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 is expressed predominantly in the vasculature in pat

14 FSH promotes late follicular development, including expr

15 FSH promotes the differentiation and proliferation of GC

16 FSH receptor integrity, and TGFbeta (transforming growth

17 FSH receptor is selectively expressed on the surface of

18 FSH released from the LH secretory pathway rescued ovari

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

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

21 FSH-FSHR signaling was shown to promote HUVEC angiogenes

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

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

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

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

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

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

28 ne thyrostimulin and design of a long-acting FSH.

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

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

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

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 as associated with slower increase in LH and FSH and decrease in AMH.

38 secretion of pituitary gonadotropins LH and FSH and impairment of reproductive function.

39 ecretion of the gonadotropic hormones LH and FSH and is critical for fertility.

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

41 Both LH and FSH increased until ~ 5 and 7 years postmenopause, respe

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

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

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

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

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

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

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

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

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

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

52 eference and E2-treated animals, and between FSH-treated and nontreated animals.

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

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

55 87877), or the MEK inhibitor PD98059 blocked FSH-dependent ERK(Thr(202)/Tyr(204)) phosphorylation, de

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

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

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

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

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

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

62 85% of transcripts that were up-regulated by FSH were increased to a comparable extent by PKA-CQR and

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

81 Overexpression of GAB2 enhances FSH-stimulated AKT phosphorylation.

82 exist between glycoforms of human and equine FSH.

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

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

85 ites were divided and treated with exogenous FSH.

86 artially rescued by treatment with exogenous FSH.

87 The tumor lymphatic vessels did not express FSH receptor.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

102 fold higher capacity than fully glycosylated FSH.

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

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

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

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

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

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

109 is the use of follicle stimulating hormone (FSH) analogs which improved sperm numbers and motility i

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

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

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

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

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

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

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

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

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

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

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

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

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

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

124 kg/m(2) and a follicle-stimulating hormone (FSH) concentration of 3.0-20.0 mIU/mL or, if no FSH meas

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

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

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

128 with exogenous follicle-stimulating hormone (FSH) is capable of rescuing phenotypes associated with c

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

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

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

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

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

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

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

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

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

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

139 Estrogen, follicular stimulating hormone (FSH), and luteinizing hormone (LH) levels were measured.

140 trogen (E2), follicular stimulating hormone (FSH), and luteinizing hormone (LH) were measured.

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

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

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

144 tration, serum follicle stimulating hormone (FSH), luteinizing hormone (LH) and testosterone levels o

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

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

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

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

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

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

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

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

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

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

155 deduced and compared between horse and human FSH preparations.

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

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

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

159 e higher in the suppressor line, implicating FSH in feedback control of GSL flux.

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

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

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

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

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

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

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

167 terised changes in reproductive hormones-LH, FSH, SHBG and AMH-by chronological age and time around t

168 ronological age contribute to changes in LH, FSH, SHBG and AMH across mid-life in women, and BMI, smo

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

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

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

172 e pituitary tumor patients [gonadotropic (LH/FSH-secreting) = 17; prolactinomas (PRL-secreting) = 11,

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

174 od from luteinizing/follicle-stimulating (LH/FSH)-secreting (n = 24), prolactinomas (n = 14), and non

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

176 Compared to LH/FSH-secreting tumors, PRL-secreting tumors showed statis

177 non-functional subtypes when compared to LH/FSH-secreting tumors.

178 rection) only in serum when compared with LH/FSH-secreting tumor patients (0.269 +/- 0.139/0.167 +/-

179 When compared with LH/FSH-secreting tumors, ACTH-secreting tumors showed stati

180 ated with reduced Th17 frequencies and lower FSH and LH concentrations, as compared to NET-EN and COC

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

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

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

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

185 Because most FSH is constitutively secreted, tight transcriptional re

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

187 ) concentration of 3.0-20.0 mIU/mL or, if no FSH measurement was available, an anti-mullerian hormone

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

204 FSH required prior exposure to low doses of FSH.

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

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

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

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

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

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

211 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

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

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

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

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

216 e with ERK phosphorylated in the presence of FSH.

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

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

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

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

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

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

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

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

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

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

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

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

229 lycoprotein hormones that suppress pituitary FSH production.

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

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

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

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

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

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

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

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

238 ce as efficiently as constitutively secreted FSH.

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

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

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

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

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

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

245 A signaling and decrease activin-stimulated FSH synthesis.

246 9 results in diminished basal and stimulated FSH secretion only in females, resulting in alterations

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

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

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

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

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

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

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

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

255 This suggests that FSH negatively regulates osteoblast number.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

271 aling corridor necessary for transducing the FSH signal.

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

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

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

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

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

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

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

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

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 ed with the patients that were responsive to FSH therapy versus those that were non-responsive.

284 important role in gonadal responsiveness to FSH.

285 SH) dependence] and increased sensitivity to FSH.

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

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

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

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

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

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

292 tions, as compared to NET-EN and COCPs, with FSH concentrations and Th17 frequencies correlating sign

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

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

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

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

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