protein

Murine FGF-23

MBS695607

0.005 mg

125 USD

Recombinant Protein

Murine FGF-23

FGF-23

fibroblast growth factor 23; 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

FGF23; FGF23; ADHR; FGFN; HYPF; HPDR2; PHPTC; HYPF; FGF-23

FGF23_HUMAN

Species Reactivity: Mouse

-20 Degree C

10190674

NP_065689.1

NM_020638.2

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

0.005 mg

125 USD

0.02 mg

195