ライフサイエンスコーパス: FSH

1 FSH activates multiple signaling pathways to regulate ge

2 FSH acts on granulosa cells within the immature follicle

3 FSH aggregation was associated with reduced receptor bin

4 FSH and inhibin B levels correlated with menstrual statu

5 FSH and LH, alone or combined, markedly upregulated ESR3

6 FSH and luteinizing hormone (LH) are secreted constituti

7 FSH and sex steroid levels were not altered.

8 FSH containing this heptapeptide enters the regulated pa

9 FSH first binds to the high-affinity hormone-binding sub

10 FSH glycosylation varies due to inhibition of FSHbeta N-

11 FSH induction of select steroidogenic enzyme mRNAs, incl

12 FSH is a heterodimer consisting of an alpha subunit, als

13 FSH promotes late follicular development, including expr

14 FSH promotes the differentiation and proliferation of GC

15 FSH receptor integrity, and TGFbeta (transforming growth

16 FSH receptor is selectively expressed on the surface of

17 FSH released from the LH secretory pathway rescued ovari

18 FSH via PKA acts to sensitize IRS1 to the tyrosine kinas

19 FSH, a glycoprotein hormone, and the FSH receptor (FSHR)

20 FSH-FSHR signaling was shown to promote HUVEC angiogenes

21 FSH-stimulated ERK phosphorylation on Thr(202)/Tyr(204)

22 FSH-stimulated phosphorylation of YB-1(Ser(102)) is prev

23 ociations between urinary MP or BP and day-3 FSH or AFC, or between urinary MP, PP, or BP and ovarian

24 lue (ptrend) = 0.07] as well as higher day-3 FSH with higher urinary PP tertiles [mean change (95% CI

25 A FSH motif, conserved in 1-Cys Prxs, precedes the active

26 Furthermore: 1) Leptin stimulated PRL/ACTH/FSH- but not LH/TSH-release; 2) adiponectin stimulated P

27 The loss of activin/FSH down-regulation leads to prolonged metestrus-diestru

28 ted by other GPCRs such as beta2-adrenergic, FSH and CXCR4 receptors, but does not affect the beta-ar

29 date the mechanism by which the GPCR agonist FSH via PKA activates the PI3K/AKT cascade.

30 Although FSH levels rise sharply in parallel, a direct effect of

31 In summary, the use of an FSH mutant-occludin peptide conjugate is a feasible nano

32 the data prompt the future development of an FSH-blocking agent as a means of uncoupling bone formati

33 Treatment with an FSH-antiserum, which suppressed primordial follicle form

34 ormed to determine the optimal inhibin B and FSH values for identifying patients with azoospermia.

35 iple hormonal stimuli including estrogen and FSH and demonstrate compromised granulosa cell survival.

36 ized as </= 31 ng/L or more than 31 ng/L and FSH was dichotomized as </= 11.5 mIU/mL or more than 11.

37 The coordinated secretion of LH and FSH are critical for reproductive functions.

38 Risk of lower testosterone and higher LH and FSH levels was significantly increased for TCSs at all t

39 ide mass increased from 1482 to 2327, LH and FSH receptor-binding affinities of the dual-specificity

40 ORs for increased LH and FSH were 4.4 (95% CI, 3.1 to 6.5) and 18.9 (95% CI, 11.0

41 entrations (estradiol, progesterone, LH, and FSH; P < 0.05) and positively associated with the risk o

42 ted the respective roles of both oocytes and FSH in the transition of preantral granulosa cells to cu

43 ovary that antagonizes activin signaling and FSH synthesis in the pituitary.

44 ection fraction <55%, menopausal status, and FSH were not associated with BNP and NT-proBNP.

45 xenograft tumors, after perfusion with anti-FSH-receptor antibodies coupled to colloidal gold, showe

46 the stimulatory action of CREB to attenuate FSH beta transcription at high GnRH pulse frequencies, t

47 binding domain, mutation of which attenuates FSH/cAMP-induced Cyp19a1 mRNA accumulation.

48 SH) receptor expression, which then augments FSH-mediated follicle growth and development.

49 On binding, FSH undergoes a concerted conformational change that aff

50 We show that the FSH antibody binds FSH specifically and blocks its action on osteoclast for

51 e 9-beta-d-arabinofuranoside (araA), blocked FSH- or AR-induced meiotic resumption and ACC phosphoryl

52 87877), or the MEK inhibitor PD98059 blocked FSH-dependent ERK(Thr(202)/Tyr(204)) phosphorylation, de

53 Both FSH and PKA-CQR stimulated the phosphorylation of protei

54 rn analysis demonstrated active AMPK in both FSH- or AR-treated GV-stage oocytes within 6 h.

