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Cultured cells expressed the FSH receptor. Paper-12143837.
Both normal and hpg mouse testes expressed FSHR(+) mRNA. Paper-9636168.
Main outcome measures were response to CC and FSHR genotype. Paper-13889428.
USF family members inhibit FSH-R gene activity by acting via these elements. Paper-10561105.
OBJECTIVE: To evaluate the association between FSH efficacy and FSHR alleles. Paper-9981327.
The LHR and FSHR genes are very large and contain 10 and 11 exons respectively. Paper-1706359.
We suggest that mutations in FSHR gene are rare in women with POF in Argentine. Paper-10519884.
These give rise to different FSHR haplotypes that modify the action of FSH. Paper-11127110.
The FSHR gene spans a region of 54 kb and consists of 10 exons and 9 introns. Paper-623895.
To this aim, the possible role of three FSHR SNP was evaluated in male infertility. Paper-12356875.
Exon 7 of the FSHR gene was first amplified using a pair of biotinylated primers. Paper-1676605.
INTERVENTION(S): Exon 10 of the FSHR gene was screened for the G2105A/S680N mutation. Paper-9037531.
FSH concentrations did not differ between FSHR polymorphisms or between ethnic groups. Paper-15924970.
FSH concentrations did not differ between FSHR polymorphisms or between ethnic groups. Paper-15172531.
The half-life of hFSHR mRNA was 3.6 +/- 0.2 h by NPA and 3.1 +/- 0.1 h by RT-PCR. Paper-10711754.
It has been found recently that the FSHR knockout mouse exhibits hypertension. Paper-12085301.
FSH regulates normal ovarian follicle development and spermatogenesis through FSHR. Paper-13188485.
Expression of the human follicle-stimulating hormone receptor in the baculovirus system. Paper-102371.
Importantly, 14-3-3tau co-immunoprecipitated with FSHR stably expressed in HEK 293 cells. Paper-10480884.
Unoccupied FSHR exhibited strong fluorescence resonance energy transfer profiles in situ. Paper-13188485.
Recently, single-nucleotide polymorphisms ( SNPs) have been assigned to the FSHR gene. Paper-11127110.
Silencing of Fshr occurs through a conserved, hypersensitive site in the first intron. Paper-11156606.
Oocyte donation is an effective infertility treatment for women with FSHR mutations. Paper-9349959.
In males, homozygous inactivation of the FSH receptor can also be associated with infertility. Paper-1506477.
CONCLUSION: Hormone-refractory prostate cancer cells express FSH and biologically active FSHR. Paper-1749289.
MAIN OUTCOME MEASURE: DNA sequencing of the hFSHR gene was the main outcome measure. Paper-13278194.
The influence of FSH receptor ( FSHR) variants on male infertility is not completely understood. Paper-15100087.
In contrast, the significance of FSHR R gene SNP in the male is poorly understood. Paper-12356875.
Human granulosa cells, the site of FSHR expression in the ovary, were found to contain 14-3-3tau. Paper-10480884.
Properties of follicle-stimulating-hormone receptor in cell membranes of bovine testis. Paper-2392200.
The expression of FSHR in isolated caprine follicles increased from the preantral to antral phase. Paper-16042771.
FSHR was found to have a distinguished role in precipitation of epithelial ovarian cancer. Paper-13278557.
Characterization of the 5' flanking region of the human follicle-stimulating hormone receptor gene. Paper-7902286.
FSHR was identified in PC3 and Du145 cells, as well as in human adenocarcinoma of the prostate. Paper-1749289.
There were no indications for an expression of tissue-specific isoforms of FSHR in testis and ovary. Paper-12232881.
In conclusion, we did not identify inactivating mutations in exons 6, 7, 9, and 10 of the FSHR gene. Paper-12866118.
Current literature shows that perimenopausal ovarian surface epithelium (OSE) can also express FSHR. Paper-10797853.
The size of the FSH-R reverse transcription-PCR product was the same as in normal ovarian follicles. Paper-8627328.
Absence of 566C>T mutation in exon 7 of the FSHR gene in Indian women with premature ovarian failure. Paper-13748556.
FSHR gene polymorphisms influence bone mineral density and bone turnover in postmenopausal women. Paper-15178255.
This finding showed that the combination of heterozygous FSHR can be responsible for male infertility. Paper-14066927.
These results suggest that photoperiod regulates FSH receptor numbers particularly in the testis. Paper-7753293.
Evidence for cycle-dependent expression of follicle-stimulating hormone receptor in human endometrium. Paper-11475605.
As expected, the 5A FSH-R-mediated cAMP accumulation was enhanced, and its internalization was reduced. Paper-12289852.
In the ovary, they can help in follicular maturation and ovulation by inducing the FSH receptor ( FSHR). Paper-10797853.
Follicle-stimulating hormone (FSH) mediated by its receptor ( FSHR) is pivotal for normal gametogenesis. Paper-15120407.
In this system, the rat Sertoli cell membrane FSH receptor also showed a molecular mass of 240 kDa. Paper-7315600.
ActD caused a time-dependent decrease in FSHR mRNA content in hFSHR-Y1 cell lines with a lag time of 1 h. Paper-10711754.
Cryptic FSH binding sites in the LRD may enable alternate spliced forms of the FSHR to interact with FSH. Paper-12370475.
FSH concentrations did not differ between the various ethnic groups, or the different FSHR polymorphisms. Paper-15924970.
FSH concentrations did not differ between the various ethnic groups, or the different FSHR polymorphisms. Paper-15172531.
The FSHR mRNA isoforms had a similar migration pattern for the normal ovary and the granulosa cell tumors. Paper-8596161.
Follitropin and the follitropin receptor are essential for normal gamete development in males and females. Paper-9403883.
Ovarian hyperstimulation syndrome (OHSS) due to mutations in the follicle-stimulating hormone receptor. Paper-15098077.
Follicle stimulating hormone receptor in ovarian surface epithelium and epithelial ovarian cancer. Paper-14462561.
In females, inactivating mutations in the FSHR result in ovarian dysgenesis with amenorrhea and infertility. Paper-15083507.
A rational pharmacogenetic approach that combines FSH dose according to the FSHR haplotype is envisaged. Paper-11127110.
The FSHR gene variations Asn680Ser as well as Ile160Thr may be contributing factors in unexplained sterility. Paper-12671846.
Follicle-stimulating hormone receptor gene haplotype distribution in normozoospermic and azoospermic men. Paper-11761546.
Using a single-strand RNA probe, we demonstrated that FSHR mRNA expression is strongest in Graafian follicles. Paper-458676.
We have examined the entire open reading frame of the FSH receptor gene in ovarian granulosa cell tumors. Paper-1887276.
The FSH receptor levels per testis were significantly lower in cryptorchidism than in control testes. Paper-5436451.
We can now conclude that FSH is present in Sertoli cells and in round germinal cells, both expressing the FSHR. Paper-1529441.
The cloning of the human follicle stimulating hormone receptor and its expression in COS-7, CHO, and Y-1 cells. Paper-7539170.
However, following cell permeabilization all four antibodies stained hFSH-R in Golgi and endoplasmic reticulum. Paper-8447471.
A high frequency of two polymorphisms that are in linkage disequilibrium was found in exon 10 of the FSHR gene. Paper-12866118.
Age at natural menopause is not linked with the follicle-stimulating hormone receptor region: a sib-pair study. Paper-10395579.
Ontogeny of follicle-stimulating hormone receptor gene expression in isolated human ovarian follicles. Paper-1217327.
Follicle-stimulating hormone receptor polymorphisms in women with normogonadotropic anovulatory infertility. Paper-10127349.
Activation of the FSHR leads to the phosphorylation of residues in the first and third intracellular loops. Paper-9974123.
Residues in both ends of the iL3 are important for signal transduction in a number of GPCRs, including the FSHR. Paper-12370463.
These findings contradict the hypothesized role of FSH as a risk factor in ovarian carcinogenesis. Paper-13872681.
Gonads in trouble: follicle-stimulating hormone receptor gene mutation as a cause of inherited streak ovaries. Paper-532907.
This mutation has previously been associated with intracellular retention of the FSHR and impaired cAMP production. Paper-15545308.
The haplotype of two FSHR polymorphisms in ovarian cancer--a potential role of ethnology in risk modification. Paper-13634726.
Ovarian size and small ovarian follicles on transvaginal sonography were not associated with FSHR genetic variants. Paper-12866118.
OBJECTIVE: FSH, via its receptor ( FSHR), influences bone remodeling and osteoclast proliferation and activity. Paper-15178255.
Follicle-stimulating hormone receptor is expressed in human ovarian surface epithelium and fallopian tube. Paper-458676.
A distribution of two SNPs in exon 10 of the FSHR gene among the women with a diminished ovarian reserve in Ukraine. Paper-13641083.
