reduced nuclear progesterone levels.

115 of this population positively correlated to progesterone levels.

116 ntribute to these adverse events by altering progesterone levels.

117 Here we report that in vitro progesterone-liganded nuclear PRB forms a complex includ

118 gnenolone sulfate exerted similar effects as progesterone, likely binding to the same site.

119 tra-individual fluctuations in estradiol and progesterone may provide unique insight into the effects

120 These data demonstrate that progesterone mediates a phenotypic change in BAT, which

121 d testosterone), progestins and metabolites (progesterone, medroxyprogesterone acetate, megestrol ace

122 nd placental expression of genes involved in progesterone metabolism in 42 human immunodeficiency vir

123 effect of HIV from that of PI-based cART on progesterone metabolism.

124 3alpha-5alpha-Tetrahydroprogesterone, a progesterone metabolite also known as allopregnanolone,

125 ad previously been analyzed for estrogen and progesterone metabolites and human chorionic gonadotropi

126 Our discovery that sulfated progesterone metabolites are a prognostic indicator for

127 r as a result of increased expression of the progesterone-metabolizing enzyme 20alpha HSD and reduced

128 uantum dots) for ultrasensitive detection of progesterone molecules.

129 ion scores in the second and third estradiol/progesterone months did not significantly differ.

130 ts increased LH pulse frequency and impaired progesterone negative feedback in adult females, mimicki

131 sociation was higher for those with estrogen/progesterone-negative tumors [1.67 (0.91, 3.05) relative

132 primary BAT cultures show a direct impact of progesterone on expression of Ucp1.

133 the influence of testosterone, estradiol and progesterone on initiation and maintenance of hedonic re

134 n, the differential effects of estradiol and progesterone on these uterine leiomyoma subtypes emphasi

135 rs, the effect of estradiol, with or without progesterone, on CIMT progression differed between the e

136 novel observation that treatment with either progesterone or a synthetic analog found in hormonal con

137 pregnant mare serum gonadotropin followed by progesterone or vehicle.

138 f hormone receptor overexpression (androgen, progesterone, or estrogen receptor).

139 mbed to P. aeruginosa challenge earlier than progesterone- or vehicle-supplemented mice (P = 0.0003).

140 mplant (OVX+E) or E implant plus cyclic oral progesterone (OVX+EP).

141 mals receiving estradiol (E) alone or E with progesterone (P).

142 and that ovarian-derived estradiol (E2) and progesterone (P4) are essential for this response.

143 Progesterone (P4) has been used for several decades in e

144 We and others have demonstrated that progesterone (P4) increases CK5+ breast cancer cells.

145 Progesterone (P4) inhibits primordial follicle formation

146 Clasically, progesterone (P4) is known to inhibit the expression of

147 Progesterone (P4) signaling is crucial for the deciduali

148 The mechanisms whereby progesterone (P4), acting via the progesterone receptor

149 Whether progesterone (P4), one of the dominant sex hormones that

150 In addition to their intended use, progesterone (P4)-based contraceptives promote anti-infl

151 secreted (group X) PLA2s in spontaneous and progesterone (P4)-induced AR by using a set of specific

152 Progesterone (P4)-stimulated proliferation resulted in a

153 n (miR-26b-5p) by estrogen was suppressed by progesterone plus PR-A were critical for the PR-A-ER cro

154 Recent studies reported that progesterone prevented premature LH surges during ovaria

155 esults demonstrate that SCAP is required for progesterone production induced by concurrent inhibition

156 enic acute regulatory protein expression and progesterone production.

157 Serum progesterone profiles, myometrium and cervix function, a

158 We assessed plasma levels of progesterone, prolactin, and lipids and placental expres

159 Progesterone promotes the Cxcl1 gradient to favor neutro

160 f the study was to determine whether vaginal progesterone prophylaxis given to reduce the risk of pre

161 ant recurrence, but the status regarding the progesterone receptor (in 54,115 patients) and human epi

162 N1ICD) in the reproductive tract driven by a progesterone receptor (Pgr) -Cre.

163 ble gene 6 (Mig-6) is a critical mediator of progesterone receptor (PGR) action in the uterus.

