Cloning and sequencing of human FSH receptor cDNA

Please cite this article as: Meduri, G., Bachelot, A., Cocca, M.P., Vasseur, C., Rodien, P., Kuttenn, F., Touraine, P., Misrahi, M., Molecular Pathology of the FSH receptor: new insights into FSH physiology, Molecular and Cellular Endocrinology (2007), doi:10.1016/j.mce.2007 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

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“…The large FSH-R gene is situated on chromosome 2p21 and comprises ten exons (Minegishi et al, 1991).…”

Section: Page 5 Of 40mentioning

confidence: 99%

Molecular pathology of the FSH receptor: New insights into FSH physiology

Meduri

Bachelot

Cocca

et al. 2008

Molecular and Cellular Endocrinology

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“…4 -6 The human FSHR gene is localized to 2p21 to p16 and is composed of 10 exons. 7 The 5Ј-flanking region of the gene has neither a TATA nor a CCAAT box and exhibits promoter-type features that are seen in housekeeping genes. 8 Inactivating mutations in the FSHR gene have been reported to cause hereditary hypergonadotropic ovarian failure in women.…”

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confidence: 99%

Mutation of the Follicle-Stimulating Hormone Receptor Gene 5′-Untranslated Region Associated With Female Hypertension

et al. 2006

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Abstract-Inactivating mutations in the follicle-stimulating hormone receptor (FSHR) gene have been reported to cause hereditary hypergonadotropic ovarian failure. It has been found recently that the FSHR knockout mouse exhibits hypertension. 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). We selected 5 SNPs in the gene (rs1394205, rs2055571, rs11692782, rs1007541, and rs2268361) and performed 2 genetic case-control studies in different populations. A confirmative case-control study was performed using 1035 EH patients and 1058 age-matched controls. Transcriptional activities were measured with a luciferase assay system. The first case-control study found that the A allele of rs1394205 was significantly higher in EH females (Pϭ0.010). In addition, in the confirmative case-control study, there was a significant difference for this SNP between female normotensive subjects (44.5%) and EH patients (50.7%) (Pϭ0.043). Multiple logistic regression analysis in female subjects also revealed a significant association of subjects with the A allele of rs1394205 with EH (Pϭ0.033), with the odds ratio calculated as 1.68 (95% CI: 1.04 to 2.73). Transcriptional activity of the A allele was 56Ϯ8% (meanϮSD) of that observed for the G-type allele (Pϭ0.001). Serum estradiol levels were significantly lower in patients with the A/A genotype than in patients without the A/A genotype (Pϭ0.004). The SNP in the 5Ј-untranslated region of the FSHR gene affects levels of transcriptional activity and is a susceptibility mutation of EH in women. Key Words: hypertension, essential Ⅲ hormones Ⅲ case-control studies I t is likely that essential hypertension (EH) is a polygenic disorder that results from the inheritance of a number of susceptibility genes. The causal genes identified may contribute from 30% to 50% of the variations in blood pressure seen among individuals. 1 These genetic determinants interact with environmental factors, such as dietary salt, to produce the final disease phenotype. Despite significant recent progress in genomic and statistical tools, the genetic dissection of human EH remains a major challenge. 2 The effects of follicle-stimulating hormone (FSH) are mediated by its interaction with specific receptors and the activation of G s , the stimulatory guanine nucleotide binding protein, which stimulates the enzyme adenylyl cyclase. 3 The FSH receptor (FSHR) belongs to the superfamily of G proteincoupled receptors that are characterized by the common structural feature of 7 transmembrane domains. They differ structurally from other G protein-coupled receptors in that they contain a large extracellular domain in the amino-terminal part of the receptor protein, which is required for interaction with complex glycoprotein hormones. 4 -6 The human FSHR gene is localized to 2p21 to p16 and is composed of 10 exons. 7 The 5Ј-flanking region of the gene has neither a TATA nor a CCAAT box and...