The association of arrestin-3 with the follitropin receptor depends on receptor activation and phosphorylation. Paper-9974123.
In conclusion, we suggest that FSHR haplotypes are not considerable risk factors for spermatogenic failure. Paper-14175127.
A fluorescence resonance energy transfer assay was used to determine whether full-length native FSHR is an oligomer. Paper-13188485.
In all species studied so far the FSH-receptor primary transcript has been shown to undergo alternate splicing. Paper-950092.
AA genotype at -29 position of FSHR gene seems to be associated with increased serum FSH levels in the study subjects. Paper-15174655.
Mutation of the follicle-stimulating hormone receptor gene 5'-untranslated region associated with female hypertension. Paper-12085301.
A 240 kDa protein isolated from bovine calf testis has been shown to have properties characteristic of an FSH receptor. Paper-7315600.
We now describe a novel phenotype related to mutations provoking a partial loss of function of the FSHR. Paper-1610375.
Diverse mutations in FSH-receptor ( FSHR) gene have been described as possible cause of premature ovarian failure (POF). Paper-10519884.
The level of FSHR protein was positively correlated with the peak level of serum E(2) and the number of mature oocytes. Paper-13270510.
FSHR extracellular domain (ECD) is predicted to have 8-9 alphabeta or leucine-rich repeat motif elements. Paper-8846886.
These observations are consistent with a role for ubiquitination in the regulation of hFSHR cell surface residency. Paper-10004096.
The deletion size was narrowed down by array analysis to approximately 163 kb, involving exons 9 and 10 of the FSHR gene. Paper-15120407.
In the present study, a functional analysis of the FSHR carboxyl-terminal segment cysteine residues was carried out. Paper-14406332.
Here we report the first germline mutation responsible for sOHSS (c.383C>A, p.Ser128Tyr), located in the ECD of the FSHR. Paper-12672497.
For the FSHR, one activating mutation was found in a patient with normal spermatogenesis without detectable gonadotropins. Paper-2151191.
We fused an ovine FSHR promoter to a luciferase gene to understand the promoter regulation in two gonadal cell lines. Paper-8731934.
Clinical features of primary ovarian failure caused by a point mutation in the follicle-stimulating hormone receptor gene. Paper-711755.
Homozygous inactivating mutations of the LH and FSH receptor invariably lead to amenorrhea in genotypical female subjects. Paper-1506477.
BACKGROUND: Inactivating mutations of the FSH receptor ( FSHR) are a rare cause of hypergonadotrophic hypogonadism in women. Paper-9784048.
This was probably due to upregulation of mRNA synthesis resulting from inhibition of porcine FSHR protein translation. Paper-11603407.
A mutation in the follicle-stimulating hormone receptor as a cause of familial spontaneous ovarian hyperstimulation syndrome. Paper-10204405.
The FSH receptor mRNA was abundant in the preovulatory follicle, with expression decreased by about 50% in the corpus luteum. Paper-1143346.
The FSH receptor ( FSHR) is expressed only in granulosa cells of the ovary and Sertoli cells of the testis. Paper-1654439.
Inactivating mutations of the FSH receptor ( FSHR) are known to cause ovarian failure with amenorrhea and infertility in women. Paper-9198110.
HEK293 cells expressing different hFSHR allelic combinations were studied for their responsiveness to recombinant (r)hTSH. Paper-13278194.
Inactivating FSHR mutations are known to cause hypergonadotropic hypogonadism with disturbed follicular maturation in females. Paper-15120407.
Breakthrough discovery of nonapeptide FSHR antagonist molecules, like suramin, compound 1 and compound 10 are noted. Paper-13278557.
There were no significant differences in the rate of FSHR mRNA degradation between the two methods of mRNA quantification. Paper-10711754.
It seems worthwhile to see what is new research on FSHR and whether they will be of any help in epithelial ovarian cancer. Paper-13278557.
No evidence of mutations in the follicle-stimulating hormone receptor gene in Mexican women with 46,XX pure gonadal dysgenesis. Paper-8708819.
FSH activates its receptor ( FSHR) located exclusively on Sertoli cells in the testis and granulosa cells in the ovary. Paper-13358547.
Furthermore, this receptor complex attenuated the hFSHR receptor protein level within the cells, which impaired cAMP production. Paper-11156661.
Interestingly, the expression of L477A, L477D and L477P FSHR mutants conferred elevated basal cAMP levels to HEK-293 cells. Paper-9235037.
Different concentrations of pXGH5 and pSG5 containing normal or mutated FSHR cDNA were transfected in COS-7 cells by lipofection. Paper-780144.
The expression of FSH receptor ( FSH-R) was detected also in epithelial cells of the caput epididymis of rat and monkey. Paper-15109177.
The mechanisms of retinoic acid-induced regulation on the follicle-stimulating hormone receptor in rat granulosa cells. Paper-8405047.
Role of G protein-coupled receptor kinases on the agonist-induced phosphorylation and internalization of the follitropin receptor. Paper-1922687.
Follicle-stimulating hormone receptor gene haplotypes and male infertility in estonian population and meta-analysis. Paper-14175127.
METHODS: The hormonal profiles and treatment of all patients were analyzed and FSHR polymorphism was examined by PCR and RFLP. Paper-12030650.
The FSHR expression in the ovary and fallopian tube was confirmed by reverse transcription polymerase chain reaction. Paper-458676.
Single nucleotide polymorphisms of follicle-stimulating hormone receptor are associated with ovarian cancer susceptibility. Paper-12051625.
RESULTS: Antipeptide antibodies to regions 15-31, 216-235, 285-300 and 327-341 hFSHR inhibited both FSH binding and cAMP production. Paper-11504620.
Neither of the two FSHR mutations (566C-->T or1255G-->A) was identified in 40 other Finnish patients with premature ovarian failure. Paper-9198110.
Our results suggest that FSHR and its ligand may play a role in the regulation of the growth of hormone-refractory prostate cancers. Paper-1749289.
DESIGN: The hFSHR gene was sequenced from eight pediatric patients displaying gonadal hyperstimulation due to primary hypothyroidism. Paper-13278194.
The functional effects of identified mutations were assessed by expression of the wild-type or the F591S mutant FSH-R in COS-7 cells. Paper-973346.
Our results suggested that the two FSHR SNPs might affect the susceptibility of women to specific subtypes of ovarian cancer. Paper-12051625.
Furthermore, it was also found that overexpression of FSHR in Chinese hamster ovary (CHO) cells leads to cell proliferation. Paper-10627688.
A mutant single nucleotide polymorphism of follicle-stimulating hormone receptor is associated with a lower risk of endometriosis. Paper-15586409.
We have described previously in the Finnish population an inactivating point mutation (566C-->T) in the human FSH receptor ( FSHR) gene. Paper-1676605.
OBJECTIVE: To characterize novel single-nucleotide polymorphisms ( SNPs) in the human FSH receptor ( FSHR) promoter region. Paper-11211382.
However, there is currently no biochemical data that demonstrate that FSHR exists as a dimer or higher-order oligomer in cell membranes. Paper-13188485.
In homozygous Ser(680)/Ser(680) type women, the FSH receptor appears to be more resistant to FSH action even in normal menstrual cycles. Paper-11153011.
In women, FSH sensitivities during the menstrual cycle and different cycle lengths are observed, depending on the FSHR haplotype. Paper-11127110.
Single-nucleotide polymorphisms in the promoter region influence the expression of the human follicle-stimulating hormone receptor. Paper-11211382.
AIMS: Dysfunction of the FSH receptor ( FSHR) may be involved in some form of male infertility with azoospermia or oligozoospermia. Paper-14066927.
Our study results appear in agreement with these experimental data and with known biological actions of FSH/ FSHR system in bone homeostasis. Paper-15178255.
Conditional logistic regression was used to estimate the odds ratio (OR) across increasing thirds of FSH concentrations. Paper-13872681.
We review studies that propose follicle-stimulating hormone ( FSH) as a physiologic stimulator of osteoclastic bone resorption. Paper-12644214.
One of the hFSHR mutations examined in this context was the substitution of a highly conserved aspartate (D581) in TM6 with glycine. Paper-9285629.
CONCLUSIONS: We could not confirm the FSHR Ala307-Ser680 haplotype as a risk factor for epithelial ovarian cancer in Caucasian women. Paper-13634726.
Cell-surface hFSHR levels increased when expressed at nonpermissive temperature in a temperature-sensitive, ubiquitination-defective cell line. Paper-10004096.
Ovarian surface epithelium and fallopian tube epithelium, not previously recognized to express FSHR, were both strongly positive. Paper-458676.
By in situ hybridisation we found that the transgenic FSHR was highly expressed in Sertoli cells, spermatocytes and round spermatids. Paper-10123949.