164 correlates with estrogen receptor (ER+) and progesterone receptor (PGR) expression and longer progre

165 The progesterone receptor (PGR) is a ligand-activated transc

166 status, tumor size, estrogen receptor (ER), progesterone receptor (PgR), human epidermal growth fact

167 r (Gr), mineralocorticoid receptor (Mr), and progesterone receptor (Pgr)] with sets of steroid target

168 Each imaging finding, progesterone receptor (PR) and human epidermal growth fa

169 xpression of the estrogen receptor (ER), the progesterone receptor (PR) and the ERBB2 (also known as

170 Estrogen receptor alpha (ERalpha) and progesterone receptor (PR) are important steroid hormone

171 defined by cancer estrogen receptor (ER) and progesterone receptor (PR) content, and HER2 content (hu

172 Progesterone receptor (PR) is a master regulator in fema

173 Furthermore, we find that while nuclear progesterone receptor (PR) is liganded during human preg

174 Progesterone receptor (PR) is usually co-localized with

175 also led to reduced expression of the ER and progesterone receptor (PR), and diminished responsivenes

176 ms whereby progesterone (P4), acting via the progesterone receptor (PR), inhibits proinflammatory/con

177 tion factor SMAD family member 4 (SMAD4) and progesterone receptor (PR), is necessary to inhibit uter

178 r (ER)-positive breast cancers coexpress the progesterone receptor (PR), which can directly and globa

179 duced Dgcr8 conditional knock-out mice using progesterone receptor (PR)-Cre (Dgcr8(d/d)) and demonstr

180 ry cues, social context, and sex hormones on progesterone receptor (PR)-expressing neurons in the ven

181 Invasive tumors overexpress the short progesterone receptor A (PR-A) isoform.

182 ene and grade and negatively correlated with progesterone receptor and estrogen receptor.

183 e PTBs induced by bacterial endotoxin LPS or progesterone receptor antagonist mifepristone more often

184 Moreover, progesterone receptor antagonist RU-486 partially revers

185 Progesterone receptor antagonist RU-486 were further app

186 However, microinjection of the progesterone receptor antagonist, RU486, into the AVPV r

187 t express estrogen receptor-alpha (Esr1) and progesterone receptor are essential for male but not fem

188 ee energies for three ligands binding to the progesterone receptor are in very good agreement with ex

189 st cancer in which the estrogen receptor and progesterone receptor are not expressed, and human epide

190 Membrane progesterone receptor as well as classical progesterone

191 ers, hyperactive Akt signaling downregulates progesterone receptor B (PRB) transcriptional activity,

192 3) A tendency for decreased expression of progesterone receptor co-activators (NCOA1, -2 and -3, a

193 l and in the neonatal mouse uterus using the progesterone receptor Cre (Pgr-Cre) model.

194 our-cell density involving microRNA-mediated progesterone receptor downregulation, and was reversible

195 r estrogen receptor expression (90%) and for progesterone receptor expression (40%) and had a Ki-67 s

196 tumor was strongly positive for estrogen and progesterone receptor expression and had a Ki-67 score o

197 mical analysis was positive for estrogen and progesterone receptor expression and negative for human

198 ogen receptor expression (50%), negative for progesterone receptor expression, and had a Ki-67 score

199 n in vitro organ culture system to show that progesterone receptor membrane component 1 (PGRMC1) medi

200 Progesterone receptor membrane component-1 (PGRMC1) was

201 positive (OR, 5.17; 95% CI, 1.64 to 17.01), progesterone receptor negative (OR, 2.63; 95% CI, 1.58 t

202 st cancers were diagnosed [3479 estrogen and progesterone receptor positive (ER+PR+); 1021 ER and PR

203 95% CI: 1.20, 4.67; P-heterogeneity with ER+/progesterone receptor positive = 0.06).

204 mone receptor status (oestrogen receptor and progesterone receptor positive vs others), and region.

205 re estrogen receptor positive, 67 (80%) were progesterone receptor positive, and 19 (23%) were human

206 2 of 3, that was estrogen receptor positive, progesterone receptor positive, and HER2 negative.

207 atory breast cancer, and by oestrogen and/or progesterone receptor positivity.

