FGFR1/alpha-Klotho Reporter Assay System (human)

This is an all-inclusive cell-based luciferase reporter assay kit targeting the Human Fibroblast Growth Factor Receptor 1c and alpha-Klotho (FGFR/alpha-Klotho). INDIGO's FGFR/alpha-Klotho reporter assay utilizes proprietary mammalian cells that have been engineered to provide constitutive expression of the Human Fibroblast Growth Factor Receptor 1c and alpha-Klotho. In addition to FGFR/alpha-Klotho Reporter Cells, this kit provides two optimized media for use during cell culture and in diluting the user's test samples, a reference agonist, Luciferase Detection Reagent, and a cell culture-ready assay plate. The principal application of this assay is in the screening of test samples to quantify any functional activity, either agonist or antagonist, that they may exert against human FGFR/alpha-Klotho. This kit provides researchers with clear, reproducible results, exceptional cell viability post-thaw, and consistent results lot to lot. Kits must be stored at -80C. Do not store in liquid nitrogen. Note: reporter cells cannot be refrozen or maintained in extended culture. Features Ready to Use Upon Receipt Includes All Needed Components Contains Transfected Reporter Cells Eliminates Cell Licensing Fees Clear, Reproducible Results Consistent Results Lot to Lot Product Specifications Target Type Growth Factor Receptor Species Human Receptor Form Hybrid Assay Mode Agonist, Antagonist Kit Components FGFR/alpha-Klotho Reporter Cells Cell Recovery Medium (CRM) Compound Screening Medium (CSM) FGF-23, (ref. activator, in PBS/0.1% BSA ) Detection Substrate Detection Buffer White, sterile, cell-culture ready assay plate. Shelf Life: 6 months. Shipping Requirements: Dry Ice. Storage temperature: -80 °C. Target Background: The family of Fibroblast Growth Factors (FGFs) comprise approximately 23 members that are related by core sequence and structure conservation, with the majority of FGFs being secreted signaling proteins. Secreted FGFs are predominantly autocrine and paracrine factors, with only three members evolved to function as endocrine factors. Paracrine FGFs show high affinity towards the extracellular matrix (ECM) component heparin sulfate (HS) and are thus retained in the ECM and function locally. In contrast, the atypical endocrine subfamily of FGFs, that comprise FGF-19, FGF-21, and FGF-23, have reduced affinity for HS and can therefore escape from the ECM into the circulation to distant reach target distant organs. FGFs bind and activate FGF Receptors (FGFRs) which, themselves, are members of the family of high-affinity tyrosine kinase receptors. The endocrine FGF-23 activates the receptor complex FGFR1c and its co-receptor alpha-Klotho (FGFR1c/alpha-Klotho). FGF-23 is a principal regulator in the maintenance of serum phosphorus concentration by inhibiting renal tubular phosphate reabsorption. Unfortunately, various FGF-23-mediated disorders exist. The most common of these is X-linked hypophosphoatemia (XLH). Additional disorders of FGF-23 signaling include autosomal dominant and recessive hypophosphophatemic rickets, fibrous dysplasia, and tumor-induced osteomalacia. Consequently, FGF-23 and FGFR1c/alpha-Klotho command considerable interest as therapeutic targets in drug development and drug safety screening. Protein function: Tyrosine-protein kinase that acts as cell-surface receptor for fibroblast growth factors and plays an essential role in the regulation of embryonic development, cell proliferation, differentiation and migration. Required for normal mesoderm patterning and correct axial organization during embryonic development, normal skeletogenesis and normal development of the gonadotropin-releasing hormone (GnRH) neuronal system. Phosphorylates PLCG1, FRS2, GAB1 and SHB. Ligand binding leads to the activation of several signaling cascades. Activation of PLCG1 leads to the production of the cellular signaling molecules diacylglycerol and inositol 1,4,5-trisphosphate. Phosphorylation of FRS2 triggers recruitment of GRB2, GAB1, PIK3R1 and SOS1, and mediates activation of RAS, MAPK1/ERK2, MAPK3/ERK1 and the MAP kinase signaling pathway, as well as of the AKT1 signaling pathway. Promotes phosphorylation of SHC1, STAT1 and PTPN11/SHP2. In the nucleus, enhances RPS6KA1 and CREB1 activity and contributes to the regulation of transcription. FGFR1 signaling is down-regulated by IL17RD/SEF, and by FGFR1 ubiquitination, internalization and degradation. [The UniProt Consortium]