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“…20 The cDNA of FSHR was then obtained by PCR amplification using the above primers in reverse-transcribed products from human ovarian tissue. Subsequently, 2 pairs of composite primers were used for FSHR competitor construction ( Fig.…”

Section: Primers and Templates For Fshr Competitive Rt-pcrmentioning

confidence: 99%

Quantitative analysis of follicle‐stimulating hormone receptor in ovarian epithelial tumors: A novel approach to explain the field effect of ovarian cancer development in secondary mullerian systems

Wang

Lin

Parkash

et al. 2002

Intl Journal of Cancer

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The role of FSHR expression in ovarian cancer development is not clear. We examined quantitative expression of FSHR in different types of OET, presumed precursor lesions and peritoneal implants and further discussed FSH as a key growth-promotion factor for the process of ovarian epithelial tumorigenesis. Thirty-five primary OET specimens, including 5 serous cystadenomas, 4 papillary serous cystadenomas, 9 SBTs and 17 serous carcinomas, were examined for quantitative FSHR expression. Ten paired samples (3 benign cystadenomas, 5 SBTs and 2 carcinomas) were obtained from several morphologically different areas, including benignlooking, borderline and cancerous areas in the same OETs, and from the remaining ovarian tissue and contralateral ovaries. Competitive RT-PCR was performed to measure the quantitative expression of FSHR in each tissue sample. FSHR expression levels were compared among nonpaired samples and within paired samples. We found that OSE had the lowest FSHR expression, whereas antral follicles had the highest level. Within benign OETs, papillary serous cystadenomas have 4.9-fold higher FSHR levels than nonpapillary serous cystadenomas. SBTs had the highest level of FSHR expression, which was 12.8-fold, 2.7-fold and 2.4-fold higher than that of serous cystadenomas, papillary serous cystadenomas and grade 1 carcinomas, respectively. A similarly high level of FSHR mRNA was found in peritoneal implants, which were associated with SBTs. FSHR levels among serous carcinomas decreased with an increase in carcinoma grade. Grade 3 carcinomas had the lowest FSHR level, which was similar to that of serous cystadenomas, while grade 1 carcinomas had 6.5-fold higher FSHR levels than those in serous cystadenomas. Our results suggest that not only serum FSH but also FSHR in ovarian epithelium may play important roles in ovarian OET development. Both the receptor and ligand may act in a synergistic way to promote tumor growth. The observation that high FSHR levels are present in peritoneal implants suggests that FSH may also play a similar role in the development of peritoneal serous tumors. From this perspective, circulating FSH may be considered a driving force in the field effect theory for the development of both ovarian neoplasms and their associated peritoneal implants. However, the exact role of FSH and/or FSHR in the development of epithelial tumors arising in both the ovary and peritoneum needs further investigation. © 2002 Wiley-Liss, Inc. Key words: gonadotropin; hormone receptor; ovarian cancer; field effectOETs are a heterogeneous group of tumors that include benign cystadenomas, borderline tumors and OECs. Although significant efforts have been made to understand the process of tumorigenesis, a full etiologic description has not been made.The understanding of tumor progression was first advanced by Foulds, 1 who proposed that tumors are in constant evolution based on the observation of tumor heterogeneity. Tumor heterogeneity is due to an intrinsic instability of the tumor genetic material, resulting in ...

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Cloning and sequencing of human FSH receptor cDNA

Cited by 206 publications

References 11 publications

Molecular pathology of the FSH receptor: New insights into FSH physiology

Molecular pathology of the FSH receptor: New insights into FSH physiology

Mutation of the Follicle-Stimulating Hormone Receptor Gene 5′-Untranslated Region Associated With Female Hypertension

Quantitative analysis of follicle‐stimulating hormone receptor in ovarian epithelial tumors: A novel approach to explain the field effect of ovarian cancer development in secondary mullerian systems

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