|Application ||WB, E|
|Other Accession||NP_065689, 8074|
|Calculated MW||27954 Da|
|Other Names||Fibroblast growth factor 23, FGF-23, Phosphatonin, Tumor-derived hypophosphatemia-inducing factor, Fibroblast growth factor 23 N-terminal peptide, Fibroblast growth factor 23 C-terminal peptide, FGF23, HYPF|
|Format||0.5 mg IgG/ml in Tris saline (20mM Tris pH7.3, 150mM NaCl), 0.02% sodium azide, with 0.5% bovine serum albumin|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||Goat Anti-FGF23 Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Regulator 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.|
|Cellular Location||Secreted. Note=Secretion is dependent on O-glycosylation|
|Tissue Location||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).|
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Provided below are standard protocols that you may find useful for product applications.
The protein encoded by this gene is a member of the fibroblast growth factor (FGF) family. FGF family members possess broad mitogenic and cell survival activities and are involved in a variety of biological processes including embryonic development, cell growth, morphogenesis, tissue repair, tumor growth and invasion. The product of this gene inhibits renal tubular phosphate transport. This gene was identified by its mutations associated with autosomal dominant hypophosphatemic rickets (ADHR), an inherited phosphate wasting disorder. Abnormally high level expression of this gene was found in oncogenic hypophosphatemic osteomalacia (OHO), a phenotypically similar disease caused by abnormal phosphate metabolism. Mutations in this gene have also been shown to cause familial tumoral calcinosis with hyperphosphatemia.
Common genetic variants associate with serum phosphorus concentration. Kestenbaum B, et al. J Am Soc Nephrol, 2010 Jul. PMID 20558539.
Levels and dynamic changes of serum fibroblast growth factor 23 in hypophosphatemic rickets/osteomalacia. Xia WB, et al. Chin Med J (Engl), 2010 May. PMID 20529556.
The associations of fibroblast growth factor 23 and uncarboxylated matrix Gla protein with mortality in coronary artery disease: the Heart and Soul Study. Parker BD, et al. Ann Intern Med, 2010 May 18. PMID 20479029.
Infantile hypercalcemia and hypercalciuria: new insights into a vitamin D-dependent mechanism and response to ketoconazole treatment. Nguyen M, et al. J Pediatr, 2010 Aug. PMID 20394945.
Personalized smoking cessation: interactions between nicotine dose, dependence and quit-success genotype score. Rose JE, et al. Mol Med, 2010 Jul-Aug. PMID 20379614.
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