GnRHR Antibody, mAb, Mouse
- Known as:
- GnRHR Antibody, mAb, Mouse
- Catalog number:
- A00086
- Product Quantity:
- 100ug
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- GnRHR Antibody mAb Mouse
Related genes to: GnRHR Antibody, mAb, Mouse
- 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, mAb, Mouse
Related articles to: GnRHR Antibody, mAb, Mouse
- 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 - Depression is a common comorbidity of chronic pain. Gonadotropin-releasing hormone (GnRH) and its receptor (GnRHR) expressed in the central nervous system are involved in non-reproductive functions. Herein, we aimed to elucidate the role and mechanism of action of GnRH in pain-related depression like behaviour in a mouse model. And we found that both GnRH and GnRHR were down-regulated in the anterior cingulate cortex of mice that were subjected to chronic pain-induced depression with complete Freund's adjuvant. Specifically, either systemic treatment with GnRH agonists or GnRH overexpression in the anterior cingulate cortex effectively ameliorated the chronic pain-induced depression-like behaviour via GnRHR signalling. Moreover, GnRHR co-localized with both excitatory and inhibitory neurons, and GnRH agonists or overexpressed GnRH rescued the complete Freund's adjuvant-stimulated imbalance of excitatory-inhibitory neurons in the anterior cingulate cortex. Chemogenetic activation of anterior cingulate cortex neurons reversed GnRH agonist-induced improvement in depression-like behaviour in complete Freund's adjuvant-treated mice. Furthermore, this specific role of GnRH was dependent on the activation of protein kinase C and Erb-B2 receptor tyrosine kinase 4 signalling pathway. Therefore, our findings indicate that GnRH/GnRHR is involved in the development of chronic pain-related depression, which may through rebalancing the excitatory-inhibitory neurons via the activation of protein kinase C/Erb-B2 receptor tyrosine kinase 4 pathway. Thus, GnRH could be a potential target for the treatment of chronic pain-related depression. - Source: PubMed
Publication date: 2026/04/16
Huang YanmeiChen YunfengLiu XueqinXu YangChen LingCao WenyuZhong Xiaolin - This study reviews the main candidate genes involved in the pathophysiology of Polycystic Ovary Syndrome (PCOS). PCOS is a common endocrine-metabolic disorder in women of reproductive age, characterized by menstrual irregularity, hyperandrogenism, and polycystic ovarian morphology. It is associated with increased metabolic and cardiovascular risk and is a leading cause of infertility. Although its pathophysiology is not fully understood, alterations in the hypothalamic-pituitary-ovarian axis, insulin metabolism, and steroidogenesis have been described. Polymorphisms in genes encoding hormones, enzymes, and receptors in these pathways contribute to clinical variability and ethnic differences, offering potential for early diagnosis and personalized medicine. This review summarizes key candidate genes related to insulin metabolism (INS, INSR, IRS-1), the hypothalamic-pituitary-ovarian axis (LHβ, LHCGR, FSHR, GnRHR, AMH, AMHR2, KISS1, CAPN10), steroidogenesis (CYP11A, CYP17A1, CYP19A1, CYP21, 17β-HSD, SHBG, AR, STAR), and other clinically relevant mechanisms such as obesity, lipid metabolism (PPARG, VDR, FTO), and follicular development (ACE). - Source: PubMed
Publication date: 2026/04/19
Cepero-González María de Los AngelesAguilar-Galarza AdrianaRodríguez-García Víctor ManuelGarcía-Gasca TeresaMoreno Celis Ulisses - The eastern and northern parts of Xinjiang are the main camel breeding areas in the region. Currently, there is a lack of systematic comparative genetic studies of local populations with significant phenotypic differences at the whole-genome level. Previous research has shown significant differences in milk production traits between Bactrian camels in the eastern and northern regions of Xinjiang. To further elucidate the genetic differences between the Bactrian camel populations in these two areas and the molecular basis of their lactation traits, this study selected 106 Bactrian camels—55 from three camel farms in the northern region and 51 from one farm in the eastern region—for whole-genome resequencing. - Source: PubMed
Publication date: 2026/03/30
Li YongqingCai ShudongTulafu HanikeziLiu ShihaoLin ChangchunWu WeiweiHuang Juncheng - ImportanceIdiopathic hypogonadotropic hypogonadism (IHH) associated with congenital hemi-arrhinia is rare but can substantially impact patients' quality of life. The underlying genetic etiology remains to be clarified, and surgical approaches for reconstructing congenital hemi-arrhinia are sparsely reported.ObjectiveTo provide a reference for clinical diagnosis and management by reporting the patient's genetic findings and surgical outcomes.DesignCase report.SettingTertiary public referral hospital.ParticipantsA patient diagnosed with IHH and congenital hemi-arrhinia.Intervention or ExposuresWhole-exome sequencing was performed, and the patient's nose was reconstructed using the contralateral nasal dorsum flap as the inner lining, an L-strut of rib and costal cartilage graft as the structural support, and a pre-expanded forehead flap as the outer skin envelope.Main Outcome MeasuresOne-year postoperative outcomes were evaluated using the Rhinoplasty Outcome Evaluation (ROE) and Nasal Obstruction Symptom Evaluation (NOSE) scales.ResultsWhole-exome sequencing revealed maternally and paternally inherited missense mutations in Gonadotropin-Releasing Hormone Receptor (GNRHR) (c.719G > A) and KISS1 (c.58G > A), respectively. One-year follow-up demonstrated stable nasal reconstruction, with the ROE score improving from 4 to 17 out of 24. The NOSE score remained 1 out of 20 pre- and postoperatively, indicating no significant change in nasal airflow perception.ConclusionsThe 4-stage surgical procedure is a viable and effective reconstructive option for hemi-arrhinia.RelevanceOur genetic findings may serve as a reference for investigating the underlying causes of IHH. The described surgical approach provides a practical reference for surgeons performing hemi-nose reconstruction. - Source: PubMed
Publication date: 2026/03/28
Liu YunhanKhoong YiminHuang XinGu ShuchenZan Tao