ReviewFrontiers in endocrinology2015
Genetic Models for the Study of Luteinizing Hormone Receptor Function.
Review in Frontiers in endocrinology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
26 citing papers in PubMed, 54 citations in OpenAlex.
- Empty Follicle Syndrome: Current Therapeutic Approaches and the Role of Triggering Agents in Assisted Reproductive Technology.Medical sciences (Basel, Switzerland) · 2026Review
- Cryptorchidism: Novel genetic insights into CCDC149 mutations.Andrology · 2026Article
- Developmental and functional landscape of theca cells in ovarian biology.Biological research · 2026Review
- LHCGR phamacodynamic effects during follicular maturation.Frontiers in endocrinology · 2026Review
- Article
- ZW and XY Sex Chromosomes Drive Rapid and Distinctive Evolution of Sex-Biased Gene Expression.Molecular ecology · 2025Article
- Targeted gene silencing in mouse testicular Sertoli and Leydig cells using adeno-associated virus vectors.Asian journal of andrology · 2025Article
- 3D Bioprinted Coaxial Testis Model Using Human Induced Pluripotent Stem Cells:A Step Toward Bicompartmental Cytoarchitecture and Functionalization.Advanced healthcare materials · 2025Article
- A case of familial partial lipodystrophy type 2 masquerading as Cushing syndrome: Explaining an atypical phenotype by whole-exome sequencing.Archives of endocrinology and metabolism · 2025Article
- Precise Correction of Lhcgr Mutation in Stem Leydig Cells by Prime Editing Rescues Hereditary Primary Hypogonadism in Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- The Effect of Statins on Male Reproductive Parameters: A Mechanism Involving Dysregulation of Gonadal Hormone Receptors and TRPV1.International journal of molecular sciences · 2023Article
- Genetics of pubertal delay.Clinical endocrinology · 2022Review
- Adult Exposure to Di-N-Butyl Phthalate (DBP) Induces Persistent Effects on Testicular Cell Markers and Testosterone Biosynthesis in Mice.International journal of molecular sciences · 2022Article
- Effects ofMolecules (Basel, Switzerland) · 2022Article
- Aberrant activation of KRAS in mouse theca-interstitial cells results in female infertility.Frontiers in physiology · 2022Article
- Large-scale DNA demethylation occurs in proliferating ovarian granulosa cells during mouse follicular development.Communications biology · 2021Article
- Human Chorionic Gonadotropin Modulates the Transcriptome of the Myometrium and Cervix in Late Gestation.Reproductive sciences (Thousand Oaks, Calif.) · 2021Article
- A Case of Familial Male-limited Precocious Puberty with a Novel MutationJournal of clinical research in pediatric endocrinology · 2021Article
- Androgens regulate ovarian gene expression by balancing Ezh2-Jmjd3 mediated H3K27me3 dynamics.PLoS genetics · 2021Article
- Enrichment analyses of diseases and pathways associated with precocious puberty using PrecocityDB.Scientific reports · 2021Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
The luteinizing hormone/chorionic gonadotropin receptor (LHCGR) is essential for fertility in men and women. LHCGR binds luteinizing hormone (LH) as well as the highly homologous chorionic gonadotropin. Signaling from LHCGR is required for steroidogenesis and gametogenesis in males and females and for sexual differentiation in the male. The importance of LHCGR in reproductive physiology is underscored by the large number of naturally occurring inactivating and activating mutations in the receptor that result in reproductive disorders. Consequently, several genetically modified mouse models have been developed for the study of LHCGR function. They include targeted deletion of LH and LHCGR that mimic inactivating mutations in hormone and receptor, expression of a constitutively active mutant in LHCGR that mimics activating mutations associated with familial male-limited precocious puberty and transgenic models of LH and hCG overexpression. This review summarizes the salient findings from these models and their utility in understanding the physiological and pathological consequences of loss and gain of function in LHCGR signaling.
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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.