208 tients with luminal B tumors irrespective of progesterone receptor status or baseline Ki-67 expressio

209 0.0001), high tumor grade, negative estrogen/progesterone receptor status, and human epidermal growth

210 e interval (CI), 0.94-1.39], by estrogen and progesterone receptor status, or by ages at first-term b

211 measureable lesion; and known oestrogen and progesterone receptor status.

212 The expression of progesterone receptor target genes including the Indian

213 present characterization of the human sperm progesterone receptor that is conveyed by the orphan enz

214 e progesterone receptor as well as classical progesterone receptor trafficked to the membrane mediate

215 id receptor, mineralocorticoid receptor, and progesterone receptor) and their endogenous ligands.

216 positive family history, estrogen receptor+, progesterone receptor+, and/or human epidermal growth fa

217 ers that are negative for estrogen receptor, progesterone receptor, and ERBB2 (triple-negative breast

218 No biomarker except for estrogen receptor, progesterone receptor, and human epidermal growth factor

219 tumor size and grade, and estrogen receptor, progesterone receptor, and Ki-67 expression levels.

220 ferences were detected in estrogen receptor, progesterone receptor, beta-catenin, or vimentin express

221 histopathologic markers (estrogen receptor, progesterone receptor, Ki-67, human epidermal growth fac

222 id not vary based on age, estrogen receptor, progesterone receptor, or HER2 status.

223 BC does not express estrogen receptor-alpha, progesterone receptor, or the HER2 oncogene; therefore,

224 ncoded by the MKI67 gene, estrogen receptor, progesterone receptor, tumor size, and RS were univariat

225 r (TNBC), as compared to estrogen receptor-, progesterone receptor- or human epidermal growth factor

226 th higher percentages of estrogen receptor-, progesterone receptor-, or ki67-positive mammary epithel

227 we conditionally ablated uterine ALK5 using progesterone receptor-cre mice to define the physiologic

228 al knockout (cKO) of Fst in the uterus using progesterone receptor-cre to study the roles of uterine

229 Women with estrogen receptor- and progesterone receptor-negative (< 10% positive cells by

230 HER2+) tumors and triple-negative (TN) (ER-, progesterone receptor-negative (PR-) and normal HER2) tu

231 cer was found for retinol in relation to ER-/progesterone receptor-negative tumors (OR: 2.37; 95% CI:

232 irmed estrogen receptor (ER)-positive (90%), progesterone receptor-negative, HER2-negative recurrent

233 sided, T2N1, grade 3, estrogen receptor- and progesterone receptor-negative, human epidermal growth f

234 vs hormone receptor-negative [oestrogen and progesterone receptor-negative]), nodal status (0, 1-3,

235 , we examined estrogen receptor-positive and progesterone receptor-positive breast tumors from five p

236 oid reexcision in estrogen receptor-positive progesterone receptor-positive cancer and 63% for estrog

237 patients with estrogen receptor-negative and progesterone receptor-positive cancer).

238 tus (hormone receptor-positive [oestrogen or progesterone receptor-positive or both] vs hormone recep

239 lly confirmed oestrogen receptor-positive or progesterone receptor-positive, or both, locally advance

240 ion of the estrogen responsive genes pS2 and progesterone receptor.

241 ancer and 63% for estrogen receptor-negative progesterone- receptor-negative cancer.

242 primary human MCs lack classical estrogen or progesterone receptors (ER or PR).

243 (TNBC) that lack expression of estrogen and progesterone receptors (ER/PR), or amplification or over

244 ast cancer that is negative for estrogen and progesterone receptors (ER/PR-negative).

245 Here we investigated the mechanisms by which progesterone receptors (PR) and retinoic acid receptors

246 In addition to estrogen and progesterone receptors and human epidermal growth factor

247 arcinoma, strongly positive for estrogen and progesterone receptors and negative for human epidermal

248 C) nuclei, while the region-specific role of progesterone receptors in these nuclei remains unknown.

249 oid receptor family (estrogen, androgen, and progesterone receptors) reveals variation in oligomeriza

250 Devoid of the estrogen and progesterone receptors, along with the receptor tyrosine

251 induced by 3-ketosteroids lacked ERalpha and progesterone receptors, expressed stem cell marker, CD44

252 variant, strongly positive for estrogen and progesterone receptors.

253 physiologic estrogen (17beta-estradiol) and progesterone reciprocally regulate melanin synthesis.

