ArticleEndocrinology2010
Female mice expressing constitutively active mutants of FSH receptor present with a phenotype of premature follicle depletion and estrogen excess.
Article in Endocrinology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- American Thyroid Association Guide to investigating thyroid hormone economy and action in rodent and cell models.Thyroid : official journal of the American Thyroid Association · 2014Guideline
- Review
- FSHR and LHR functional compensation reveals the mechanism and treatment of Ovarian Hyperstimulation Syndrome.Nature communications · 2026Article
- A rare germline BMP15 missense mutation causes hereditary ovarian immature teratoma in human.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Alterations in gonadotropin, apoptotic and metabolic pathways in granulosa cells warrant superior fertility of the Dummerstorf high fertility mouse line 1.Journal of ovarian research · 2023Article
- Knockout of cyclin B1 in granulosa cells causes female subfertility.Cell cycle (Georgetown, Tex.) · 2022Article
- Endocrine and molecular factors of increased female reproductive performance in the Dummerstorf high-fertility mouse line FL1.Journal of molecular endocrinology · 2022Article
- The Roles of Luteinizing Hormone, Follicle-Stimulating Hormone and Testosterone in Spermatogenesis and Folliculogenesis Revisited.International journal of molecular sciences · 2021Review
- The Luteinizing Hormone Receptor Knockout Mouse as a Tool to Probe the In Vivo Actions of Gonadotropic Hormones/Receptors in Females.Endocrinology · 2021Article
- MC4R mutant mice develop ovarian teratomas.Scientific reports · 2021Article
- Article
- Gain-of-Function Genetic Models to Study FSH Action.Frontiers in endocrinology · 2019Review
- Mouse models for the analysis of gonadotropin secretion and action.Best practice & research. Clinical endocrinology & metabolism · 2018Review
- Constitutively active follicle-stimulating hormone receptor enables androgen-independent spermatogenesis.The Journal of clinical investigation · 2018Article
- Molecular regulation of follicle-stimulating hormone synthesis, secretion and action.Journal of molecular endocrinology · 2018Review
- Regulation of reproduction via tight control of gonadotropin hormone levels.Molecular and cellular endocrinology · 2018Review
- Role of Follicle-Stimulating Hormone in Spermatogenesis.Frontiers in endocrinology · 2018Review
- In Vitro Effects of the Endocrine Disruptor p,p'-DDT on Human Follitropin Receptor.Environmental health perspectives · 2016Article
- Infertility in Female Mice with a Gain-of-Function Mutation in the Luteinizing Hormone Receptor Is Due to Irregular Estrous Cyclicity, Anovulation, Hormonal Alterations, and Polycystic Ovaries.Biology of reproduction · 2015Article
- Inactivation of Retinoblastoma Protein (Rb1) in the Oocyte: Evidence That Dysregulated Follicle Growth Drives Ovarian Teratoma Formation in Mice.PLoS genetics · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
Abstract
Strong gain-of-function mutations have not been identified in humans in the FSH receptor (FSHR), whereas such mutations are common among many other G protein-coupled receptors. In order to predict consequences of such mutations on humans, we first identified constitutively activated mutants of the mouse (m) Fshr and then expressed them under the human anti-Müllerian hormone promoter in transgenic mice or created knock-in mutation into the mouse genome. We show here that mutations of Asp580 in the mFSHR significantly increase the basal receptor activity. D580H and D580Y mutations of mFSHR bind FSH, but the activity of the former is neither ligand-dependent nor promiscuous towards LH/human choriogonadotropin stimulation. Transgenic expression of mFshr(D580H) in granulosa cells leads to abnormal ovarian structure and function in the form of hemorrhagic cysts, accelerated loss of small follicles, augmented granulosa cell proliferation, increased estradiol biosynthesis, and occasional luteinized unruptured follicles or teratomas. The most affected mFshr(D580H) females are infertile with disturbed estrous cycle and decreased gonadotropin and increased prolactin levels. Increased estradiol and prolactin apparently underlie the enhanced development of the mammary glands, adenomatous pituitary growth, and lipofuscin accumulation in the adrenal gland. The influence of the mFSHR(D580Y) mutation is milder, mainly causing hemorrhagic cysts in transgenic mFSHR(D580Y) and mFSHR(D580Y) -knock-in mice. The results demonstrate that gain-of-function mutations of the FSHR in mice bring about distinct and clear changes in ovarian function, informative in the search of similar mutations in humans.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.