55 Prolonged AKT activation by FSH stimulation of the FSH receptor (FSHR) promotes gank

56 Stimulation of GCs by FSH leads to their proliferation and differentiation, ev

57 B-1(S102A) mutant prevented the induction by FSH of Egfr, Cyp19a1, Inha, Lhcgr, Cyp11a1, Hsd17b1, and

58 research focused on the phosphoregulation by FSH of ERK within GCs.

59 85% of transcripts that were up-regulated by FSH were increased to a comparable extent by PKA-CQR and

60 the transcripts that were down-regulated by FSH, 76% were also down-regulated by PKA-CQR.

61 Transcripts regulated similarly by FSH and PKA-CQR are involved in steroidogenesis and diff

62 ned at an immature stage until stimulated by FSH secreted by pituitary gonadotropes.

63 To characterize FSH glycosylation, FSH isoforms in pituitary gland extra

64 We suggest that high circulating FSH causes hypogonadal bone loss.

65 females had increased levels of circulating FSH and higher expression of the Fshb subunit in the pit

66 ting in the regulated (LH) and constitutive (FSH) secretion pathways.

67 In contrast, FSH stimulated the phosphorylation of p38 MAP kinase but

68 that FSHR binds Asnalpha(52)-deglycosylated FSH at a 3-fold higher capacity than fully glycosylated

69 of glycosylated FSH, but not deglycosylated FSH, would increase 3-fold, and that the dissociated mon

70 Immunoelectron microscopy was used to detect FSH receptor in mouse tumors.

71 epitopes and in situ hybridization to detect FSH receptor in tissue samples from patients with a wide

72 noclonal antibodies that recognize different FSH receptor epitopes and in situ hybridization to detec

73 Thus, while biologically active dimeric FSH and LH can be produced by the human fetal pituitary

74 The combination of low-dose FSH with tamoxifen (TamFSH-IVF) or letrozole (Letrozole-

75 ries, but the decline was restored by either FSH or LH replacement on D4 afternoon.

76 ypogonadal bone loss despite having elevated FSH, suggesting that TNFalpha is critical to the effect

77 ility may develop in the context of elevated FSH levels thereby closely mimicking the hallmark featur

78 ition that has been associated with elevated FSH in women.

79 oss is caused, at least in part, by enhanced FSH secretion, which in turn increases TNFalpha producti

80 Overexpression of GAB2 enhances FSH-stimulated AKT phosphorylation.

81 exist between glycoforms of human and equine FSH.

82 In all 1336 patients examined, FSH receptor was expressed by endothelial cells in tumor

83 rkably, supplying a single dose of exogenous FSH activity to Fshb(-/-) females is sufficient to incre

84 The tumor lymphatic vessels did not express FSH receptor.

85 The endothelial cells that expressed FSH receptor were located at the periphery of the tumors

86 n profiles of lutropin (LH) and follitropin (FSH) differ.

87 monstrate that beta-catenin is essential for FSH/cAMP-regulated gene expression in the ovary, identif

88 , one at alphaAsn52, the critical glycan for FSH function, and the other at betaAsn24.

89 eported that ERK activation is necessary for FSH to induce key genes that define the preovulatory GC.

90 ERK/RSK-2 signaling pathway is necessary for FSH-mediated expression of target genes required for mat

91 The results for FSH/FSHR were analyzed on the basis of the crystal struc

92 esults demonstrate an unanticipated role for FSH in establishing the signaling axis that coordinates

93 re we identify a previously unknown role for FSH in this signaling cascade.

94 The specificity for FSH was 74.1%, and the positive predictive value was 65.

95 similarly to mesenchymal cells isolated from FSH receptor (FSHR)(-/-) mice.

96 ion of YB-1(Ser(102)) in the absence of FSH; FSH did not further increase YB-1(Ser(102)) phosphorylat

97 completely restored their ovarian function (FSH < 10 IU/L), but the anti-Mullerian hormone values we

98 rast to the alpha and LH beta subunit genes, FSH beta subunit transcription is preferentially stimula

99 fold higher capacity than fully glycosylated FSH.

100 r into monomers, the binding of glycosylated FSH, but not deglycosylated FSH, would increase 3-fold,

101 To characterize FSH glycosylation, FSH isoforms in pituitary gland extracts and a variety o

102 higher LH levels at both surveys and higher FSH at SI.