Also, an oligonucleotide that represented the sequence of the terminal deoxynucleotidyltransferase InR displaced the complexes at the FSHR InR. Paper-829710.
The area under the ROC curve for seminal plasma inhibin-B was significantly larger than that for FSH and testicular volume. Paper-11151392.
Poor ovarian response to gonadotropin stimulation is associated with low expression of follicle-stimulating hormone receptor in granulosa cells. Paper-13270510.
Delineation of regions in the extracellular domain of follicle-stimulating hormone receptor involved in hormone binding and signal transduction. Paper-11504620.
Three polymorphisms at nucleotide position -29 and codons 307 and 680 of the FSHR gene were genotyped by Taqman allelic discrimination and RFLP. Paper-15827874.
FSHR sequence analysis revealed a novel non-synonymous point mutation in exon 10 (c.1760C>A, p.Pro587His), but no wild-type allele. Paper-15120407.
Absence of mutation in the follicle-stimulating hormone receptor gene in severe primary hypothyroidism associated with gonadal hyperstimulation. Paper-12524890.
Earlier studies indicate that transcription of Fshr in the gonads requires elements outside the gene's immediate 5' flanking sequence. Paper-11156606.
An increase in steady-state levels of FSHR mRNA as well as a change in alternative splicing appear to be important during early folliculogenesis. Paper-14993186.
The interaction between follicle-stimulating hormone (FSH) and the FSH receptor ( FSHR) is essential for normal oogenesis and spermatogenesis. Paper-11127110.
A homozygous missense mutation, C566T, in the follicle stimulation hormone receptor ( FSHR) gene has been linked to premature ovarian failure. Paper-14268734.
The FSHR cDNA was cloned in the pSG5 expression vector and mutagenized (Ala307-->Thr) by oligonucleotide-mediated, site-directed mutagenesis. Paper-780144.
Real-time PCR analyses revealed that FSHR mRNA was highly expressed in early yolk-stage follicles but decreased at the end of vitellogenesis. Paper-15884285.
Prediction of severity of symptoms in iatrogenic ovarian hyperstimulation syndrome by follicle-stimulating hormone receptor Ser680Asn polymorphism. Paper-10616703.
It might well be that mutations occur with the same frequency, but that activating mutations of the FSHR do not result in any particular phenotype. Paper-2151191.
Overexpression of FSHR may be associated with an elevated level of OET cell proliferation via an enhanced activity of potential oncogenic pathways. Paper-13705300.
This study aimed to investigate the effects of the FSHR polymorphisms on idiopathic male infertility and serum FSH levels in Han-Chinese population. Paper-15827874.
Overexpression of upstream stimulating factor-1 (USF1) suppresses the activity of the human FSH-R promoter/enhancer via Inr and E-box elements. Paper-10561105.
Comparisons were also made with gain-of-function mutations of lutropin/choriogonadotropin (LH/ CGR) and follicle-stimulating hormone receptors ( FSHR). Paper-8357128.
Thus, differences in the residual activity of mutated FSHR led to differences in the clinical, biological, and histological phenotypes of the patient. Paper-8346965.
CONCLUSIONS: Our findings suggest that increased serum FSH levels in subjects with primary amenorrhea correlated to FSHR genotype at position -29. Paper-15174655.
Effects of trilostane on HPG-related endpoints in exposed males were less pronounced, although, as in females, up-regulation of gonadal fshr was seen. Paper-16136181.
In this retrospective study, we explored the impact and action of two distinct FSHR isoforms, Thr307/Asn680 and Ala307/Ser680, in a large group of men. Paper-9228476.
However, rat testis FSH receptor has, on the basis of cloning experiments, been found to have a much lower molecular mass of 75 kDa (peptide only). Paper-7315600.
To our knowledge, this is the first description of a compound heterozygosity of an inactivating FSHR point mutation unmasked by a partial deletion. Paper-15120407.
Sequence analysis indicated that the buffalo FSHR cDNA sequence comprised of an open reading frame of 2085bp encoding a 695 amino acid protein. Paper-12988409.
RECENT FINDINGS: FSHR polymorphisms consist of single nucleotide changes within the coding and regulatory regions and/or alternatively spliced products. Paper-15855260.
In addition, it has been shown that genetic factors such as the patient's FSH-receptor genotype also determine individual response to FSH treatment. Paper-11152998.
A yeast two-hybrid screen of an ovarian cDNA library was employed to identify potential interacting partners with human FSHR intracellular loops 1 and 2. Paper-10499371.
A linked construct of the first and second intracellular loops (iL1-iL2 bait) of FSHR was used as bait and a human ovarian cDNA library was used as prey. Paper-10480884.
An FSH bioassay that employed a stable chimeric cell line expressing the human FSH-R was used to provide an accurate measurement of FSH bioactivity. Paper-2153312.
Pregnancies after oocyte donation in women with ovarian failure caused by an inactivating mutation in the follicle stimulating hormone receptor. Paper-9349959.
Whether the effect of RA and FSH on FSH-R mRNA levels was the result of decreased transcription and/or altered mRNA stability was also investigated. Paper-8405047.
We hypothesize that, in addition to low estrogen, a rising FSH contributes to the increased bone resorption and bone loss in hypergonadism. Paper-12644214.
We conclude that, in contrast to the data obtained with the LHR, the association of arrestin-3 with the FSHR is dependent on receptor phosphorylation. Paper-9974123.
We conclude that the FSHR haplotype does not associate with different serum FSH levels but it is differently distributed in normal and azoospermic men. Paper-11761546.
Follicle-stimulating hormone (FSH) is fundamental for Sertoli cell function stimulating spermatogenesis and follicular growth by a specific receptor ( FSHR). Paper-14486584.
Immunofluorescence microscopy showed that mAbs 106.318 and 106.156 stained the surface of fixed, intact CHO cells expressing wild type hFSH-R. Paper-8447471.
We examined the chronology of OSE changes, including tumor appearance, in a mouse model where ovulation never occurs due to deletion of follitropin receptor. Paper-13322451.
Thus truncated hFSH-R variants do not reach the medial or trans Golgi where high mannose oligosaccharides are trimmed and sialic acid is added. Paper-8447471.
As a control, human FSH was administered in vitro to the Y1 mouse cell line, which was stably transfected with cDNA for FSHR and devoid of endogenous FSH. Paper-1529441.
Evaluating the roles of follicle-stimulating hormone receptor polymorphisms in gonadal hyperstimulation associated with severe juvenile primary hypothyroidism. Paper-13278194.
Monoclonal antibodies raised against the human follicle-stimulating hormone receptor failed to detect the latter in the epidermal structures and in the dermis. Paper-2112539.
Single nucleotide polymorphisms ( SNPs) Thr307Ala and Asn680Ser were two non-synonymous variations in the coding region of the FSH receptor ( FSHR) gene. Paper-12051625.
The leucine-rich repeat domain (LRD) of the FSHR also appears to contain a cryptic FSH binding site that is obscured by other parts of the extracellular domain. Paper-12370475.
In the last years, follice-stimulating hormone (FSH) receptor ( FSHR) gene polymorphisms have been studied as potential risk factors for spermatogenetic failure. Paper-16092219.
Presence and absence of follicle-stimulating hormone receptor mutations provide some insights into spontaneous ovarian hyperstimulation syndrome physiopathology. Paper-10835345.
We generated a novel polyclonal HinR antibody that specifically stimulates cAMP production by HEK 293 cells expressing FSHR in a hormone-independent manner. Paper-13587526.
Accordingly, the spatial organization of signaling and adapter proteins with FSHR likely facilitates and finely regulates the signal transduction induced by FSH. Paper-12370460.
The regulatory regions of the FSHR gene are more akin to 'housekeeping' genes than to a highly regulated gene, and there is an E box in the promoter region. Paper-14993186.
In denuded human preovulatory oocytes, FSH receptor mRNA was detected at a concentration per cell exceeding by about 20-fold that present in granulosa cells. Paper-9451684.
Conversely, the substitution of Y614 of the rFSHR with the cognate hFSHR residue ( histidine) fully suppresses the constitutive activity of the rFSHR (D580G) mutant. Paper-9285629.
The amplified DNA sequence shows a high degree of homology to the available turkey and human luteinizing and follicle stimulating hormone receptor coding sequences. Paper-8409444.
The FSHR expression at both mRNA and protein levels was determined by either reverse transcription-polymerase chain reaction or Western blot in granulosa cells. Paper-13270510.
Sequence analysis of this exon revealed an open reading frame corresponding to base positions 855-2085 of the FSHR cDNA, thereby coding for 410 amino acids. Paper-135610.
