Ask about this productRelated genes to: GnRHR antibody
- Gene:
- GNRHR NIH gene
- Name:
- gonadotropin releasing hormone receptor
- Previous symbol:
- GRHR
- Synonyms:
- LHRHR
- Chromosome:
- 4q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-01-15
- Date modifiied:
- 2016-10-05
Related products to: GnRHR antibody
Related articles to: GnRHR antibody
- Reproductive efficiency in Nellore heifers is fundamental to the profitability and sustainability of beef production in tropical regions, where environmental stress can cause genotype-environment (G×E) interactions that affect fertility. Using 200,258 and 299,885 phenotypic records for heifer early pregnancy (HP) and heifer rebreeding (HR), respectively, we investigated the genetic basis of reproductive plasticity via single-step genomic reaction norms across a continuous environmental gradient (EG) defined from yearling weight records as a proxy for environmental quality. Genomic analyses included 22,556 animals (21,456 females and 1,100 sires) with genotypes imputed to 409,617 single-nucleotide polymorphisms (SNPs). We then performed genome-wide association analyses of the reaction norm intercept (genetic merit) and slope (environmental sensitivity), followed by multi-trait summary analyses and Bayesian fine-mapping of significant loci using imputed whole-genome sequence variants within ±100 kb windows around lead SNPs. - Source: PubMed
Publication date: 2026/06/08
Mota Lucio F MArikawa Leonardo MSantos Daniel J ABrito Luiz FFonseca Larissa F SOliveira Henrique NAlbuquerque Lucia G - A mid-adolescent boy presented with pubertal delay and micropenis. His sister had amenorrhoea. Laboratory evaluation confirmed hypogonadotropic hypogonadism. Brain MRI showed normal pituitary and hypothalamus, though the olfactory bulbs assessment was limited by artefacts. Testosterone therapy enabled the development of secondary sexual characteristics. Subsequent genetic testing identified compound heterozygous pathogenic variants in the gonadotropin-releasing hormone receptor gene, establishing the molecular basis of isolated hypogonadotropic hypogonadism (IHH). Identifying a genetic cause allowed proper counselling regarding prognosis, fertility induction and familial risk. Management focuses on completing sexual maturation, fertility induction and genetic counselling. This case emphasises that mid-adolescents with absent sexual characteristics apart from pubic hair should be evaluated for hypogonadotropic hypogonadism. Early recognition and prompt investigation support timely pubertal induction, fertility preservation and genetic counselling, improving long-term outcomes. Furthermore, this report highlights the pivotal role of genetic testing in guiding the diagnosis and long-term treatment management in patients with IHH. - Source: PubMed
Publication date: 2026/06/01
Lucas Miguelda Bernarda Rodrigues InêsRosmaninho-Salgado JoanaMirante Alice - Gonadotropins are glycoprotein hormones that are often secreted from the gonadotrope cells of the pituitary gland. These hormones play an essential role in growth, reproduction and sexual function. - Source: PubMed
Kheiri FarshidFaghani MostafaBerenjegani Mohammad MohammadiGouran Somayeh TirbakhshDomakani Matin Rahimi - Zearalenone (ZEA) is a potent estrogenic mycotoxin known to disrupt reproductive functions, but its precise central neuroendocrine mechanisms remain unclear. This study investigated the effects of ZEA on the hypothalamic-pituitary Kiss1/GPR54 signaling pathway in weaned gilts. A total of 32 gilts were randomly assigned to four dietary treatments contained with 0, 0.15, 1.5, or 3.0 mg/kg ZEA for a 32-day feeding trial. Histopathology, immunohistochemistry, and mRNA/protein expression analyses of GPR30, Kiss1, GPR54, GnRH, and GnRHR in the hypothalamus and pituitary gland were conducted. ZEA exposure induced significant histological damage in both tissues. In the hypothalamus, Kiss1, GPR54, GnRH, and GnRHR exhibited a non-linear response, increasing at moderate doses and decreasing at 3.0 mg/kg ZEA, whereas GPR30 expression was continuously upregulated. In the pituitary gland, GnRHR showed a similar non-linear pattern. Furthermore, high-dose ZEA down-regulated pituitary Kiss1 and GPR54 while up-regulating GnRH and GPR30 expressions. In conclusion, ZEA induces reproductive neuroendocrine toxicity through a complex, dose-dependent modulation of the Kiss1/GPR54 signaling axis. The persistent upregulation of GPR30 suggests it acts as a crucial mediator in disrupting this endocrine feedback loop within the hypothalamus and pituitary gland. - Source: PubMed
Publication date: 2026/04/22
Yuan ZixueZhou MinLuan YueKong LeiYang WeirenJiang Shuzhen - Several reproductive issues in both men and women are caused by changes in the pulsatile secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH). For males to sustain spermatogenesis and Leydig cell function, and for females to ensure orderly folliculogenesis, ovulation, and ovarian steroidogenesis, precise coordination of LH and FSH secretion is necessary. Pituitary responsiveness, the frequency or amplitude of gonadotropin-releasing hormone pulses, or the dysregulation of feedback signals mediated by sex steroids and inhibins all disrupt the balance between LH and FSH secretion. Oligozoospermia, luteal-phase abnormalities, anovulation, or complete spermatogenic failure are possible clinical signs of these alterations. In addition to functional neuroendocrine disturbances, emerging genetic and epigenetic evidence, including pathogenic variants in genes such as gonadotropin-releasing hormone receptor, kisspeptin, kisspeptin receptor, luteinizing hormone beta subunit, follicle-stimulating hormone beta subunit, follicle-stimulating hormone receptor, and luteinizing hormone/choriogonadotropin receptor, has highlighted the role of inherited and acquired molecular defects in disrupting gonadotropin regulation. This narrative review synthesizes contemporary mechanistic, clinical, translational, and genetic evidence elucidating how dysregulated secretion of LH and FSH contributes to reproductive dysfunction. The molecular processes that regulate gonadotropin synthesis and release, as well as neuroendocrine regulation, gene-level determinants of hypothalamic-pituitary-gonadal (HPG) axis dysfunction, and the clinical phenotypes that result from their disruption, are all given special attention. We conclude with a discussion of new treatment strategies that target local intragonadal regulators to enhance gametogenic capacity, modulate gonadotropin signaling, or restore physiological gonadotropin-releasing hormone (GnRH) pulsatility, with consideration of how genetic insights may inform personalized therapeutic approaches. - Source: PubMed
Publication date: 2026/03/31
Zikopoulos AthanasiosMoustakli EfthaliaPotiris AnastasiosParaschos Vasilis SebastianKatopodis PeriklisMachairoudias PavlosAntsaklis PanagiotisKathopoulis NikolaosAnagnostaki IsminiStavros Sofoklis