103 We have shown that the pituitary hormone FSH, the levels of which are high during late perimenopa

104 n [indicative of follicle stimulant hormone (FSH) dependence] and increased sensitivity to FSH.

105 Follicle stimulating hormone (FSH) acts through receptors (FSHR) on the Sertoli cell t

106 Serum follicle-stimulating hormone (FSH) and E2 were measured at baseline and over 2 years.

107 rmones such as follicle-stimulating hormone (FSH) and estrogen.

108 monitoring of follicle-stimulating hormone (FSH) and inhibin A and B levels.

109 the levels of follicle-stimulating hormone (FSH) and inhibin B are correlated with sperm concentrati

110 by regulating follicle-stimulating hormone (FSH) and luteinizing hormone (LH) gene expression in the

111 signaling and follicle-stimulating hormone (FSH) and luteinizing hormone (LH) secretion.

112 ropic hormones follicle-stimulating hormone (FSH) and luteinizing hormone (LH), and that ovarian ster

113 gonadotropin's follicle-stimulating hormone (FSH) and luteinizing hormone (LH), both of which are het

114 gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), under the control of

115 hormone (LH), follicle-stimulating hormone (FSH) and sex hormone-binding globulin (SHBG) levels were

116 Follicle-stimulating hormone (FSH) and syt-9 are highly co-localized in female, but no

117 the roles that follicle-stimulating hormone (FSH) and testosterone play in regulating spermatogenesis

118 Follicle-stimulating hormone (FSH) and the EGF-like peptide, amphiregulin (AR), are po

119 between human follicle-stimulating hormone (FSH) and the N-terminal hormone-binding fragment of the

120 Follicle-stimulating hormone (FSH) glycosylation is regulated by feedback from the gon

121 and levels of follicle-stimulating hormone (FSH) in the postmenopausal range.

122 ly showed that follicle-stimulating hormone (FSH) induces the expression of an 80-kDa AKAP (AKAP 80)

123 Follicle-stimulating hormone (FSH) is an essential regulator of gonadal function and f

124 Follicle-stimulating hormone (FSH) is central to reproduction in mammals.

125 Follicle stimulating hormone (FSH) is one of the important hormones that regulate gona

126 lly engineered follicle-stimulating hormone (FSH) mutant protein was produced in Spodoptera furgiperd

127 a recombinant follicle-stimulating hormone (FSH) mutant, which serves as its 'carrier'.

128 e GPCR agonist follicle-stimulating hormone (FSH) promotes the protein kinase A (PKA)-dependent phosp

129 ollitropin, or follicle-stimulating hormone (FSH) receptor (FSHR), is a G protein-coupled receptor be

130 rogens enhance follicle-stimulating hormone (FSH) receptor expression, which then augments FSH-mediat

131 lt humans, the follicle-stimulating hormone (FSH) receptor is expressed only in the granulosa cells o

132 Follicle-stimulating hormone (FSH) regulates follicular growth and stimulates estrogen

133 ase A (PKA) by follicle stimulating hormone (FSH) transduces the signal that drives differentiation o

134 ng hormone and follicle-stimulating hormone (FSH), act through their cognate receptors to initiate a

135 hormone (AMH), follicle-stimulating hormone (FSH), and inhibin B and urinary level of FSH.

136 gonadotropins, follicle-stimulating hormone (FSH), and luteinizing hormone (LH).

137 rve were day-3 follicle-stimulating hormone (FSH), antral follicle count (AFC), and ovarian volume.

138 erved close to follicle-stimulating hormone (FSH), luteinizing hormone (LH) and growth hormone (GH) c

139 hormone (LH), follicle-stimulating hormone (FSH), prolactin, fasting plasma glucose, and insulin lev

140 NP, NT-proBNP, follicle-stimulating hormone (FSH), total testosterone, and sex hormone-binding globul

141 controlled by follicle-stimulating hormone (FSH), which regulates transcription of the aromatase gen

142 mone (LH), and follicle-stimulating hormone (FSH), which were measured < or =8 times/cycle, and incid

143 expression of follicle-stimulating hormone (FSH)- and testosterone-induced target genes.

144 teraction with follicle-stimulating hormone (FSH)-driven proliferation in ovarian cancer has been stu

145 rmone (LH) and follicle stimulating hormone (FSH).

146 erum levels of follicle-stimulating hormone (FSH).

147 actor (EGF) or follicle-stimulating hormone (FSH).

