Rabbit Anti-KISS1R Recombinant Antibody (EG1794) (CBMAB-EN2142-LY)

Name: Rabbit Anti-KISS1R Recombinant Antibody (EG1794)
SKU: CBMAB-EN2142-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

Rabbit

Clone

EG1794

Application

IF: 1:100~1:500 ELISA: 1:5000

Immunogen

The antibody was produced against synthesized peptide derived from internal of human KISSR.

Specificity

Human

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

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

KISS1 Receptor

Introduction

The protein encoded by this gene is a galanin-like G protein-coupled receptor that binds metastin, a peptide encoded by the metastasis suppressor gene KISS1. The tissue distribution of the expressed gene suggests that it is involved in the regulation of endocrine function, and this is supported by the finding that this gene appears to play a role in the onset of puberty. Mutations in this gene have been associated with hypogonadotropic hypogonadism and central precocious puberty. [provided by RefSeq, Jul 2008]

Entrez Gene ID

84634

UniProt ID

Q969F8

Alternative Names

KISS1 Receptor; G-Protein Coupled Receptor OT7T175; G Protein-Coupled Receptor 54; Kisspeptins Receptor; Hypogonadotropin-1; Metastin Receptor; HOT7T175; KISS-1R;

Function

Receptor for metastin (kisspeptin-54 or kp-54), a C-terminally amidated peptide of KiSS1. KiSS1 is a metastasis suppressor protein that suppresses metastases in malignant melanomas and in some breast carcinomas without affecting tumorigenicity. The metastasis suppressor properties may be mediated in part by cell cycle arrest and induction of apoptosis in malignant cells. The receptor is essential for normal gonadotropin-released hormone physiology and for puberty. The hypothalamic KiSS1/KISS1R system is a pivotal factor in central regulation of the gonadotropic axis at puberty and in adulthood. The receptor is also probably involved in the regulation and fine-tuning of trophoblast invasion generated by the trophoblast itself. Analysis of the transduction pathways activated by the receptor identifies coupling to phospholipase C and intracellular calcium release through pertussis toxin-insensitive G(q) proteins.

Biological Process

G protein-coupled receptor signaling pathway1 PublicationNAS:UniProtKB
Neuropeptide signaling pathwayManual Assertion Based On ExperimentIBA:GO_Central

Cellular Location

Cell membrane

Involvement in disease

Hypogonadotropic hypogonadism 8 with or without anosmia (HH8):
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).
Precocious puberty, central 1 (CPPB1):
A condition defined as the development of secondary sexual characteristics in boys and girls at a chronological age that is 2.5 standard deviations below the mean age at onset of puberty in the population. Central precocious puberty results from premature activation of the hypothalamic-pituitary-gonadal axis.

Topology

Extracellular: 1-46
Helical: 47-67
Cytoplasmic: 68-78
Helical: 79-101
Extracellular: 102-120
Helical: 121-138
Cytoplasmic: 139-157
Helical: 158-178
Extracellular: 179-202
Helical: 203-223
Cytoplasmic: 224-263
Helical: 264-284
Extracellular: 285-305
Helical: 306-328
Cytoplasmic: 329-398

Li, Z., Liu, J., Inuzuka, H., & Wei, W. (2022). Functional analysis of the emerging roles for the KISS1/KISS1R signaling pathway in cancer metastasis. Journal of Genetics and Genomics, 49(3), 181-184.

Siahpoosh, Z., Farsimadan, M., Pazhohan, M., Vaziri, H., & Mahmoudi Gomari, M. (2021). KISS1R polymorphism rs587777844 (Tyr313His) is linked to female infertility. British Journal of Biomedical Science, 78(2), 98-100.

Pagani, S., Calcaterra, V., Acquafredda, G., Montalbano, C., Bozzola, E., Ferrara, P., ... & Bozzola, M. (2020). MKRN3 and KISS1R mutations in precocious and early puberty. Italian Journal of Pediatrics, 46(1), 1-6.

Kapustin, R. V., Drobintseva, A. O., Alekseenkova, E. N., Onopriychuk, A. R., Arzhanova, O. N., Polyakova, V. O., & Kvetnoy, I. M. (2020). Placental protein expression of kisspeptin-1 (KISS1) and the kisspeptin-1 receptor (KISS1R) in pregnancy complicated by diabetes mellitus or preeclampsia. Archives of gynecology and obstetrics, 301(2), 437-445.

Moalla, M., Hadj Kacem, F., Al-Mutery, A. F., Mahfood, M., Mejdoub-Rekik, N., Abid, M., ... & Hadj Kacem, H. (2019). Nonstop mutation in the Kisspeptin 1 receptor (KISS1R) gene causes normosmic congenital hypogonadotropic hypogonadism. Journal of assisted reproduction and genetics, 36, 1273-1280.

Ke, R., Ma, X., & Lee, L. T. (2019). Understanding the functions of kisspeptin and kisspeptin receptor (Kiss1R) from clinical case studies. Peptides, 120, 170019.

Cao, Y., Li, Z., Jiang, W., Ling, Y., & Kuang, H. (2019). Reproductive functions of Kisspeptin/KISS1R Systems in the Periphery. Reproductive Biology and Endocrinology, 17, 1-9.

Guzman, S., Brackstone, M., Radovick, S., Babwah, A. V., & Bhattacharya, M. M. (2018). KISS1/KISS1R in cancer: friend or foe?. Frontiers in endocrinology, 9, 437.

Wahab, F., Atika, B., Ullah, F., Shahab, M., & Behr, R. (2018). Metabolic impact on the hypothalamic kisspeptin-kiss1r signaling pathway. Frontiers in endocrinology, 9, 123.

Fratangelo, F., Carriero, M. V., & Motti, M. L. (2018). Controversial role of Kisspeptins/KiSS-1R signaling system in tumor development. Frontiers in endocrinology, 9, 192.

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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)
Proteogenomic
Other Protocols

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

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