LHRH (7-10)
- Known as:
- LHRH (7-10)
- Catalog number:
- L-0824
- Product Quantity:
- 5mg
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- LHRH (7-10)
Related genes to: LHRH (7-10)
- Gene:
- ADGRV1 NIH gene
- Name:
- adhesion G protein-coupled receptor V1
- Previous symbol:
- USH2C, MASS1, GPR98
- Synonyms:
- DKFZp761P0710, KIAA0686, FEB4, VLGR1
- Chromosome:
- 5q14.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-09-17
- Date modifiied:
- 2019-04-23
- Gene:
- C1orf198 NIH gene
- Name:
- chromosome 1 open reading frame 198
- Previous symbol:
- -
- Synonyms:
- FLJ14525, MGC10710, FLJ16283, DKFZp667D152, FLJ38847
- Chromosome:
- 1q42.2
- Locus Type:
- gene with protein product
- Date approved:
- 2006-02-15
- Date modifiied:
- 2017-08-01
- Gene:
- EBLN3P NIH gene
- Name:
- endogenous Bornavirus like nucleoprotein 3, pseudogene
- Previous symbol:
- EBLN3
- Synonyms:
- LOC100506710
- Chromosome:
- 9p13.2
- Locus Type:
- pseudogene
- Date approved:
- 2014-06-05
- Date modifiied:
- 2019-02-18
- Gene:
- GACAT3 NIH gene
- Name:
- gastric cancer associated transcript 3
- Previous symbol:
- LINC01458
- Synonyms:
- lncRNA-AC130710
- Chromosome:
- 2p24.3
- Locus Type:
- RNA, long non-coding
- Date approved:
- 2014-06-25
- Date modifiied:
- 2018-07-25
- Gene:
- GNRH1 NIH gene
- Name:
- gonadotropin releasing hormone 1
- Previous symbol:
- GRH, GNRH, LHRH
- Synonyms:
- -
- Chromosome:
- 8p21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1993-12-15
- Date modifiied:
- 2016-10-05
Related products to: LHRH (7-10)
(3,5-Diiodo-Tyr5)-LHRH 98% C55H73I2N17O13 CAS: 73644-49-2(D-2-Nal6)-LHRH
Nafarelin 98% C66H83N17O13 CAS: 76932-56-4(D-2-Nal6)-LHRH (Nafarelin) - EIA Kit,(D-2-Nal6)-LHRH (Nafarelin) - EIA Kit, Host Rabbit, High Sensitivity, CE-marked(D-2-Nal6)-LHRH (Nafarelin) - EIA Kit, Host RabbitHigh SensitivityCE-marked(D-2-Nal6)-LHRH (Nafarelin) - EIA Kit, Host: Rabbit, High Sensitivity, CE-marked(D-2-Nal6)-LHRH (Nafarelin) - EIA Kit, Host: Rabbit, High Sensitivity, CE-marked(D-2-Nal6)-LHRH (Nafarelin), High Sensitivity ELISA(D-Ala6)-LHRH
(D-Ala6)-GnRH, (D-Ala6)-Gonadorelin 98% C56H77N17O13 CAS: 51230-19-4(D-His2)-LHRH
(D-His2)-Gonadorelin, (D-His2)-GnRH 98% C55H75N17O13 CAS: 53634-19-8(D-His2,D-Trp6)-LHRH
(D-His2)-Triptorelin 98% C64H82N18O13 CAS: 321709-34-6(D-Leu6)-LHRH (1-8) (free acid)
(Des-Pro-NHEt9)-Leuprolide, (Des-Pro-NHEt9)-Leuprorelin 98% C52H72N14O12 CAS: 112642-14-5(D-Leu6,Pro-NHEt9)-LHRH (4-9)
Leuprolide (4-9), Leuprorelin (4-9) 98% C37H62N10O8 CAS: 202333-85-5(D-Leu7)-LHRH
(D-Leu7)-Gonadorelin 98% C55H75N17O13 CAS: 53728-75-9(D-Lys6)-LHRH
(D-Lys6)-Gonadorelin 98% C59H84N18O13 CAS: 130751-49-4 Related articles to: LHRH (7-10)
- This study aimed to investigate the effects of dietary supplementation of N-carbamylglutamate (NCG) on the laying performance of layers and explore the underlying endocrine mechanism involving the hypothalamic-pituitary-ovarian (HPO) axis. Ninety-six 12-week-old layers of the Zhuanghe Dagu breed were divided into two groups: CON and TRT, with four replicates and 12 birds per replicate. The experimental period lasted 24 weeks, during which the CON group received a basal diet while the TRT group received a basal diet supplemented with 0.12% NCG. The results showed that NCG supplementation in the diet resulted in an increase in the egg production rate and an advancement in the timing of egg-laying compared to the CON group. To gain insights into the underlying molecular mechanisms, transcriptomics analysis was conducted on the hypothalamus, pituitary, and ovary. Differential gene expression analysis identified 156 differentially expressed genes (DEGs) in the hypothalamus, 208 DEGs in the pituitary, and 229 DEGs in the ovary. Pathway analysis revealed that these DEGs were enriched in 2 pathways in the hypothalamus, 8 pathways in the pituitary, and 9 pathways in the ovary, all of which are related to reproduction. Of particular interest, the expression of specific genes involved in the HPO axis, such as and in the hypothalamus, and in the pituitary, and , , , , , and in the ovary, was significantly regulated by NCG supplementation. These findings were further validated by quantitative real-time polymerase chain reaction, which confirmed the expression profiles of the aforementioned genes observed in the RNA-seq results. Overall, these findings provide valuable insights into the endocrine mechanisms underlying the improvement of laying performance in layers through NCG supplementation. - Source: PubMed
Publication date: 2025/10/02