148 rmone (LH) and follicle-stimulating hormone (FSH)], with adrenocorticomelanotropic cells [corticotrop

149 re (POF) rate (follicle-stimulating hormone [FSH] >/= 40 IU/L) after 1 year of follow-up.

150 deduced and compared between horse and human FSH preparations.

151 a partially deglycosylated complex of human FSH bound to the extracellular hormone-binding domain of

152 Use of human FSH/thyroid-stimulating hormone (TSH) receptor chimeras

153 Currently, purified and recombinant human FSH are the only FSH receptor (FSH-R) agonists available

154 rminal hormone-binding fragment of the human FSH receptor (FSHR) extracellular domain (ECD).

155 ction in Y1 cells transfected with the human FSH-R (EC50 = 980 nm) and estradiol production from prim

156 e agonists (EC50's = 20 microm) of the human FSH-R.

157 53)) of the FSHR ECD identified in the human FSH.FSHR ECD crystal structure as contact sites with the

158 er, these results support a role for AMPK in FSH and AR-induced maturation in vitro and hCG-induced m

159 UCC-555) caused a dose-dependent decrease in FSH levels in ovariectomized mice.

160 eclined significantly, while the decrease in FSH receptor-binding affinity for eFSH was not significa

161 rmone (AMH) and inhibin B and an increase in FSH with age corresponding to the experimental data.

162 ligands, could play more important roles in FSH synthesis than GnRH.

163 GDF9 exposure increased FSH secretion in rat primary pituitary cells.

164 dly elevated inhibin B was unable to inhibit FSH secretion, indicating a status of pituitary inhibin

165 However, these low levels (0.005 or 0.025 IU FSH/ml) suppressed expression of Slc38a3 and Amh, two tr

166 e the clinico-endocrinological profiles (LH, FSH, SHBG, DHEAS, and testosterone levels) of men with e

167 d PRL-, inhibited ACTH- and did not alter LH/FSH/TSH-release; and 3) resistin increased ACTH-release

168 The mean FAI and LH/FSH ratio were was also increased in the AGA group.

169 reased ACTH-release and did not alter PRL/LH/FSH/TSH-secretion.

170 The LH/FSH ratio was not significantly different among the PCOS

171 etition experiments with the cognate ligand, FSH, indicated that the interaction at the FSHR-ECD usin

172 ional regulation is critical for maintaining FSH levels within a narrow physiological range.

173 The mean FSH values were higher in the control group than in the

174 d cyclin D1 expression, ultimately mediating FSH-driven ovarian cancer cell proliferation.

175 The small molecule FSH receptor agonists described here could lead to an or

176 Because most FSH is constitutively secreted, tight transcriptional re

177 gonadotrope cells, mice make essentially no FSH and females are sterile.

178 Neither serum inhibin B nor FSH is a suitable surrogate for determination of sperm c

179 Neither FSHbeta nor FSH receptor (FSHR) null mice have bone loss despite sev

180 ng, SMAD4, is absolutely required for normal FSH synthesis in both male and female mice.

181 EGF required the presence of oocytes but not FSH during the culture period.

182 erwent expansion in response to EGF, but not FSH.

183 Knockdown of PP1beta blocks the ability of FSH to activate PI3K in the presence of endogenous IGF-1

184 /Tyr(204)) phosphorylation in the absence of FSH to levels comparable with ERK phosphorylated in the

185 ively dephosphorylates ERK in the absence of FSH, allowing MEK-phosphorylated ERK to accumulate in th

186 IGF1 receptor (IGF1R) but, in the absence of FSH, fails to stimulate YXXM phosphorylation of IRS1 (in

187 We report that in the absence of FSH, granulosa cells secrete a subthreshold concentratio

188 rylation of YB-1(Ser(102)) in the absence of FSH; FSH did not further increase YB-1(Ser(102)) phospho

189 tion, suggesting that the skeletal action of FSH is estrogen independent.

190 e formation, a yet uncharacterized action of FSH that we report herein.

191 ad become established between the actions of FSH and androgen through the Sertoli cells.

192 otein kinase A (PKA) mediates the actions of FSH by signaling through multiple targets to activate PI

193 ulogenesis and fertility, the development of FSH mimetics has been sought to treat infertility.

194 were cultured with or without a low dose of FSH (0.005 IU/ml) and isolated PAGCs were cultured with

195 FSH required prior exposure to low doses of FSH.

196 g that TNFalpha is critical to the effect of FSH on bone mass.

197 rise sharply in parallel, a direct effect of FSH on the skeleton has never been explored.