CONCLUSIONS: We did not find any activating mutation in exon 10 of the FSHR in our patients, and one patient developed precocious puberty after removal of her tumor. Paper-13849438.
RA, either alone or in combination with FSH, did not affect intracellular cAMP levels, while it inhibited the effect of 8-Br-cAMP on FSH-R mRNA production. Paper-8405047.
Besides the expected expression of FSH-R and LH-R mRNA in the gonads similarly strong signals for LH-R were also obtained in male gill, and in female and male brain. Paper-13554890.
Follicle-stimulating hormone receptor polymorphism (Thr307Ala) is associated with variable ovarian response and ovarian hyperstimulation syndrome in Indian women. Paper-13070672.
Basal, rhFSHR- and rhTSH receptor-stimulated cAMP levels were assayed in HEK293 cells transfected with the hTSH receptor or different hFSHR allelic combinations. Paper-13278194.
The patient was a compound heterozygote for two mutations in the FSHR gene: 566C-->T, the Finnish founder mutation, and 1255G-->A, a previously unidentified mutation. Paper-9198110.
MAIN OUTCOME MEASURE(S): Relative expression of mRNA and protein of FSHR in granulosa cells, serum E(2), FSH level in serum and FF, and the number of mature follicles. Paper-13270510.
METHODS: FSHR gene SNPs were analyzed by PCR and RFLP. "Poor responders" (ovarian dysfunction) group and "good responders" group constituted the study group. Paper-13641083.
The steady decline of FSHR expression from benign cystadenoma to borderline tumor to carcinoma suggests that FSH may be needed in early ovarian cancer development. Paper-2077996.
Identification of the first germline mutation in the extracellular domain of the follitropin receptor responsible for spontaneous ovarian hyperstimulation syndrome. Paper-12672497.
The present study indicates that photoperiod is a more important environmental factor than temperature for the regulation of FSH receptor in the Djungarian hamster. Paper-5825092.
The immunocytochemistry also demonstrated that myometrial smooth muscle cells, as rat ovary and human granulosa cells, contain FSH receptor immunostaining. Paper-545269.
We sequenced the transmembrane region of FSHR (located on chromosome 2) in 21 unrelated mothers of dizygotic twins and found no differences to the published sequence. Paper-8701335.
Exons 6, 7, 9, and 10 of the FSHR gene were analyzed by PCR, restriction enzyme analysis, denaturing gradient gel electrophoresis, and direct sequencing. Paper-12866118.
Similarly, after treatment with proteasome inhibitors, HEK293 cells stably transfected with an hFSHR expression plasmid showed an increase in follitropin binding. Paper-10004096.
PURPOSE: This retrospective study was designed to analyze the FSHR gene variants in subjects with primary and secondary amenorrhea with hypergonadotropic hypogonadism. Paper-15174655.
This highly specific pattern of gene expression asserts that transcriptional events unique to these two cell types are responsible for activation of the FSHR gene. Paper-1654439.
Delayed puberty and primary amenorrhea associated with a novel mutation of the human follicle-stimulating hormone receptor: clinical, histological, and molecular studies. Paper-9813657.
CONCLUSION: A 1.5kb 5'-region of the human FSHR drives mRNA expression of the transgene in the testis but leads to ectopic expression in germ cells and in the brain. Paper-10123949.
These findings suggest that the proband is hemizygous, with an inherited or de-novo microdeletion, or alternatively a de-novo gene conversion, of the accompanying FSHR allele. Paper-9784048.
Further mutational and functional analysis of the AFN region in the LHR and FSHR revealed that the integrity of this amino acid sequence is crucial for receptor function. Paper-9240313.
The objective of this study was to examine whether FSHR is expressed in OETs and to investigate the possible different roles of the gonadotropins in ovarian cancer development. Paper-2077996.
Studies on FSH-receptor mRNA levels during granulosa cell luteinization show that there is complete loss of full-length transcripts soon after luteinization. Paper-950092.
FSH receptor ( FSHR), a member of the G protein-coupled receptor superfamily, is present in the plasma membrane of ovarian granulosa cells and testicular Sertoli cells. Paper-13188485.
Toward gene therapy of premature ovarian failure: intraovarian injection of adenovirus expressing human FSH receptor restores folliculogenesis in FSHR(-/-) FORKO mice. Paper-14268734.
This shows that although the FSHR does not normally bind hCG, it contains a cryptic lutropin binding site that has the potential to recognize hCG in a manner similar to the LHR. Paper-12370475.
More importantly, this study shows the feasibility of evaluating FSHR expression by both in situ hybridization and reverse transcription polymerase chain reaction. Paper-458676.
Site directed mutagenesis of the FSHR and the expression of resulting mutants in HEK-293 cells were performed in order to corroborate the effects of these substitutions. Paper-9235037.
Following extraction of genomic DNA, the FSHR polymorphism at position 680 was determined by polymerase chain reaction and restriction fragment length polymorphism analysis. Paper-12201523.
These results indicated that the FSHR is a potential marker for superovulation response and can be used as a predictor for superovulation in Chinese Holstein cows. Paper-14769711.
Importantly and consistent with the foregoing results, dodecyl phosphocholine induced a significant increase in the ordered secondary structure of the purified hFSHR ECD as well. Paper-8780226.
In this article, we review existing knowledge of FSHR in ovary, in OSE, and in epithelial ovarian cancer and try to establish relative importance of this receptor over its ligand. Paper-14462561.
The overall clinical pregnancy rate in patients stimulated with recombinant FSH was 10.91%, compared with 22.22% in the group stimulated with urinary gonadotropins. Paper-14027924.
The specificity of the FSHR detected on prostate cancer tissues or cells by IHC and Western blotting was confirmed by preabsorbing the antibodies with the immunizing antigens. Paper-1749289.
We investigated the effects of bilateral intra-ovarian injection of an adenovirus expressing a normal copy of human FSHR on the reproductive system of 6-10 weeks female FORKO mice. Paper-14268734.
A C566T transition in exon 7 of FSHR predicting an Ala to Val substitution at residue 189 in the extracellular ligand-binding domain segregated perfectly with the disease phenotype. Paper-361286.
Since the FSH actions could be receptor mediated, we investigated the presence of FSH receptor mRNA transcripts and protein in freshly dispersed myometrial smooth muscle cells. Paper-545269.
Functional and structural roles of conserved cysteine residues in the carboxyl-terminal domain of the follicle-stimulating hormone receptor in human embryonic kidney 293 cells. Paper-14406332.
A reverse transcription-polymerase chain reaction amplification was used to detect the expression of different isoforms of the FSH receptor mRNA in human corpus luteum and placenta. Paper-1143346.
Inactivation of FSHR causes in otherwise normally masculinized men small testis size and variably reduced spermatogenesis, but not azoospermia or absolute infertility. Paper-12348947.
To further define the repertoire of proteins involved in FSH-induced signal transduction, several signaling and adapter proteins were examined for the ability to associate with FSHR. Paper-12370460.
Northern blotting demonstrated that myometrial smooth muscle cells, just as rat ovary, a classical target of FSH action, contain multiple FSH receptor mRNA transcripts. Paper-545269.
By using a peptide derived from FSH (amino acids 33-53 of the FSH beta chain, named as FSH33), we developed a conjugated nanoparticle, FSH33-NP, to target FSHR in ovarian cancer. Paper-13930151.
Female mice carrying mutated FSHR gene, called follitropin receptor knockout (FORKO), display similar phenotype and are sterile because of a folliculogenesis block at a primary stage. Paper-14268734.
The FSH molecule has been localized by monoclonal antibodies on plasma membranes and vesicles, and the FSHR mRNA was found scattered in the cytoplasm after in situ hybridization. Paper-1529441.
Cell type was identified by fluorescence immunocytochemistry (ICC); the cells expressed cimentin, but not cytoceratin and follicular stimulation hormone receptor ( FSHR). Paper-13697337.
The human follicle-stimulating hormone (FSH) receptor ( FSHR) gene possesses single nucleotide polymorphisms (SNP) in exon 10, which influence serum FSH levels in women, but not in men. Paper-11761546.
Here, we show that the A189 V FSHR stably expressed in HEK293N cells provoked ERK MAP kinases phosphorylation through β-arrestins, independently of the canonical cAMP/PKA pathway. Paper-15545308.
In order to define more precisely the peptide domains involved, we synthesized truncated peptide amides corresponding to FSHR residues 551-555 (KIAKR) and 650-653 (RKSH), respectively. Paper-679511.
Ovarian sex cord tumors (n = 13), small cell carcinomas of the ovary (n = 3), and control DNA specimens (n = 116) were screened for mutations in the transmembrane domains of the FSH-R. Paper-973346.
A common single nucleotide polymorphism in exon 10 of the human follicle stimulating hormone receptor is a major determinant of length and hormonal dynamics of the menstrual cycle. Paper-11242611.
