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Mouse Anti-KISS1 Recombinant Antibody (1F7) (CBMAB-K0955-LY)

This product is antibody recognizes KISS1. The antibody 1F7 immunoassay techniques such as: ELISA, WB.
See all KISS1 antibodies
Published Data
Fig. 1 Spindle cell type UM displaying nuclear staining for KISS1 (original magnification × 400).
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Summary

Host Animal
Mouse
Specificity
Human
Clone
1F7
Antibody Isotype
IgG2a, κ
Application
ELISA, WB

Basic Information

Immunogen
KISS1 (NP_002247, 46 a.a. ~ 146 a.a) partial recombinant protein with GST tag
Specificity
Human
Antibody Isotype
IgG2a, κ
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
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.

Target

Full Name
KiSS-1 Metastasis Suppressor
Introduction
This gene is a metastasis suppressor gene that suppresses metastases of melanomas and breast carcinomas without affecting tumorigenicity. The encoded protein may inhibit chemotaxis and invasion and thereby attenuate metastasis in malignant melanomas. Studies suggest a putative role in the regulation of events downstream of cell-matrix adhesion, perhaps involving cytoskeletal reorganization. A protein product of this gene, kisspeptin, stimulates gonadotropin-releasing hormone (GnRH)-induced gonadotropin secretion and regulates the pubertal activation of GnRH nuerons. A polymorphism in the terminal exon of this mRNA results in two protein isoforms. An adenosine present at the polymorphic site represents the third position in a stop codon. When the adenosine is absent, a downstream stop codon is utilized and the encoded protein extends for an additional seven amino acid residues. [provided by RefSeq, Mar 2012]
Entrez Gene ID
3814
UniProt ID
Q15726
Alternative Names
KiSS-1 Metastasis Suppressor; Prepro-Kisspeptin; Kisspeptin-1; Malignant Melanoma Metastasis-Suppressor; Metastasis-Suppressor KiSS-1; KiSS-1 Metastasis-Suppressor;
Function
Metastasis suppressor protein in malignant melanomas and in some breast cancers. May regulate events downstream of cell-matrix adhesion, perhaps involving cytoskeletal reorganization. Generates a C-terminally amidated peptide, metastin which functions as the endogenous ligand of the G-protein coupled receptor GPR54. Activation of the receptor inhibits cell proliferation and cell migration, key characteristics of tumor metastasis. Kp-10 is a decapeptide derived from the primary translation product, isolated in conditioned medium of first trimester trophoblast. Kp-10, but not other kisspeptins, increased intracellular Ca(2+) levels in isolated first trimester trophoblasts. Kp-10 is a paracrine/endocrine regulator in fine-tuning trophoblast invasion generated by the trophoblast itself. The receptor is also essential for normal gonadotropin-released hormone physiology and for puberty. The hypothalamic KiSS1/GPR54 system is a pivotal factor in central regulation of the gonadotropic axis at puberty and in adulthood.
Biological Process
Cytoskeleton organizationManual Assertion Based On ExperimentTAS:ProtInc
G protein-coupled receptor signaling pathwayManual Assertion Based On ExperimentIBA:GO_Central
Generation of ovulation cycle rhythmIEA:Ensembl
Negative regulation of cell population proliferationIEA:Ensembl
Positive regulation of cytosolic calcium ion concentrationManual Assertion Based On ExperimentIBA:GO_Central
Positive regulation of cytosolic calcium ion concentration involved in phospholipase C-activating G protein-coupled signaling pathwayIEA:Ensembl
Positive regulation of growth hormone secretionIEA:Ensembl
Positive regulation of luteinizing hormone secretionIEA:Ensembl
Positive regulation of MAPK cascadeIEA:Ensembl
Positive regulation of synaptic transmissionIEA:Ensembl
Cellular Location
Secreted
Involvement in disease
Hypogonadotropic hypogonadism 13 with or without anosmia (HH13):
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).
PTM
Processed by MMP2 and MMP9.

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.

Ly, T., Harihar, S., & Welch, D. R. (2020). KISS1 in metastatic cancer research and treatment: potential and paradoxes. Cancer and Metastasis Reviews, 39(3), 739-754.

Talbi, R., & Navarro, V. M. (2020). Novel insights into the metabolic action of Kiss1 neurons. Endocrine connections, 9(5), R124-R133.

Ikegami, K., Goto, T., Nakamura, S., Watanabe, Y., Sugimoto, A., Majarune, S., ... & Uenoyama, Y. (2020). Conditional kisspeptin neuron-specific Kiss1 knockout with newly generated Kiss1-floxed and Kiss1-Cre mice replicates a hypogonadal phenotype of global Kiss1 knockout mice. Journal of Reproduction and Development, 66(4), 359-367.

Ulasov, I. V., Borovjagin, A. V., Timashev, P., Cristofanili, M., & Welch, D. R. (2019). KISS1 in breast cancer progression and autophagy. Cancer and Metastasis Reviews, 38, 493-506.

Yeo, S. H., Kyle, V., Blouet, C., Jones, S., & Colledge, W. H. (2019). Mapping neuronal inputs to Kiss1 neurons in the arcuate nucleus of the mouse. PloS one, 14(3), e0213927.

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.

Vazquez, M. J., Toro, C. A., Castellano, J. M., Ruiz-Pino, F., Roa, J., Beiroa, D., ... & Tena-Sempere, M. (2018). SIRT1 mediates obesity-and nutrient-dependent perturbation of pubertal timing by epigenetically controlling Kiss1 expression. Nature communications, 9(1), 4194.

Kostakis, I. D., Agrogiannis, G., Vaiopoulos, A. G., Mylona, E., Patsouris, E., Kouraklis, G., & Koutsilieris, M. (2018). KISS1 and KISS1R expression in gastric cancer. J buon, 23(01), 79-84.

Chakravarthi, V. P., Khristi, V., Ghosh, S., Yerrathota, S., Dai, E., Roby, K. F., ... & Rumi, M. K. (2018). ESR2 is essential for gonadotropin-induced Kiss1 expression in granulosa cells. Endocrinology, 159(11), 3860-3873.

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

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