KiSS1-derived Peptide Family Related Drug Discovery Products
Creative Biolabs has the assays you can rely on for high throughput screening, lead optimization, characterizing and discovering targets, and uncovering the complexity of disease pathways. We can offer membrane protein in vitro assay kits that save valuable laboratory time and is ideal for high throughput screening.
Membrane protein stable cell lines are widely used in many areas of biomedical research. Creative Biolabs can offer membrane protein stable cell lines to stablish in vitro models for High Throughput Screening.
Creative Biolabs offers high-quality, innovative tools to help research groups accelerate membrane protein drug discovery. They can be found by targets. If there is no product that meets your needs, please contact us.
The hypothalamic-pituitary-gonadal axis, which controls puberty and reproductive processes, is crucially activated by KiSS1. Kisspeptins, which are peptides generated from KiSS1, communicate by way of the G-protein coupled receptor GPR54. By inhibiting cell migration and invasion, KiSS1 signaling prevents metastases from occurring and keeps disseminated malignant cells dormant in cancer. Moreover, by switching the energy production towards oxidative phosphorylation and β-oxidation, KiSS1 modifies the metabolism of glucose and lipids. The loss or reduced expression of KiSS1, which is mediated in part by promoter hypermethylation, is associated with metastases in a variety of cancer types. KiSS1 appears to play a role in modulating autophagy, the intrinsic apoptotic pathway, and cell defense components in response to chemotherapeutic drugs, however its exact function is yet unclear.
Fig.1 KiSS1 and regulation of metabolism. (O’Mahony, 2011)
Creative Biolabs offers high-quality KiSS1-derived peptide family related tools for our clients to help them accelerate drug discovery:
KiSS1-Derived Peptide GPCR Assays 
GPCR Assay Kits 
GPCR Cell Lines 
GPCR Membranes 
Membrane Protein Tools
Overview of KiSS1-derived Peptide Family
KiSS1R/GPR54 is expressed in the placenta, pituitary gland, pancreas, brain, and spinal cord; interaction with its ligand causes phospholipase C to be activated, Ca2+ to be mobilized, and ERK1/2 and p38 to be phosphorylated. According to physiological theory, this signaling pathway is necessary to start the release of gonadotropins during puberty. With evidence that released KiSS1 is necessary for the prevention of organ metastasis and the maintenance of the dormant state of disseminated malignant cells, KiSS1 signaling has been associated with the inhibition of metastasis in tumor cells. It has been suggested that the KiSS1/GPR54 axis is crucial for mammalian fertility, with neurons in the hypothalamus producing kisspeptins. The gonadotropin releasing hormone (GnRH), which is produced by hypothalamic neurons when kisspeptin binds to KiSS1R, induces the release of pituitary gonadotropins and sexual steroids. Evidence that mutations of these genes are linked to hypogonadotropic hypogonadism, infertility, or even the absence of pubertal development for loss of function GPR54 mutations supports a role for KiSS1 and its receptor in human reproduction.
Fig.2 Schematic representation of the role of KiSS1. (O’Mahony, 2011)
KiSS1-derived Peptide Family Drug Discovery
The majority of neoplastic disorders are difficult to effectively control because of metastatic spread. With further examination of its role in modulating tumor cell responsiveness to chemotherapeutic drugs, KiSS1 appears to be a critical player in the regulation of metastases, as well as exploitable as a biomarker to monitor disease progression and to monitor therapeutic response. KiSS1, which is released by tumor cells and produces peptides that can be detected in biological fluids, seems to be a possible biomarker that will be useful for use in regular tests in the future.
Reference
- O’Mahony, L.; et al. Regulation of the immune response and inflammation by histamine and histamine receptors. Journal of Allergy and Clinical Immunology. 2011, 128(6): 1153-1162.