254 nd transmission electron microscopy supports progesterone recognition lead to the generation of bulk

255 nd ARC respectively, which are essential for progesterone regulation of oestrous cyclicity in rats.

256 flammatory condition that is associated with progesterone resistance and cell proliferation, resultin

257 ases proinflammatory, estrogen-dominant, and progesterone-resistant molecular environment of the endo

258 ry for P4 activation and contains a putative progesterone response element (PRE).

259 onfirmed that PGR proteins were recruited on progesterone response element of Gpr64 gene in the uteri

260 we showed that rs2071473 is located within a progesterone-responsive cis-regulatory element that func

261 These results demonstrated that progesterone's inhibitory effect on the GnRH/LH surge an

262 ered 0, 4, 8, 24 and 48 h after removal of a progesterone-secreting pellet).

263 ction effects of hCG and DHT on estrogen and progesterone secretion in CMKLR1 KO mice, but not in WT

264 not the longer PR-B isoform, with increased progesterone sensitivity when PR-A was overexpressed.

265 own as RANKL) is a key paracrine effector of progesterone signaling and that RANKL and its receptor T

266 ting evidence points to amplification of the progesterone signaling axis in precancerous tissue from

267 of luminal progenitor cells, and deregulated progesterone signaling has been implicated in BRCA1-asso

268 We further show that the inhibition of progesterone signaling is caused by hypermethylation of

269 eceptor RANK are downstream effectors of the progesterone signaling pathway.

270 um does not respond properly to estrogen and progesterone signals and remains unreceptive to embryo a

271 When exposed to progesterone-spiked sand, fathead minnows (Pimephales pr

272 o yield 16,17alpha-dihydroxypregnenolone and progesterone, suggesting the presence of an active perfe

273 Three progesterone sulfate compounds, whose concentrations hav

274 Delineation of a progesterone sulfate-TGR5 pruritus axis identifies a the

275 ancy = 29/100), demonstrating that all three progesterone sulfates are prognostic for ICP.

276 Finally, we show mechanistically that progesterone sulfates mediate itch by evoking a Tgr5-dep

277 Concentrations of progesterone sulfates were associated with itch severity

278 a third group of first-trimester samples all progesterone sulfates were significantly elevated in ser

279 ), but not Levonorgestrel, Norethisterone or progesterone, suppressed the anti-HIV effect of TFV by r

280 Progesterone suppresses uterine contractility acting thr

281 the major steroid 21-hydroxylase, converting progesterone to 11-deoxycorticosterone and 17alpha-hydro

282 Higher (vs lower) progesterone levels and progesterone to estradiol ratios were associated with re

283 enstrual cycle by blocking the conversion of progesterone to its 5alpha-reduced neurosteroid metaboli

284 inhibitor dutasteride to block conversion of progesterone to its neurosteroid metabolite allopregnano

285 In vitro, we found the pregnancy hormone progesterone to robustly increase Treg frequencies via p

286 components that account for the capacity of progesterone to target specific subsets of male-pheromon

287 and 17alpha-hydroxyprogesterone (17alpha-OH-progesterone) to 11-deoxycortisol.

288 o the ARC shortened LH pulse interval in the progesterone treated rats.

289 Furthermore, exogenous progesterone treatment inhibited estrous cycles in wild-

290 splantation into wild-type hosts or estrogen/progesterone treatment rescued outgrowth and hormone rec

291 hermore, we found that combinatorial MK-2206+progesterone treatments decreased angiogenesis and proli

292 that 15 microRNAs (miRNAs) are regulated by progesterone via PR-A, but not the longer PR-B isoform,

293 In this work, the detection of progesterone was examined by integrating novel aptamer d

294 Vaginal progesterone was not associated with reduced risk of pre

295 catalyzing the conversion of pregnenolone to progesterone, which is mediated by the inner mitochondri

296 troviral therapy (cART) have lower levels of progesterone, which put them at risk of adverse birth ou

297 Older pregnant mice also had delayed progesterone withdrawal and impaired myometrial function

298 elated to putative mechanisms for functional progesterone withdrawal.

299 creased during menstrual phase and 24 h post-progesterone-withdrawal respectively.

300 s significantly increased at 8 and 24 h post-progesterone-withdrawal.