Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all synonyms
Human Polyclonal FGF23 Primary Antibody for IP, ELISA - ABIN188699
Orfanidou, Malizos, Varitimidis, Tsezou et al.: 1,25-Dihydroxyvitamin D(3) and extracellular inorganic phosphate activate mitogen-activated protein kinase pathway through fibroblast growth factor 23 contributing to hypertrophy and mineralization ... in Experimental biology and medicine (Maywood, N.J.) 2012
Show all 2 Pubmed References
Human Polyclonal FGF23 Primary Antibody for IF, ELISA - ABIN1534408
Sun, Zou, Yang, Morita, Gong, Shiba, Akagawa, Yuan: Inorganic polyphosphates stimulate FGF23 expression through the FGFR pathway. in Biochemical and biophysical research communications 2012
Human Polyclonal FGF23 Primary Antibody for IF (p), IHC (p) - ABIN714461
Andersen, Huntley, Sandberg, Heublein, Burnett: Elevation of circulating but not myocardial FGF23 in human acute decompensated heart failure. in Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association 2016
Mouse (Murine) Polyclonal FGF23 Primary Antibody for ELISA, WB - ABIN4311599
Mirza, Alsiö, Hammarstedt, Erben, Michaëlsson, Tivesten, Marsell, Orwoll, Karlsson, Ljunggren, Mellström, Lind, Ohlsson, Larsson: Circulating fibroblast growth factor-23 is associated with fat mass and dyslipidemia in two independent cohorts of elderly individuals. in Arteriosclerosis, thrombosis, and vascular biology 2010
FGF23 functions as a hypocalcemic hormone in zebrafish.
This study showed that stanniocalcin 1 (stc1 (show STC1 Antibodies))modulates cation levels in trpm7 (show TRPM7 Antibodies) mutants and in the wild type; levels of cations are restored to normal in trpm7 (show TRPM7 Antibodies) mutants when stc1 (show STC1 Antibodies) activity is blocked.
A decrease in serum FGF23 and hepcidin (show HAMP Antibodies) levels was observed in chronic hemodialysis patients treated with lanthanum carbonate.
serum FGF23 levels were significantly higher and soluble Klotho (show KL Antibodies) levels significantly lower in the autosomal-dominant polycystic kidney disease group than in the non-diabetic chronic kidney disease group matched for estimated glomerular filtration rate
Higher serum fibroblast growth factor 23 concentration was associated with kidney function decline, height-adjusted total kidney volume percentage increase, and death in patients with autosomal dominant polycystic kidney disease.
This study indicates a possible mechanism by which excessive levels of FGF23 are involved in endothelial thrombomodulin (show THBD Antibodies) disruption, which has been implicated as a potential cardiovascular risk factor in patients with chronic kidney disease, especially in hemodialysis patients
Novel relationships were identified between higher plasma FGF23 concentrations and absence of APOL1 (show APOL1 Antibodies) renal-risk genotypes with higher mortality in African Americans with diabetes.
FGF23 is an integral part of a complex pathway, associated with higher cardiac mass in African-Americans males with excess adiposity.
found no independent association between FGF-23 and cardiac changes. LVH remains the most common cardiac change seen in children with CKD
Fibroblast Growth Factor-23 was higher in alcoholics than in controls, especially among cirrhotics, and soluble alpha Klotho (show KL Antibodies) levels were also higher among cirrhotics.
Dietary factors other than phosphate are associated with FGF23 levels in young adults.
Novel CLCN5 (show CLCN5 Antibodies) (c.1205G>A, p.W402*) and FGF23 (c.526C>G, p.R176G) mutations were found in two patients from the remaining two families
the main physiological function of Klotho (show KL Antibodies) for mineral homeostasis in vivo is its role as co-receptor mediating Fgf23 action.
our study provided histological evidences that sclerostin (show SOST Antibodies) tends to be secreted in osteocytes of remodeled mature bone, while FGF23 would be differently synthesized in osteoblasts and osteocytes according to the developmental stages
these results indicate that Nf1 (show NF1 Antibodies) deficiency in osteocytes dramatically increases FGF23 production and causes a mineralization defect (ie, hyperosteoidosis) via the alteration of calcium-phosphorus metabolism.
FGF23 promotes myocardial fibrosis and exacerbates diastolic dysfunction induced by myocardial infarction or ischemia/reperfusion , which is associated with the upregulation of active beta-catenin (show CTNNB1 Antibodies) and TGF-beta (show TGFB1 Antibodies)
deleting FGF23 within early osteoblasts and osteocytes demonstrated that both cell types contribute to baseline circulating FGF23 concentrations, and that targeting osteoblasts/osteocytes for FGF23 production can modify systemic responses to changes in serum phosphate concentrations and rescue the Hyp (show PHEX Antibodies) genetic syndrome
Thus, monotherapy with 1,25D improves growth, skeletal microarchitecture, and bone strength in the absence of phosphate supplementation despite enhancing FGF23 expression, demonstrating that 1,25D has direct beneficial effects on the skeleton in XLH (show PHEX Antibodies), independent of its role in phosphate homeostasis
FGF23 augments pro-fibrotic signalling cascades in injury-primed renal fibroblasts via activation of FGFR4 (show FGFR4 Antibodies)
Zinc13407541 also inhibited FGF-23 signaling in isolated renal tubules ex vivo and partially reversed the hypophosphatemic effects of excess FGF-23 in a mouse model. These chemical probes provide a platform to develop lead compounds to treat disorders caused by excess FGF-23.
FGF23 may be an important modulator of PTH (show PTH Antibodies) signaling in bone and kidney.
EPO (show EPO Antibodies) dependent regulation pathway of FGF23 gene expression
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).
fibroblast growth factor 23
, tumor-derived hypophosphatemia inducing factor