ELISA/assay

Porcine Intact Fibroblast Growth Factor 23 ELISA Kit

MBS749770

48-Strip-Wells

470 USD

ELISA Kit

Porcine Intact Fibroblast Growth Factor 23 ELISA Kit

Intact Fibroblast Growth Factor 23

FGF23; 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

IFGF-23

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

FGF23_HUMAN

Porcine

This assay has high sensitivity and excellent specificity for detection of iFGF-23. No significant cross-reactivity or interference between iFGF-23 and analogues was observed. NOTE: Limited by current skills and knowledge, it is impossible for us to complete the cross-reactivity detection between iFGF-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: Competitive. Sensitivity: 0.1 ng/mL.

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

Cancer

Principle of the assay: iFGF-23 ELISA kit applies the competitive enzyme immunoassay technique utilizing a monoclonal anti-iFGF-23 antibody and an iFGF-23-HRP conjugate. The assay sample and buffer are incubated together with iFGF-23-HRP conjugate in pre-coated plate for one hour. After the incubation period, the wells are decanted and washed five times. The wells are then incubated with a substrate for HRP enzyme. The product of the enzyme-substrate reaction forms a blue colored complex. Finally, a stop solution is added to stop the reaction, which will then turn the solution yellow. The intensity of color is measured spectrophotometrically at 450nm in a microplate reader. The intensity of the color is inversely proportional to the iFGF-23 concentration since iFGF-23 from samples and iFGF-23-HRP conjugate compete for the anti-iFGF-23 antibody binding site. Since the number of sites is limited, as more sites are occupied by iFGF-23 from the sample, fewer sites are left to bind iFGF-23-HRP conjugate. A standard curve is plotted relating the intensity of the color (O.D.) to the concentration of standards. The iFGF-23 concentration in each sample is interpolated from this standard curve.

9964292

AAG09917.1

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: Secreted; Secreted, signal peptide; Cytokine. 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; fibroblast growth factor receptor signaling pathway; phosphoinositide-mediated signaling; nerve growth factor receptor signaling pathway; negative regulation of hormone secretion; positive regulation of transcription, DNA-dependent; phosphate metabolic process; negative regulation of bone mineralization; cellular phosphate ion homeostasis; insulin receptor signaling pathway; innate immune response; negative regulation of osteoblast differentiation; phosphate ion homeostasis; cell differentiation; vitamin D catabolic process. Disease: Hypophosphatemic Rickets, Autosomal Dominant

48-Strip-Wells

470 USD

96-Strip-Wells

675