Target:FGF-23
Fields:MAPK signaling pathway;Ras signaling pathway;Rap1 signaling pathway;Calcium signaling pathway;PI3K-Akt signaling pathway;Regulation of actin cytoskeleton;Parathyroid hormone synthesis, secretion and action;Pathways in cancer;Melanoma;Breast cancer;Gastric cancer
Gene Name:FGF23
Protein Name:Fibroblast growth factor 23
Human Gene Id:8074
Human Swiss Prot No:Q9GZV9
Mouse Gene Id:64654
Mouse Swiss Prot No:Q9EPC2
Rat Gene Id:170583
Rat Swiss Prot No:Q8VI82
Immunogen:The antiserum was produced against synthesized peptide derived from human FGF23. AA range:151-200
Specificity:FGF-23 Polyclonal Antibody detects endogenous levels of FGF-23 protein.
Formulation:Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
Source:Polyclonal, Rabbit,IgG
Dilution:WB 1:500 - 1:2000. ELISA: 1:20000. IF 1:100-300 Not yet tested in other applications.
Purification:The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.
Concentration:1 mg/ml
Storage Stability:-15°C to -25°C/1 year(Do not lower than -25°C)
Other Name:FGF23;HYPF;Fibroblast growth factor 23;FGF-23;Phosphatonin;Tumor-derived hypophosphatemia-inducing factor
Observed Band(KD):27kD
Background: 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],
Function:disease:Defects in FGF23 are a cause of hyperphosphatemic familial tumoral calcinosis (HFTC) [MIM:211900]. HFTC is a severe autosomal recessive metabolic disorder that manifests with hyperphosphatemia and massive calcium deposits in the skin and subcutaneous tissues.,disease:Defects in FGF23 are the cause of autosomal dominant hypophosphataemic rickets (ADHR) [MIM:193100]. ADHR is characterized by low serum phosphorus concentrations, rickets, osteomalacia, leg deformities, short stature, bone pain and dental abscesses.,PTM:After secretion it is processed into a N-terminal fragment and a C-terminal fragment. The processing is effected by the proprotein convertases.,similarity:Belongs to the heparin-binding growth factors family.,
Subcellular Location:Secreted . Secretion is dependent on O-glycosylation.
Expression:Expressed in osteogenic cells particularly during phases of active bone remodeling. In adult trabecular bone, expressed in osteocytes and flattened bone-lining cells (inactive osteoblasts).