ELISA/assay

Mouse Fibroblast growth factor 23 ELISA Kit

MBS720442

48-Strip-Wells

470 USD

ELISA Kit

Mouse Fibroblast growth factor 23 ELISA Kit

Fibroblast growth factor 23

fibroblast growth factor 23; Fibroblast growth factor 23; fibroblast growth factor 23; phosphatonin; tumor-derived hypophosphatemia inducing factor; fibroblast growth factor 23; Phosphatonin; Tumor-derived hypophosphatemia-inducing factorCleaved into the following 2 chains:Fibroblast growth factor 23 N-terminal peptide; Fibroblast growth factor 23 C-terminal peptide

FGF-23

FGF23; FGF23; ADHR; FGFN; HYPF; HPDR2; PHPTC; HYPF; UNQ3027/PRO9828; FGF-23

FGF23_HUMAN

Mouse

This assay has high sensitivity and excellent specificity for detection of FGF-23. No significant cross-reactivity or interference between FGF-23 and analogues was observed. NOTE: Limited by current skills and knowledge, it is impossible for us to complete the cross-reactivity detection between FGF-23 and all the analogues, therefore, cross reaction may still exist in some cases.

Store all reagents at 2-8 degree C.

Samples: Serum, plasma, cell culture supernatants, body fluid and tissue homogenate. Assay Type: Sandwich. Sensitivity: 1.0 pg/mL.

Intended Uses: This FGF-23 ELISA kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of Mouse FGF-23. This ELISA kit for research use only, not for therapeutic or diagnostic applications!

Cardiovascular

Principle of the Assay: FGF-23 ELISA kit applies the quantitative sandwich enzyme immunoassay technique. The microtiter plate has been pre-coated with a monoclonal antibody specific for FGF-23. Standards or samples are then added to the microtiter plate wells and FGF-23 if present, will bind to the antibody pre-coated wells. In order to quantitatively determine the amount of FGF-23 present in the sample, a standardized preparation of horseradish peroxidase (HRP)-conjugated polyclonal antibody, specific for FGF-23 are added to each well to "sandwich" the FGF-23 immobilized on the plate. The microtiter plate undergoes incubation, and then the wells are thoroughly washed to remove all unbound components. Next, substrate solutions are added to each well. The enzyme (HRP) and substrate are allowed to react over a short incubation period. Only those wells that contain FGF-23 and enzyme-conjugated antibody will exhibit a change in color. The enzyme-substrate reaction is terminated by addition of a sulphuric acid solution and the color change is measured spectrophotometrically at a wavelength of 450 nm. A standard curve is plotted relating the intensity of the color (O.D.) to the concentration of standards. The FGF-23 concentration in each sample is interpolated from this standard curve.

10190674

NP_065689.1

NM_020638.2

27,954 Da

Activated Point Mutants Of FGFR2 Pathway (645281); Adaptive Immune System Pathway (366160); Constitutive PI3K/AKT Signaling In Cancer Pathway (685535); DAP12 Interactions Pathway (685549); DAP12 Signaling Pathway (685550); Disease Pathway (530764); Downstream Signal Transduction Pathway (106385); Downstream Signaling Events Of B Cell Receptor (BCR) Pathway (576250); Downstream Signaling Of Activated FGFR Pathway (160957); FGF Signaling Pathway (137989)

This gene encodes a member of the fibroblast growth factor family of proteins, which possess broad mitogenic and cell survival activities and are involved in a variety of biological processes. The product of this gene regulates phosphate homeostasis and transport in the kidney. The full-length, functional protein may be deactivated via cleavage into N-terminal and C-terminal chains. Mutation of this cleavage site causes autosomal dominant hypophosphatemic rickets (ADHR). Mutations in this gene are also associated with hyperphosphatemic familial tumoral calcinosis (HFTC). [provided by RefSeq, Feb 2013]

FGF23: Regulator of phosphate homeostasis. Inhibits renal tubular phosphate transport by reducing SLC34A1 levels. Upregulates EGR1 expression in the presence of KL. Acts directly on the parathyroid to decrease PTH secretion. Regulator of vitamin-D metabolism. Negatively regulates osteoblast differentiation and matrix mineralization. Defects in FGF23 are the cause of autosomal dominant hypophosphataemic rickets (ADHR). ADHR is characterized by low serum phosphorus concentrations, rickets, osteomalacia, leg deformities, short stature, bone pain and dental abscesses. Defects in FGF23 are a cause of hyperphosphatemic familial tumoral calcinosis (HFTC). HFTC is a severe autosomal recessive metabolic disorder that manifests with hyperphosphatemia and massive calcium deposits in the skin and subcutaneous tissues. Belongs to the heparin-binding growth factors family. Protein type: Cytokine; Secreted; Secreted, signal peptide. Chromosomal Location of Human Ortholog: 12p13.3. Cellular Component: extracellular space; extracellular region. Molecular Function: growth factor activity; type 1 fibroblast growth factor receptor binding. Biological Process: epidermal growth factor receptor signaling pathway; negative regulation of bone mineralization; cellular phosphate ion homeostasis; phosphoinositide-mediated signaling; fibroblast growth factor receptor signaling pathway; nerve growth factor receptor signaling pathway; negative regulation of hormone secretion; positive regulation of transcription, DNA-dependent; insulin receptor signaling pathway; innate immune response; negative regulation of osteoblast differentiation; phosphate ion homeostasis; cell differentiation; phosphate metabolic process; vitamin D catabolic process. Disease: Hypophosphatemic Rickets, Autosomal Dominant

48-Strip-Wells

470 USD

96-Strip-Wells

675