Product Information
Molecular Weight27954DaObserved Band:27KD
Protein NameFibroblast growth factor 23
Human Gene Id8074
Human Swiss Prot NoQ9GZV9
Mouse Gene Id64654
Mouse Swiss Prot NoQ9EPC2
Rat Gene Id170583
Rat Swiss Prot NoQ8VI82
SpecificityFGF-23 Polyclonal Antibody detects endogenous levels of FGF-23 protein.
FormulationLiquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
Concentration1 mg/ml
Storage Stability-20°C/1 year
Other NameFGF23; HYPF; Fibroblast growth factor 23; FGF-23; Phosphatonin; Tumor-derived hypophosphatemia-inducing factor
Functiondisease: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 LocationSecreted . Secretion is dependent on O-glycosylation.
ExpressionExpressed in osteogenic cells particularly during phases of active bone remodeling. In adult trabecular bone, expressed in osteocytes and flattened bone-lining cells (inactive osteoblasts).,
Backgroundfibroblast growth factor 23(FGF23) Homo sapiens 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],