Alanine replacement of C(627) had no effect on hFSHR expression and function, whereas the same mutation at C(629) altered membrane expression and signal transduction. Paper-12370463.
One single nucleotide polymorphism (SNP) of G-278A located in the 5' upstream region of bovine FSHR gene was found in 118 Chinese Holstein cows treated for superovulation. Paper-14769711.
Mutation of the phosphorylation sites in the third intracellular loop of the rat ( r) FSHR partially reduces phosphorylation but has no effect on arrestin-3 association. Paper-9974123.
While these findings may potentially suggest that FSH action is not absolutely required for spermatogenesis, it cannot be ruled out that these individuals have some residual FSHR activity. Paper-15083507.
In the hFSHR, C(629) may be a target for palmitoylation, and apparently it is the only cysteine residue in the Ctail domain that might play an important role in receptor function. Paper-12370463.
However, higher expression of FSHR mRNA in the granulosa layer of the less mature follicles may be involved in the differentiation and maturation of granulosa cells in these follicles. Paper-1000682.
Using the candidate gene approach, we searched for mutations in the gene encoding the FSH receptor in a woman who had given birth to two sets of dizygotic twins without fertility treatment. Paper-8659165.
CONCLUSIONS: The newly identified SNPs do not seem to influence clinical parameters substantially, but modulate expression of the FSHR via changes in transcription factor binding sites. Paper-11211382.
A single gene for the FSH receptor undergoes extensive alternate splicing generating multiple transcripts, and several of these have been cloned and characterized from the sheep testis. Paper-1279172.
These results suggest that the FSH receptor itself is not a calcium channel and, therefore, FSH must be stimulating endogenous calcium channels in rat Sertoli cell plasma membranes. Paper-7482200.
FSHR single-nucleotide polymorphisms at codon 680 of exon 10 were determined by restriction fragment length polymorphism of amplicons generated by polymerase chain reaction. Paper-15924970.
FSHR single-nucleotide polymorphisms at codon 680 of exon 10 were determined by restriction fragment length polymorphism of amplicons generated by polymerase chain reaction. Paper-15172531.
We performed direct sequencing of all 10 exons of the FSHR gene in seven sporadic patients and two sisters with 46,XX pure gonadal dysgenesis, to investigate the cause of their disorder. Paper-8708819.
In germinal cells, our observations demonstrate the presence of FSH and the FSHR mRNA: the first on the plasma membrane and in endocytotic vesicles, and the second scattered in the cytoplasm. Paper-1529441.
Furthermore, molecular-cytogenetic analyses of the breakpoint region on chromosome 2 showed the translocation to be unbalanced, containing a deletion with one breakpoint within the FSHR gene. Paper-15120407.
Our results indicated that the FSHR is expressed in a cell-specific fashion at different stages of follicular development and is also expressed in ovarian surface and fallopian tube epithelia. Paper-458676.
Monitoring the transfection efficiency of the human follicle-stimulating hormone receptor cDNA in COS-7 cells: evaluation of the growth hormone transient gene expression assay system. Paper-780144.
When relative expression was analysed at different stages of sexual maturation, levels for FSH-R increased moderately during gonadal growth whereas those of LH-R showed a high peak at spawning. Paper-13554890.
To gain a better understanding of these processes, we used a yeast-based interaction trap to identify cytoplasmic proteins in a human ovarian cDNA library that interacted with the hFSHR 3i loop. Paper-10004096.
We investigated the presence of mutations/polymorphisms in the FSH receptor ( FSHR) gene and their association with phenotype in women with premature ovarian failure (POF) in southern Brazil. Paper-12866118.
The data showed that in the Italian population, FSHR genotypes have no influence on FSH concentrations both in normal and infertile males and do not associate with spermatogenetic impairment. Paper-12356875.
RESULTS: FSH receptor mRNA was expressed by human endometrium, and its peptide was located immunohistochemically in both proliferative and secretory endometrial epithelial and stromal cells. Paper-11475605.
The first mutation identified in the FSHR gene was a missense mutation (566C-->T, predicting Ala189Val transition) found in several Finnish patients with primary amenorrhea due to ovarian failure. Paper-9198110.
We speculate that cryptic lutropin binding sites in the FSHR, which are also likely to be present in thyrotropin receptors (TSHR), permit the physiological regulation of ligand binding specificity. Paper-12370475.
This 566C-->T mutation, predicting an alanine to valine substitution, is located in exon 7 of the FSHR gene, in the region encoding the extracellular domain of the receptor molecule. Paper-894372.
The nFSHR 5'-flanking region exhibits new interesting putative cis-regulatory elements including those for the SRY transcription factor, which had not been previously related to the FSHR gene. Paper-14089014.
Y chromosome microdeletions were detected in 33.3% (6 out of 18) of idiopathic azoospermic patients with high serum follicle-stimulating hormone ( FSH) levels in the present study. Paper-10771368.
The aim of the present study was to investigate the association between polymorphisms in the human FSHR gene and essential hypertension (EH) by using single nucleotide polymorphisms ( SNPs). Paper-12085301.
The crystal structure of the FSH-FSHR(HB) complex provides explanations for the high affinity and specificity of FSH interaction with FSHR, and it shows an unexpected dimerization of these complexes. Paper-12370464.
RESULTS: Positive FSHR mRNA expression by RT-PCR (the most sensitive method) was found in 100% of epithelial inclusions, 100% of cystadenomas, 94% of borderline tumors, and 60% of carcinomas. Paper-2077996.
Exon 10 was found to comprise the seven transmembrane domains, the C-terminal intracellular domain and a fragment of 81 amino acids belonging to the extracellular N-terminal domain of the FSHR. Paper-135610.
In a multivariate logistic regression model, corrected for age, BMI, mean ovarian, volume, hyperandrogenism, and amenorrhoea, only FSHR and basal FSH levels were predictive for ovulation. Paper-13889428.
Rainbow trout follicular maturational competence acquisition is associated with an increased expression of follicle stimulating hormone receptor and insulin-like growth factor 2 messenger RNAs. Paper-9932289.
Although this concept remains valid, the recent reports of defects in genes encoding FSH and its receptor ( FSHR) have altered the concepts, particularly with regard to the role of FSH in spermatogenesis. Paper-1235633.
Expression of recombinant human follicle-stimulating hormone receptor: species-specific ligand binding, signal transduction, and identification of multiple ovarian messenger ribonucleic acid transcripts. Paper-66283.
The homozygous Ser/Ser genotype of FSHR polymorphism at position 680 may be associated with a reduced ovarian response to COH for IVF-ET, while Asn/Asn genotypes showed a higher pregnancy rate. Paper-12201523.
Also, studies using rcFSH demonstrate that both up- and down-regulation of FSH receptor gene expression can be induced by the homologous hormone at different stages of follicle development. Paper-53917.
These findings reveal transgenic FSHR(+) stimulated a constitutive FSH-like Sertoli cell response in gonadotropin-deficient testes, and pathways that induced LH-independent testicular steroidogenesis. Paper-9636168.
Spontaneous ovarian hyperstimulation syndrome (sOHSS) is a rare genetic condition in which human chorionic gonadotropin (hCG) promiscuously stimulates the FSHR during the first trimester of pregnancy. Paper-12672497.
Comparison of the sequences of the extracellular domains (ECD) of the receptors reveals two regions (amino acids 4-56 and 265-319 in FSH-R) that share relatively little amino acid sequence similarity. Paper-582304.
The frequency of an inactivating point mutation (566C-->T) of the human follicle-stimulating hormone receptor gene in four populations using allele-specific hybridization and time-resolved fluorometry. Paper-1676605.
We have characterized the promoter elements required for activity of the rat FSHR gene in a Sertoli cell line MSC-1, primary cultures of rat Sertoli cells, and two non-Sertoli cell lines. Paper-1654439.
Our results suggest an altered hormonal environment resulting from FSH-R loss as a cause of early changes in tight junction proteins that predispose the ovary to late-onset tumors that occur with aging. Paper-12403314.
Thus, SNPs of the FSHR determine the ovarian response and should, therefore, be considered in controlled ovarian hyperstimulation during assisted-reproduction techniques in women with normal ovarian function. Paper-11127110.
The FSHR polymorphism at position 680 was analyzed in the whole group, while position 307 was investigated in 150 subjects, both of them by single-stranded conformation polymorphism ( SSCP) gel electrophoresis. Paper-9228476.
Selection of a dominant follicle that will ovulate likely occurs by activation of cell survival pathways and suppression of death-promoting pathways in a mechanism involving FSH and its cognate receptor ( FSHR). Paper-10499371.
At 21 days of age data showed that FSH-R mRNA levels were significantly higher in both hyper- and hypothyroid rat testes compared to controls, but no differences were detected in recovered 50-day-old rats. Paper-9931180.
