Product nameAnti-FGF 23 antibody
See all FGF 23 primary antibodies
DescriptionRabbit polyclonal to FGF 23
Tested applicationsSuitable for: WBmore details
Species reactivityReacts with: Human
- This antibody gave a positive signal in the following tissue lysates: Human brain; Human heart; Human bone marrow; Human bone tumour as well as the following whole cell lysates: U2OS; U937; MOLT4.
Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C or -80°C. Avoid freeze / thaw cycle.
Storage bufferpH: 7.40
Preservative: 0.02% Sodium azide
Note: Batches of this product that have a concentration < 1mg/ml may have BSA added as a stabilising agent. If you would like information about the formulation of a specific lot, please contact our scientific support team who will be happy to help.
Concentration information loading...
PurityImmunogen affinity purified
Immunizing Peptide (Blocking)
Our Abpromise guarantee covers the use of ab98000 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||Use a concentration of 1 µg/ml. Detects a band of approximately 27 kDa (predicted molecular weight: 27 kDa).|
FunctionRegulator of phosphate homeostasis. Inhibits renal tubular phosphate transport by reducing SLC34A1 levels. Upregulates EGR1 expression in the presence of KL (By similarity). Acts directly on the parathyroid to decrease PTH secretion (By similarity). Regulator of vitamin-D metabolism. Negatively regulates osteoblast differentiation and matrix mineralization.
Tissue specificityExpressed in osteogenic cells particularly during phases of active bone remodeling. In adult trabecular bone, expressed in osteocytes and flattened bone-lining cells (inactive osteoblasts).
Involvement in diseaseDefects 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.
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.
Sequence similaritiesBelongs to the heparin-binding growth factors family.
modificationsFollowing secretion this protein is inactivated by cleavage into a N-terminal fragment and a C-terminal fragment. The processing is effected by proprotein convertases.
O-glycosylated by GALT3. Glycosylation is necessary for secretion; it blocks processing by proprotein convertases when the O-glycan is alpha 2,6-sialylated. Competition between proprotein convertase cleavage and block of cleavage by O-glycosylation determines the level of secreted active FGF23.
Cellular localizationSecreted. Secretion is dependent on O-glycosylation.
- Information by UniProt
- ADHR antibody
- FGF-23 antibody
- Fgf23 antibody
All lanes : Anti-FGF 23 antibody (ab98000) at 1 µg/ml
Lane 1 : Human brain tissue lysate - total protein (ab29466)
Lane 2 : MOLT4 (Human acute lymphoblastic leukemia cell line) Whole Cell Lysate
Lane 3 : Bone Marrow (Human) Tissue Lysate - adult normal tissue
Lane 4 : Human bone tumor tissue lysate - total protein (ab29359)
Lysates/proteins at 10 µg per lane.
All lanes : Goat Anti-Rabbit IgG H&L (HRP) preadsorbed (ab97080) at 1/5000 dilution
Developed using the ECL technique.
Performed under reducing conditions.
Predicted band size: 27 kDa
Observed band size: 27 kDa
Additional bands at: 48 kDa, 90 kDa. We are unsure as to the identity of these extra bands.
Exposure time: 30 seconds
This antibody has also given a positive signal in Human heart tissue lysate and U2OS and U937 whole cell lysates.
This product has been referenced in:
- Rodrat M et al. Prolonged exposure to 1,25(OH)2D3 and high ionized calcium induces FGF-23 production in intestinal epithelium-like Caco-2 monolayer: A local negative feedback for preventing excessive calcium transport. Arch Biochem Biophys 640:10-16 (2018). WB . Read more (PubMed: 29317227) »
- Leifheit-Nestler M et al. Impact of Altered Mineral Metabolism on Pathological Cardiac Remodeling in Elevated Fibroblast Growth Factor 23. Front Endocrinol (Lausanne) 9:333 (2018). Read more (PubMed: 29977226) »