198 umulus cells, suggesting opposing effects of FSH on cumulus cell differentiation.

199 quired for this transition-and expression of FSH receptors (FSHR), which reflects the degree of bioch

200 NT5a acts to down-regulate the expression of FSH-responsive genesin vitro, and corresponding increase

201 Within 3 h of FSH treatment, phospho-acetyl CoA carboxylase (ACC) leve

202 Given the importance of FSH in regulating folliculogenesis and fertility, the de

203 ne (FSH), and inhibin B and urinary level of FSH.

204 ng/mL; P = .01) and decreased mean levels of FSH (4.02 [2.69] vs 5.66 [1.93] mIU/mL; P < .001) and SH

205 n analysis was performed and serum levels of FSH and inhibin B were measured in 275 adult male surviv

206 ould be replaced without significant loss of FSH binding, while cAMP signaling potency was diminished

207 In contrast, the majority of FSH is secreted constitutively with an incremental incre

208 rylated ERK to accumulate in the presence of FSH because of inactivation of the phosphatase.

209 e with ERK phosphorylated in the presence of FSH.

210 th reduced TSH biopotency, over-secretion of FSH at neonatal minipuberty and macroorchidism from 3 ye

211 The recently resolved crystal structure of FSH bound to the entire FSHR ectodomain has been instrum

212 We report the crystal structure of FSH in complex with the entire extracellular domain of F

213 through which the glycosylation variants of FSH may exert distinct and differential effects at the t

214 t testicular parameters is more dependent on FSH action than androgen action mediated through the Ser

215 numbers and spermatogenesis are dependent on FSH and androgen action through the Sertoli cells.

216 nd GnRH pulse frequency-dependent effects on FSH beta transcription.

217 ified and recombinant human FSH are the only FSH receptor (FSH-R) agonists available for infertility

218 expansion transcripts in response to EGF or FSH (0.5 IU/ml).

219 n oral alternative to the current parenteral FSH treatments used clinically to induce ovarian stimula

220 With two to four N-glycans per FSH molecule, many combinations of charges distributed o

221 down-regulation of activin-induced pituitary FSH release.

222 (and higher circulating levels) of pituitary FSH, while faster pulses favor LH release.

223 Ascorbic acid may prevent FSH-induced hypogonadal bone loss by modulating the cata

224 cles of Fshb(-/-) mice, which cannot produce FSH, have a severely impaired ability to support two ess

225 endocrine changes were not observed; rather FSH, LH, inhibin B, and anti-Mullerian hormone were temp

226 mbinant human FSH are the only FSH receptor (FSH-R) agonists available for infertility treatment.

227 necting miR-7 genomic circuits that regulate FSH and LH synthesis and secretion through their effects

228 ian cystadenomas and that gankyrin regulates FSH upregulation of cyclin D1.

229 Interestingly, the rerouted FSH enhanced ovarian follicle survival, caused a dramati

230 Furthermore, the rerouted FSH vastly improved the in vivo fertilization competency

231 l and biological activities in the resulting FSH isoform preparations are generally attributed to cha

232 ce as efficiently as constitutively secreted FSH.

233 oblotting techniques involving four separate FSH-receptor-specific monoclonal antibodies that recogni

234 neral linear model was used to assess serial FSH by OFR.

235 Among AI-naive patients, serial FSH significantly increased over time (P < .001), did no

236 Women with high serum FSH values (>10 mIU/mL [n = 83]) did not have a signific

237 s11031006-G was associated with higher serum FSH levels, earlier age at menarche, earlier age at firs

238 factor beta (TGFbeta) superfamily, stimulate FSH synthesis; yet, their relative roles and mechanisms

239 A signaling and decrease activin-stimulated FSH synthesis.

240 9 results in diminished basal and stimulated FSH secretion only in females, resulting in alterations

241 e associated with high follicle-stimulating (FSH) and luteinizing (LH) hormone levels.

242 a Galpha(s)-dependent signal that suppressed FSH biosynthesis.