Western immunoblotting demonstrated that myometrial smooth muscle cells also contain a 60 kDA FSH receptor protein just as rat ovary and human granulosa cells used as positive control tissues. Paper-545269.
Because gonadotropins induce the growth, differentiation, and function of the steroid-producing cells of the ovary, we hypothesized that mutations in the FSH receptor ( FSH-R) might occur in this group of tumors. Paper-973346.
Expression of the FSH receptor ( Fshr) is restricted to testicular Sertoli cells and ovarian granulosa cells, thereby limiting the direct targets of FSH action to these somatic cells of the gonads. Paper-11156606.
In most patients who are still experiencing cyclic menstrual bleeding no FSH receptors were detected possibly due to severe disturbances in follicular FSH receptor synthesis prior to ovarian follicle exhaustion. Paper-821394.
Contrary to the mutations described previously, the p.Ser128Tyr FSHR mutant displayed increase in affinity and sensitivity toward hCG and did not show any constitutive activity, nor promiscuous activation by TSH. Paper-12672497.
The SNPs in codon 680 and at position -29 of the FSHR gene were analyzed by PCR-RFLP technique in 240 men with proven fathers, and 270 infertile men (150 nonobstructive azoospermic and 120 severe oligozoospermic). Paper-15100087.
The immunoexpression of FSH-R in the ductuli efferentes and the epididymis of men and rat: effect of FSH on the morphology and steroidogenic activity of rat epididymal epithelial cells in vitro. Paper-15109177.
The results showed that the FSHR polymorphisms were not associated with either azoo- or oligozoospermia as the distributions of alleles, genotypes, and haplotypes among patients and controls were similar. Paper-14175127.
Flow cytometry studies of this region revealed that antibody X179 against peptide R265-S296 binds to human FSHR expressed by CHO cells and can be competed against by preincubating the cells with hFSH. Paper-8541775.
In the FSHR gene, which consists of 10 exons, an homozygous mutation was reported in six Finnish families with gonadal dysgenesis; whereas two isolated French patients exhibited compound heterozygous mutations. Paper-8708819.
A hFSHR mutant with all basic amino acids present in the iL3 BXXBB motif replaced by alanine failed to bind agonist and activate effector, and was expressed as an immature < or =62kDa form of the receptor. Paper-12370463.
Effects of antisense oligodeoxynucleotide to follicle-stimulating hormone receptor on the cell proliferation and apoptosis in cells derived from human ovarian mucinous cystadenocarcinoma in Vitro. Paper-12477980.
Like pharmacoperones for other receptors, this drug was able to rescue a particular mutant hFSHR (A(189)V) associated with misrouting and endoplasmic reticulum retention, although other mutants could not be rescued. Paper-13557571.
No significant difference was found in allelic variants frequency and genotype distribution between each category of subjects when analysing the FSHR exon 10 SNP alone and in combination with the SNP at position -29. Paper-12356875.
RESULT(S): We identified two SNPs and three mutations in the promoter region of the human FSHR which could be allocated to positions -29, -37, -114, -123, and -138 upstream of the translational initiation codon. Paper-11211382.
RESULTS: FSHR Ser(680) was associated with higher levels of gonadotrophic hormones (FSH: P < 0.01, LH: P = 0.01), and testosterone ( P = 0.05) and a higher frequency of hyperandrogenism ( P = 0.04). Paper-13889430.
Perifollicular blood flow and pregnancy in superovulated intrauterine insemination (IUI) cycles: An observational comparison of recombinant follicle-stimulating hormone ( FSH) and urinary gonadotropins. Paper-14027924.
Compared with the lowest third of FSH concentrations, the OR among those in the middle and highest thirds were 0.45 [95% Confidence Interval (CI): 0.20-1.00] and 0.26 (95% CI: 0.10-0.70), respectively. Paper-13872681.
Activating mutations confer to FSHR a higher responsiveness to FSH, making it constitutively active even in the absence of the ligand, or render it able to nonspecifically respond to other tropic hormones (e.g., TSH). Paper-14339214.
This study was conducted to characterize the expression of the receptor ( FSHR) for follicle-stimulating hormone (FSH) in androgen-independent prostate cancer cell lines and in human malignant prostate tissues. Paper-1749289.
Screening of a human genomic library with a cDNA probe corresponding to the transmembrane domain of the FSH receptor ( FSHR) resulted in the identification of a positive clone with a DNA insert of approximately 17.5 kb. Paper-135610.
Pregnancy rate was analysed according to age, type of infertility, cause of infertility, duration of infertility, number of eggs collected and follicle stimulating hormone ( FSH) levels. Paper-11538726.
Taken together, these data demonstrate that FSH binding requires elements within the leucine-rich repeat motifs that form a central region of hFSHR ECD, and a conformational change occurs upon hormone binding. Paper-8846886.
When Western European women with this phenotype were examined for FSHR mutations the result was negative, suggesting that other etiologies corresponding to this clinical pattern are markedly more frequent. Paper-1610375.
Our results suggest that neither incessant ovulation nor follicle-stimulating hormone receptor presence in the OSE is required for inducing ovarian tumors; thus, other mechanisms must contribute to ovarian tumorigenesis. Paper-13322451.
In conclusion, intra-ovarian injection of an adenovirus expressing human FSHR gene is able to restore FSH responsiveness and reinitiate ovarian folliculogenesis as well as resume estrogen production in female FORKO mice. Paper-14268734.
To investigate the presence of mutations and/or polymorphisms in FSHR gene, DNA from 20 POF, 5 of which were diagnosed as resistant ovary syndrome (ROS), and from 44 controls was isolated from peripheral lymphocytes. Paper-10519884.
The FSH-R codon 680 and codon 307 genotypes did not result in different serum FSH levels either in men with normal spermatogenesis (the control group) or in men with oligoasthenoteratozoospermia (infertile men). Paper-16063835.
Complete FSH resistance caused by a mutation of the FSHR gene has demonstrated that normal FSH action is an absolute requirement for female fertility, but spermatogenesis and male fertility are possible without FSH action. Paper-1235633.
Both glycosylated truncated hFSH-R variants were sensitive to peptide-N-glycanase F and endoglycosidase H but insensitive to neuraminidase indicating that these variants possess high mannose type oligosaccharides. Paper-8447471.
Thus, the simultaneous substitution of M576 in TM6 and H615 in TM7 of the hFSHR with the cognate rFSHR residues ( threonine and tyrosine, respectively) now renders the hFSHR(D581G) mutant constitutively active. Paper-9285629.
Our investigations also demonstrate that alternate splicing of the FSH receptor gene provides a mechanism for creating receptor diversity and suggest that multiple receptors could be involved in regulation of hormone action. Paper-1279172.
Selected analogues (2, 14, and 50) were also able to block FSHR-dependent estradiol production in rat primary ovarian granulosa cells and progesterone secretion in a clonal mouse adrenal Y1 cell line. Paper-9608211.
Employing point mutations we have found that several residues present in the iL2 of the hFSHR are important for both coupling the receptor to the G(s) protein and maintaining the receptor molecule in an inactive conformation. Paper-12370463.
In the present study, the common G-29A, A919G, and A2039G polymorphisms in the FSHR gene were analysed in 150 (36 non-obstructive azoospermia and 114 individuals with oligozoospermia) patients and 208 normozoospermic men. Paper-14175127.
We created a novel transgenic model to investigate a mutant human FSH receptor ( FSHR(+)) containing a single amino acid substitution (Asp567Gly) equivalent to activating mutations in related glycoprotein hormone receptors. Paper-9636168.
Treatment of immature rats with PMSG (10 IU) to induce follicular development resulted in increased FSH receptor mRNA levels 24 h after treatment, with a further increase at 52 h, coincident with increased [125I]FSH binding. Paper-53917.
A phosphorylation cluster of five serine and threonine residues in the C-terminus of the follicle-stimulating hormone receptor is important for desensitization but not for beta-arrestin-mediated ERK activation. Paper-12289852.
We have also proposed a model to explain FSH receptor activation and from that model, begun to create small molecules predicted to induce FSH signal transduction without binding to the extracellular domain of the membrane protein. Paper-1616066.
Although a large number of naturally occurring activating mutations of the human LH receptor (hLHR) and human TSH receptor (hTSHR) have been identified, only one activating mutation of the human FSH receptor ( hFSHR) has been found. Paper-9285629.
Penetration was by the endocytosis via membrane vesicles in which the FSHR is present, whereas its messenger is largely present in the cytoplasm and is responsible for the binding and subsequent internalization of the FSH molecule. Paper-1529441.
