Mouse Anti-GNRH1 Recombinant Antibody (CBLG1-1457) (CBMAB-G4226-LY)

Name: Mouse Anti-GNRH1 Recombinant Antibody (CBLG1-1457)
SKU: CBMAB-G4226-LY
Rating: 5 (1 reviews)

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Datasheet

SDS

Request for COA

Datasheet Target References Q & As Review & reward Protocols Associated Products

Basic Information

Host Animal

Mouse

Clone

CBLG1-1457

Application

ICC, IHC-F/P, ELISA (EIA), WB

Immunogen

The antibody is a mouse monoclonal antibody raised against GnRH. It has been selected for its ability to recognize GnRH in immunohistochemical staining andwestern blotting

Specificity

Rat

Antibody Isotype

IgG

Clonality

Monoclonal

Application Notes

The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Format

Liquid

Buffer

50% glycerol

Preservative

0.02% NaN3

Concentration

0.5 mg/mL

Purity

> 95% Purity determined by SDS-PAGE.

Storage

Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freezethaw cycles.

More Infomation

Target

Full Name

Gonadotropin Releasing Hormone 1

Introduction

This gene encodes a preproprotein that is proteolytically processed to generate a peptide that is a member of the gonadotropin-releasing hormone (GnRH) family of peptides. Alternative splicing results in multiple transcript variants, at least one of which is secreted and then cleaved to generate gonadoliberin-1 and GnRH-associated peptide 1. Gonadoliberin-1 stimulates the release of luteinizing and follicle stimulating hormones, which are important for reproduction. Mutations in this gene are associated with hypogonadotropic hypogonadism. [provided by RefSeq, Nov 2015]

Entrez Gene ID

25194

UniProt ID

P07490

Alternative Names

Gnrh; Gnrha; Lhrh; Rgnrhg1; SH-4

Function

Stimulates the secretion of gonadotropins; it stimulates the secretion of both luteinizing and follicle-stimulating hormones.

Biological Process

Aging Source: Ensembl
Cell-cell signaling Source: ProtInc
Estrous cycle Source: Ensembl
Female pregnancy Source: Ensembl
Male sex determination Source: Ensembl
Multicellular organism development Source: ProtInc
Negative regulation of apoptotic process Source: Ensembl
Negative regulation of cell population proliferation Source: ProtInc
Negative regulation of immature T cell proliferation Source: Ensembl
Negative regulation of neuron migration Source: Ensembl
Regulation of gene expression Source: Ensembl
Regulation of ovarian follicle development Source: Ensembl
Reproduction Source: GO_Central
Response to corticosteroid Source: Ensembl
Response to ethanol Source: Ensembl
Response to lipopolysaccharide Source: Ensembl
Response to potassium ion Source: Ensembl
Response to prolactin Source: Ensembl
Response to prostaglandin E Source: Ensembl
Response to testosterone Source: Ensembl
Signal transduction Source: ProtInc

Cellular Location

Secreted

Involvement in disease

Hypogonadotropic hypogonadism 12 with or without anosmia (HH12):
The disease is caused by variants affecting distinct genetic loci, including the gene represented in this entry. The genetics of hypogonadotropic hypogonadism involves various modes of transmission. Oligogenic inheritance has been reported in some patients carrying mutations in GNRH1 as well as in other HH-associated genes including PROKR2 and FGFR1 (PubMed:23643382). A disorder characterized by absent or incomplete sexual maturation by the age of 18 years, in conjunction with low levels of circulating gonadotropins and testosterone and no other abnormalities of the hypothalamic-pituitary axis. In some cases, it is associated with non-reproductive phenotypes, such as anosmia, cleft palate, and sensorineural hearing loss. Anosmia or hyposmia is related to the absence or hypoplasia of the olfactory bulbs and tracts. Hypogonadism is due to deficiency in gonadotropin-releasing hormone and probably results from a failure of embryonic migration of gonadotropin-releasing hormone-synthesizing neurons. In the presence of anosmia, idiopathic hypogonadotropic hypogonadism is referred to as Kallmann syndrome, whereas in the presence of a normal sense of smell, it has been termed normosmic idiopathic hypogonadotropic hypogonadism (nIHH).

Cho-Clark, M. J., Watkins, A., & Wu, T. J. (2023). The role of GnRH metabolite, GnRH-(1-5), in endometrial cancer. Frontiers in Endocrinology, 14.

Patil, V. A., Lila, A. R., Shah, N., Ekbote, A. V., Shah, R., Bhandare, V. V., ... & Bandgar, T. (2022). GNRH1 Variants in Congenital Hypogonadotropic Hypogonadism: Single-Center Experience and Systematic Literature Review. Neuroendocrinology, 112(8), 723-732.

Li, C., Han, T., Li, Q., Zhang, M., Guo, R., Yang, Y., ... & Hu, R. (2021). MKRN3-mediated ubiquitination of Poly (A)-binding proteins modulates the stability and translation of GNRH1 mRNA in mammalian puberty. Nucleic Acids Research, 49(7), 3796-3813.

Petrucci, L., Maranesi, M., Supplizi, A. V., Dall’Aglio, C., Mandara, M. T., Quassinti, L., ... & Zerani, M. (2020). Kisspeptin/GnRH1 system in Leydig cells of horse (Equus caballus): Presence and function. Theriogenology, 152, 1-7.

Taroc, E. Z. M., Naik, A. S., Lin, J. M., Peterson, N. B., Keefe, D. L., Genis, E., ... & Forni, P. E. (2020). Gli3 regulates vomeronasal neurogenesis, olfactory ensheathing cell formation, and GnRH-1 neuronal migration. Journal of Neuroscience, 40(2), 311-326.

Taroc, E. Z. M., Katreddi, R. R., & Forni, P. E. (2020). Identifying Isl1 genetic lineage in the developing olfactory system and in GnRH-1 neurons. Frontiers in Physiology, 11, 601923.

Li, X., Xiao, J., Fan, Y., Yang, K., Li, K., Wang, X., ... & Zhou, Y. (2019). miR-29 family regulates the puberty onset mediated by a novel Gnrh1 transcription factor TBX21. Journal of Endocrinology, 242(3), 185-197.

Yellapragada, V., Liu, X., Lund, C., Känsäkoski, J., Pulli, K., Vuoristo, S., ... & Raivio, T. (2019). MKRN3 interacts with several proteins implicated in puberty timing but does not influence GNRH1 expression. Frontiers in endocrinology, 10, 48.

Taroc, E. Z. M., Lin, J. M., Tulloch, A. J., Jaworski, A., & Forni, P. E. (2019). GnRH-1 neural migration from the nose to the brain is independent from Slit2, Robo3 and NELL2 signaling. Frontiers in Cellular Neuroscience, 13, 70.

Elokil, A. A., Bhuiyan, A. A., Liu, H. Z., Hussein, M. N., Ahmed, H. I., Azmal, S. A., ... & Li, S. (2019). The capability of L-carnitine-mediated antioxidant on cock during aging: evidence for the improved semen quality and enhanced testicular expressions of GnRH1, GnRHR, and melatonin receptors MT 1/2. Poultry Science, 98(9), 4172-4181.

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Please try the standard protocols which include: protocols, troubleshooting and guide.

Enzyme-linked Immunosorbent Assay (ELISA)
Flow Cytometry
Immunofluorescence (IF)
Immunohistochemistry (IHC)
Immunoprecipitation (IP)
Western Blot (WB)
Enzyme-Linked Immunospot (ELISpot)
Proteogenomics
Other Protocols

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For research use only. Not intended for any clinical use.

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