Peng Xiao-BingWang Qing-YueZhang YanLiu NaMa WeiWang Chun-Qiang - Protracted exposure to drugs like Lupron Depot® suppresses pubertal development. How the brain responds and develops in the face of pharmacological suppression is not well understood. The present study tested the effects of daily leuprolide acetate (LEU) treatment (50 μg/kg, postnatal day (PD) 25-50) on gene expression (Kiss1, Esr1, Esr2, Ar, Gnrh1, Gnrhr) in the hypothalamus and pituitary of female and male Long-Evans rats using real-time PCR. Brains and trunk blood were harvested on PD 50. In the pituitary gland of both sexes, expression of Esr2 and Gnrhr expression was higher in LEU-treated rats than in saline controls. Esr1 expression in females was lower and Ar expression in males was higher in LEU-treated rats than saline controls. In the preoptic area of the hypothalamus in male rats, Kiss1 expression was significantly lower in LEU than in saline controls. In the mediobasal hypothalamus, Gnrh1 and Kiss1 expression was higher in LEU-treated male rats than in saline controls; for females, only Kiss1 was increased by LEU. Serum gonadal hormone levels were not significantly different in LEU-treated rats than saline controls at the end of treatment, although hormones trended lower in the LEU-treated rats. LEU affected expression of genes involved in reproduction, potentially explaining sex-specific effects of LEU on behavior reported earlier. The changes in hypothalamic and pituitary gene expression may represent compensation that permits early stages of pubertal development (e.g., VO and PPS), but not complete maturation (e.g., estrous cyclicity, sexual behavior) during LEU treatment. - Source: PubMed
Publication date: 2025/07/24
Guarraci Fay AKlepcyk Ian MThompson Lindsay MStreifer MadelineHilz Emily NHudson GraceMeerts Sarah HGore Andrea C - Genistein, an abundant phytoestrogen found in soy and soy products, can cross the placental barrier. However, impacts of prenatal genistein on male offspring reproductive development are unclear. Here, pregnant Sprague-Dawley rats were exposed to genistein at 1, 10, and 20 mg/kg·bw/day from gestational day 0-17. Medium- and high-dose prenatal genistein delayed pubertal onset in male offspring by 2-3 days, reduced body weight, increased the testis-to-body weight ratio and shortened anogenital distance. Testicular histology revealed disorganized seminiferous tubules and reduced germ cell numbers. At pubertal onset, serum levels of gonadotropin-releasing hormone, follicle-stimulating hormone, luteinizing hormone and estradiol were increased in medium- and high-dose groups, while at postnatal day 49, serum level of testosterone was decreased. Real-Time quantitative PCR revealed reduced transcription of Kiss1 and Esr1, and elevated transcription of Gnrh1 in hypothalamus; reduced transcription of Esr1, Gnrhr, Fshb and Lhb in pituitary; and elevated transcription of Esr2, Lhcgr, Cyp11a1 and Inhba in testes. Immunohistochemistry and Western-blot analyses showed dysregulated protein expression of KISS1, GnRHR, and FSHR. In conclusion, prenatal genistein exposure in rats delays pubertal onset in male offspring by affecting hypothalamic-pituitary-gonadal axis, highlighting potential transgenerational impacts of prenatal phytoestrogen on pubertal and reproductive development of male offspring. - Source: PubMed
Publication date: 2025/05/02
Zi JingMa GuochenHu YifanLi XinlongCao QianqianLi YanliuWang XiaoyuCheng GuoXiong Jingyuan - Which phenotypes can be confidently linked to a genetic etiology in males with congenital hypogonadotropic hypogonadism (CHH) resulting in absent or arrested puberty? - Source: PubMed
Castro SebastiánBrunello Franco GSansó GabrielaIzquierdo AgustínZaiat JonathanUrrutia MarielaMartí MarceloRey Rodolfo ATellechea Mariana LGrinspon Romina P - In this study, the expression and localization of gonadotropin-releasing hormone (GnRH1) and kisspeptin (KISS1) and their specific receptors in canine ovarian and uterine tissues were investigated after the application of deslorelin acetate (Suprelorin, 4.7 mg, Virbac, France) in the late prepubertal period. We hypothesized that prolonged treatment of prepubertal dogs with deslorelin would alter the expression of GnRH and kisspeptin genes in the uterus and ovaries. Ovarian and uterine samples of 25 dogs with an average age of 7.8 ± 0.2 months and from mixed breeds were used. Following implant insertion, dogs entered estrus (EST; n = 6); dogs without estrus (N-EST; n = 10) comprised the experimental groups. Nine dogs with placebo implants served as a control (CONT). Ovarian and uterine tissues were investigated for expression of GnRH1, GnRHR, KISS1, and KISS1R/GPR54 mRNA and protein by using IHC and RT-qPCR. In the uterus, expression of GnRH1 significantly decreased in response to deslorelin treatment in the N-EST, compared with the control group. Compared with CONT, KISS1R expression in ovarian samples was significantly lower in the EST group. Uterine protein expression of GnRH1 appeared weaker in N-EST than in CONT. While GnRH1-system members and KISS1 protein were localized in the follicles at various stages and stroma, no or only weak signals were detected for KISS1R in the ovarian samples. Deslorelin-mediated induction of puberty by changing the expression of some of the GnRH and KISS1-system members seems to have an effect on ovarian and uterine functionality. Deslorelin implants can, therefore, not be considered a valuable alternative to induce fertile estrus in late-prepubertal bitches. However, further studies with a larger number of animals are needed to clarify the effect of deslorelin-mediated induction of puberty. - Source: PubMed
Publication date: 2024/11/25
Karadağ Muhammet AliGram AykutSchäfer-Somi SabineAslan SelimKaya Duygu