CONCLUSIONS: Our findings suggest that the FSHR polymorphisms at the studied sites do not associate with idiopathic male infertility and have no influence on FSH levels both in normal and infertile males in the Han-Chinese population. Paper-15827874.
A phosphorylation cluster in the C terminus of the FSH-R, identified as a site of beta-arrestin recruitment, positively regulated both desensitization and internalization but negatively regulated beta-arrestin-dependent ERK activation. Paper-12289852.
These results indicate that hMG is an effective, albeit stage-dependent, inducer of superovulation in the guinea pig, and that FSH-R homologies should be taken into account when choosing hormones for superovulation. Paper-9712957.
The results suggest that it may be necessary to detect microdeletions in patients with azoospermia, especially for those with high serum FSH levels, before assisted reproductive technology (ART) is provided to them. Paper-10771368.
Single nucleotide polymorphisms were selected in GnRH (Trp16Ser [rs6185]), the FSH-receptor ( FSHR, Ala307Thr [rs6165] and Asn680Ser [ rs6166]) and the LH-receptor (18insLQ, Asn291Ser [rs12470652] and Ser312Asn [rs2293275]). Paper-13889430.
Thus, activin seems to be available as an autocrine/paracrine factor in epithelial neoplasms and may contribute to the expression of FSH-R, although the roles of activin and gonadotropin in tumorigenesis has yet to be defined. Paper-8627328.
The present investigation is the first screening study for SNP at nucleotide position -29 in the core promoter region and codon 680 in exon 10 of the FSHR and the effect of the serum levels of FSH on male infertility in Southeast Turkey. Paper-15100087.
Transgenic FSHR(+) also elevated testosterone production in hpg testes, in the absence of circulating LH (or FSH), and it was not expressed functionally on steroidogenic cells, suggesting a paracrine effect mediated by Sertoli cells. Paper-9636168.
Cis-acting sequences and associated binding factors responsible for the transcription of the TATA-less FSHR gene in Sertoli cells were analyzed with dimethylsulfate (DMS) footprinting assays and electrophoretic mobility shift assay (EMSA). Paper-8861646.
MCV152 cells with FSHR overexpression showed an increased cellular proliferation and invasive capacity, which was associated with reduced levels of prohibitin and RII-beta expression and increased levels of HER-2/neu, c-Myc, and EGFR expression. Paper-13705300.
We showed in the immunohistochemistry study the expression of FSH-R in rat and human ductuli efferentes and the caput, corpus, and cauda epididymis, moreover, by Western blot analysis in the caput and cauda epididymis of rat. Paper-15109177.
To determine receptor variant trafficking and intracellular processing in mammalian cells, the intracellular fate of intentionally truncated variants of human follicle stimulating hormone receptor ( hFSH-R) expressed in CHO cells was examined. Paper-8447471.
Chimeras of the rat and human FSH receptors (FSHRs) identify residues that permit or suppress transmembrane 6 mutation-induced constitutive activation of the FSHR via rearrangements of hydrophobic interactions between helices 6 and 7. Paper-9285629.
STUDY DESIGN: We evaluated four patients with ovarian juvenile granulosa cell tumors (age range, 2.4 to 7.2; median, 2.9 years) and five healthy pubertal girls (age range, 16 to 18.5; median, 16.8 years) for activating mutations in exon 10 of the FSHR. Paper-13849438.
Decreased Degradation of Internalized Follicle-Stimulating Hormone Caused by Mutation of Aspartic Acid 6.30550 in a Protein Kinase-CK2 Consensus Sequence in the Third Intracellular Loop of Human Follicle-Stimulating Hormone Receptor. Paper-15930324.
Testes of untreated adult Tg- FSHR* males were equivalent in weight to nontransgenic controls but exhibited increased total Sertoli cell (24%) and spermatogonia (34%) numbers and nonsignificantly elevated spermatocyte-spermatid numbers (13%-17%). Paper-11812649.
Using biochemical and imaging approaches we show here that the majority of the internalized FSH- FSHR complex accumulates in endosomes and subsequently recycles back to the cell surface where the bound, intact hormone dissociates back into the medium. Paper-10191793.
PROBLEM: To use antipeptide antibodies to potential surface-oriented regions of the extracellular domain (ECD) of the human follicle-stimulating hormone receptor ( hFSHR) to delineate regions involved in FSH binding and FSH-induced signal transduction. Paper-11504620.
Although the fates of the internalized hormone-receptor complexes formed by the lutropin/choriogonadotropin and the TSH receptors have been examined in some detail, much less is known about the fate of the internalized FSH-FSH receptor ( FSHR) complex. Paper-10191793.
After 4 wk of gonadotropin suppression, Sertoli cell numbers were reduced in Tg- FSHR* testes to levels comparable with nontransgenic testes, whereas spermatogonia numbers were maintained at higher levels relative to nontransgenic testes. Paper-11812649.
The development of ovarian tumors in these patients may have been caused by mutations at other exons of the FSHR and G protein subunits, so the association noted between central precocious puberty and granulosa cell tumors might not be coincidental. Paper-13849438.
Previously, we have shown that the beta-strands of hLH-R leucine-rich repeats 3 and 6 can confer full hCG/hLH responsiveness and binding when simultaneously introduced into a hFSH-R background without affecting the receptor's responsiveness to hFSH. Paper-10011939.
These models suggest that differences in hydrophobic interactions between TMs 6 and 7 of the rat and human FSHRs may account for the ability of TM6 of the rat, but not human, FSHR to adopt an active conformation as a result of the D580/581G mutation. Paper-9285629.
We postulated that inactivating FSH receptor mutations might be a cause of oligozoospermia or azoospermia and reviewed the clinical data of 151 male intracytoplasmic sperm injection ( ICSI) candidates with special attention to FSH serum concentrations. Paper-1650315.
Their affinity constants for 125I-hFSH did not deviate greatly from that of wild-type FSHR, in which some mutants exhibited an approximately two- to threefold reduction in Ka compared to wild-type receptor, and no mutation abolished signal transduction. Paper-8541775.
Isolated transgenic Sertoli cells had significantly higher basal ( approximately 2-fold) and FSH-stimulated ( approximately 50%) cAMP levels compared with controls, demonstrating constitutive signaling and cell-surface expression of FSHR(+), respectively. Paper-9636168.
The binding experiments show that, while the affinity of the FSH receptor does not change through the menstrual cycle, the total number of FSH receptors in the leading follicles increases by about two-fold at mid-follicular phase compared with those at other periods. Paper-1143346.
The aim of this study was to evaluate the influence of two single nucleotide polymorphisms ( SNPs) of the FSHR gene on bone mineral density (BMD) and bone turnover markers (bone alkaline phosphatase and type I collagen C-telopeptides) in postmenopausal women. Paper-15178255.
Mutation in the E-box sequence from nt -124 to -119 ( E-box 3), in the construct from -224 to nt -1 or in the Inr element, which encompasses the transcriptional start site at nt -99, resulted in a substantial reduction in the human FSH-R promoter/enhancer activity. Paper-10561105.
A statistically significant difference in the allelic distribution of G-Asn/G-Ser and G-Ser/G-Ser genotype between proven fathers and infertile men but there were not any statistically significant difference in the overall frequency of the four FSHR haplotypes. Paper-15100087.
Northern blot hybridization of testicular poly (A)+ RNA to a cRNA probe corresponding to the extracellular domain of the monkey FSHR resulted in the identification of several transcripts, indicating alternative splicing events of the primary transcript. Paper-7625753.
SUMMARY: The identification of FSHR variants in a select infertility patient population has significant clinical implications in demonstrating a possible genetic cause to female infertility and improves our understanding of the genetic basis of infertility as a whole. Paper-15855260.
These results indicate that infertility can be induced in adult male monkeys by interfering with the action of FSH using specific peptides of the extracellular domain of FSHR as antigens, without the risk of producing cross-reacting antibodies to the other glycoprotein hormones. Paper-10415751.
CONCLUSIONS: • No significant correlation between serum FSH levels and semen characteristics, or fertility status and FSH-R gene polymorphisms was found. • The combination of heterozygous Thr/ Ala + Asn/Ser genotypes increases the risk for male infertility. Paper-16063835.
In total, 23 males with OAT and five males with azoospermia were tested for mutations of the coding sequences and the intron-exon boundaries of the FSH receptor gene by polymerase chain reaction ( PCR) followed by single strand conformation polymorphism analysis ( SSCP). Paper-1650315.
For the follicle-stimulating hormone (FSH) receptor ( FSHR) loss-of-function mutations have been allocated to this region, a homozygous A189V mutation resulting in a resistant ovary syndrome and impaired spermatogenesis and a heterozygous N191I mutation with no apparent phenotype. Paper-9240313.