243 erone) levels was assessed with chi(2) test (FSH) or ordinal logistic regression analysis and express

244 expression and RNAi studies demonstrate that FSH- and cAMP-dependent regulation of this promoter is s

245 We find that FSH directly stimulates TNFalpha production from bone ma

246 We hypothesized that FSH via PKA enhances ERK phosphorylation by inhibiting t

247 These studies show that FSH induces an increase in EGFR expression during late f

248 We show that FSH is required for hypogonadal bone loss.

249 Our results show that FSH promotes an increase in the phosphorylation of YB-1

250 Together, these results suggest that FSH-stimulated ERK activation in GCs requires the PKA-de

251 This suggests that FSH negatively regulates osteoblast number.

252 The FSH-FSHR(HB) complexes form dimers in the crystal and at

253 FSH, a glycoprotein hormone, and the FSH receptor (FSHR), a G protein-coupled receptor, play

254 , thus, seems to coordinate signals from the FSH-stimulated rise in cAMP that leads to activation of

255 ts its sTyr (i.e., sulfated Tyr335) into the FSH nascent pocket, eventually leading to receptor activ

256 When injected into ovariectomized mice, the FSH antibody attenuates bone loss significantly not only

257 ce within the receptor-binding domain of the FSH beta-subunit.

258 as expected from a negative regulator of the FSH hormone.

259 ged AKT activation by FSH stimulation of the FSH receptor (FSHR) promotes gankyrin expression, which,

260 e focused on two downstream effectors of the FSH signal, cAMP and the orphan nuclear receptor steroid

261 on the basis of the crystal structure of the FSH.FSHR ECD complex, and comparative modeling was used

262 We show that the FSH antibody binds FSH specifically and blocks its actio

263 s coupled to colloidal gold, showed that the FSH receptor is exposed on the luminal endothelial surfa

264 lliculogenesis and provide evidence that the FSH-dependent increase is necessary for EGFR physiologic

265 Finally, we find that the FSH-mediated up-regulation of reporter activities for LH

266 ICER binds to the FSH beta CRE site to reduce CREB occupation and abrogate

267 t BTB integrity in vivo, was inserted to the FSH mutant by polymerase chain reaction (PCR), as well a

268 , FSHR-1, which shares equal identity to the FSH, LH, and TSH receptors from mammals.

269 did not compete with FSH for binding to the FSH-R.

270 aling corridor necessary for transducing the FSH signal.

271 ring surgery performed to remove tumors, the FSH receptor was not expressed in the normal tissues loc

272 Thus, it remains open whether the FSH-FSHR activation has a direct regulatory role in the

273 al cells isolated from mice treated with the FSH antibody show greater osteoblast precursor colony co

274 cyclic AMP response element (CRE) within the FSH beta promoter resulted in the loss of preferential G

275 in an increased regulated secretion of this FSH analog compared with wild-type FSH.

276 When this FSH mutant-occludin peptide conjugate was administered t

277 activity but was still capable of binding to FSH receptors, which are restricted to Sertoli cells in

278 n response to FSH requires prior exposure to FSH during development, while oocyte-derived factors alo

279 itions, rat GCs differentiate in response to FSH but do not proliferate unless activin is also presen

280 MAPK14 and undergo expansion in response to FSH required prior exposure to low doses of FSH.

281 ability to undergo expansion in response to FSH requires prior exposure to FSH during development, w

282 tiate the complex program of GC responses to FSH.

283 important role in gonadal responsiveness to FSH.

284 SH) dependence] and increased sensitivity to FSH.

285 n of this FSH analog compared with wild-type FSH.

286 Women with high urinary FSH values (>11.5 mIU/mg creatinine [n = 69]) did not ha

287 In contrast to positive control VEGF, FSH treatment showed no effects on tube formation, nitri

288 ith full efficacy compared with FSH that was FSH-R-selective and -dependent.

289 At proestrus, when FSH levels were decreased in Mutants, ovaries contained

290 lting in an array of glycans associated with FSH preparations derived from pools of pituitary or urin

291 H-IVF) or letrozole 5 mg in combination with FSH (Letrozole-IVF).

292 C50 = 2 nm) with full efficacy compared with FSH that was FSH-R-selective and -dependent.

293 s and related compounds did not compete with FSH for binding to the FSH-R.

294 mide-1-beta-d-ribofuranoside (AICAR) or with FSH or AR, and this staining was eliminated by compound

295 e expression profiles of GCs stimulated with FSH or expressing PKA-CQR, a constitutively active mutan

296 treated with EGF, but not those treated with FSH increased Has2, Ptgs2 and Ptx3 mRNAs to 17-96% of th

297 iated with expansion, they were treated with FSH or EGF and co-cultured with fully-grown oocytes secr

298 Treatment with FSH and increasing concentrations of exogenous IGF-1 tri

299 COCs expanded in vitro with FSH or EGF underwent the same changes, whereas those exp

300 of genes involved in signaling through Wnt, FSH, parathyroid hormone (PTH), oxytocin, and calcineuri