Deletions of this entire segment or any 10 amino acids within this segment from FSHR led to complete loss of antibody response and, surprisingly, response to the hormone as well despite all mutants exhibiting cell surface receptor density and affinity comparable with the wild type receptor. Paper-13587526.
Testis weights of transgenic FSHR(+) hpg mice were increased approximately 2-fold relative to hpg controls ( P < 0.02) and contained mature Sertoli cells and postmeiotic germ cells absent in controls, revealing FSHR(+)-initiated autonomous FSH-like testicular activity. Paper-9636168.
METHODS: FSH receptor mRNA and peptide expression were evaluated by reverse transcription-polymerase chain reaction and by immunohistochemistry in endometrium from 15 women undergoing hysteroscopy to evaluate the morphology of the uterine cavity or hysterectomy for leiomyomas. Paper-11475605.
The recent identification of mutations in the FSH receptor gene, which display an increased sensitivity to hCG and are responsible for the development of spontaneous ovarian hyperstimulation syndrome (OHSS), provides for the first time the molecular basis for the physiopathology of spontaneous OHSS. Paper-10516855.
FSHR inactivating mutations may cause primary or secondary amenorrhea, infertility, and premature ovarian failure (POF), whereas activating mutations can predispose to ovarian hyperstimulation syndrome (OHSS) as a consequence of exogenous FSH administration, or with a spontaneous onset. Paper-14339214.
We hypothesize that a rising follicle-stimulating hormone ( FSH) level during the menopausal transition, even in the face of a normal estrogen level, contributes to increased bone resorption and profound bone loss that is accompanied by trabecular perforation and diminished bone strength. Paper-13891061.
Sequence analysis of the recombinant clones revealed the existence of a truncated isoform of the human follicle stimulating hormone receptor which is spliced through a cassette exon mode without a change in the open reading frame, thereby deleting exon IX from the coding region of the receptor. Paper-75862.
The IL-2(R467H), IL-2(T470A), the triple R467A/T470A/L477A IL-2 mutant and the IL-2 of the oxytocin receptor (G(q/11)-coupled) had no effects on Wt FSHR-mediated intracellular signaling whereas the L477A mutation provoked a higher ( approximately 55%) inhibition of FSH-stimulated cAMP than the free, Wt IL-2. Paper-9235037.
In order to elucidate regulatory mechanisms during puberty final oocyte maturation and spawning, full-length sequences coding for the receptors for follicle-stimulating hormone ( FSH-R) and luteinizing hormone (LH-R) were isolated from female Atlantic cod ( Gadus morhua) by a RACE-PCR based strategy. Paper-13554890.
RESULT(S): Allele frequencies for the G2105A/ S680N substitution of the FSHR in twin mothers were not different from those of controls ( genotype (isoform) [twins vs. controls]: G/G ( S/ S) [24.1% vs. 22.3%]; A/G ( N/ S) [57.4% vs. 55.4%]; A/A ( N/ N) [18.5% vs. 22.3%]). Paper-9037531.
Active immunization of proven fertile adult male bonnet monkeys ( Macaca radiata) with phage-expressed follicle-stimulating hormone receptor (FSHR)-specific peptides from the extracellular domain resulted in a progressive drop in sperm count with all animals becoming azoospermic by day 100. Paper-10415751.
We conclude that FSHR* activity enhances Sertoli and spermatogenic development in normal testes but has limited ability to maintain spermatogenesis during gonadotropin deficiency, in which the testicular response provided by the FSHR*D567G mutation resembled typical FSH-mediated but not steroidogenic activity. Paper-11812649.
The presence of FSHR in ovarian surface epithelium and of gonadotropin-binding sites in ovarian neoplasms provide additional evidence supporting the derivation of epithelial ovarian tumors from the surface epithelium and should promote heightened interest in the gonadotropin theory of ovarian tumorigenesis. Paper-458676.
When 70 treated subjects were subdivided based on FSHR genotype, only subjects with at least one serine in position 680 showed a statistically significant increase in these sperm parameters, whereas subjects with homozygote Thr307-Asn680 showed no difference in any seminal parameters evaluated. Paper-16092219.
There is great deal of information regarding metabolism of FSHR, including regulation of its gene expression, isoforms, and pathways of desensitization and degradation with which ovarian cancer etiology researchers have to be familiar with, and there are a number of steps where manipulation may stop carcinogenesis. Paper-14462561.
In the study population with an unknown distribution of FSH receptor polymorphisms, the ovarian response to rFSH stimulation was significantly different from that of uFSH stimulation, including lower number of oocytes retrieved/ oocytes in MII, higher fertilization rates and higher good quality embryo rates. Paper-10418649.
SummaryThis study evaluated the expression of FSH receptors ( FSHR) in the different stages of goat follicle development and investigated whether the addition of increasing concentrations of FSH throughout the culture period influences the survival, growth and antral formation of in vitro-cultured caprine preantral follicles. Paper-16042771.
In order to investigate whether alternative splicing of the receptor occurs in the human testis we amplified the extracellular and the transmembrane domain of the human testicular follicle stimulating hormone receptor by reverse transcription polymerase chain reaction and subcloned the resulting DNA fragments. Paper-75862.
This observation may indicate a direct connection between tyrosine phosphorylation and follicle-stimulating hormone (FSH) receptor ( FSHR) transduction pathways, as is the case for growth factor receptors with intrinsic tyrosine kinase activity, which share several downstream signaling elements with GPCRs. Paper-2151195.
This hitherto first case-control study investigating the association between these two FSHR SNPs and the risk of ovarian cancer involved 202 histopathologically confirmed ovarian cancer patients and 266 age-matched cancer-free control subjects using restriction fragment length polymorphism assay and direct sequencing. Paper-12051625.
As a first step towards understanding the regulatory mechanisms underlying the asynchronous oogenesis in repetitive spawning fish, full-length cDNAs encoding the receptors for follicle stimulating hormone ( FSH-R) and luteinizing hormone (LH-R) were isolated from the gonads of the flatfish Atlantic halibut (Hippoglossus hippoglossus). Paper-14410718.
In the study population with a similar distribution of FSH receptor polymorphisms, the ovarian responses to rFSH were lower numbers of oocytes in MII, higher fertilization rates and higher good quality embryo rates, but the total number of oocytes retrieved was not influenced, in comparison with ovarian stimulation with uFSH. Paper-10418649.
Classically, the FSH receptor ( FSH-R) mediates its effects through coupling to guanine nucleotide-binding protein alpha S subunit (Galpha(s)) and activation of the cAMP/protein kinase A (PKA) signaling pathway. beta-Arrestins are rapidly recruited to the FSH-activated receptor and play key roles in its desensitization and internalization. Paper-12289852.
Other possibilities for the presence of 46,XX gonadal dysgenesis, such as defects in the regulatory regions of the FSHR gene promoter, in the untranslated regions of exons 1 and 10, and within introns, or the existence of other genes likely to be important for normal ovarian function on the X chromosome or on autosomes, should be considered. Paper-8708819.
In this study, we investigated the availability of ovarian oocytes during the estrous cycle, and the follicle stimulating hormone (FSH) receptor ( FSH-R) homologies between guinea pigs and other species, in order to identify an effective gonadotropin and optimal time-of-application for the induction of superovulation in the guinea pig. Paper-9712957.
Two common single nucleotide polymorphisms (SNP) within exon 10 of the human FSHR gene result in two almost equally common allelic variants exhibiting threonine ( Thr) or alanine ( Ala) at position 307 in the hinge region, respectively, asparagine ( Asn) or serine ( Ser) at codon 680 of the intracellular domain. Paper-13358547.
These synonyms are used for gene FSHR (follicle stimulating hormone receptor): ODG1, MGC141668, MGC141667, LGR1, FSHRO, FSH-R, Follitropin receptor, Follicle-stimulating hormone receptor.
These accession numbers are used for gene FSHR: Q53RW2 (UNIPROT__AC), AY429104 (NCBI_GENBANK__AC), AK292562 (NCBI_GENBANK__AC), A8K947 (UNIPROT__AC).
FSHR is a homologue of FSHR (follicle stimulating hormone receptor) from Pan troglodytes.
FSHR is a homologue of FSHR (follicle stimulating hormone receptor) from Canis lupus familiaris.
FSHR is a homologue of FSHR (follicle stimulating hormone receptor) from Bos taurus.
FSHR is a homologue of FSHR (follicle stimulating hormone receptor) from Gallus gallus.
FSHR is a homologue of Fshr (follicle stimulating hormone receptor) from Mus musculus.
FSHR is a homologue of Fshr (follicle stimulating hormone receptor) from Rattus norvegicus.
FSHR is a homologue of fshr (follicle stimulating hormone receptor) from Danio rerio.
Important links !
iHOP - Information Hyperlinked over Proteins .
Concept & Implementation by Robert Hoffmann.