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anti-Human FGF23 Antibodies:
anti-Rat (Rattus) FGF23 Antibodies:
anti-Mouse (Murine) FGF23 Antibodies:
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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.
In patients with heart failure, higher plasma FGF23 levels were associated with volume overload and increased risk of all-cause mortality and hospitalization.
serum level of FGF-23 was not correlated with a change in bone mineral density of maintenance hemodialysis patients, whereas the serum Klotho (show KL Antibodies) protein level was associated with the degree of bone mineral density
Increased insulin (show INS Antibodies) resistance in chronic kidney disease is a consequence of the uremic status and is intimately associated with disturbed phosphate metabolism and FGF23.
Increased serum levels of FGF23 were associated with loss of graft function in kidney transplant recipients.
Responses of FGF23 to salt intervention were more prominent in normotensive, older than 60 years, BMI <24 kg/m(2) and salt-resistant individuals. Furthermore, a significant inverse correlation was observed between 24-hour urinary sodium and serum concentrations of FGF23 after adjusting age, sex, BMI and hypertension status.
FGF23 is reduced in subjects with nephrotic syndrome compared to healthy controls. Reduced levels of Vitamin D, and urinary losses may contribute to lower levels of FGF23 in NS.
Pharmacological treatment of hypercalciuric patients resulted in significantly lower urinary calcium excretion, lower serum FGF23, and elevated TP/GFR (show RAPGEF5 Antibodies) and serum phosphate concentration, without significant changes in PTH (show PTH Antibodies).
Carboxy-terminal fragment of FGF-23 induces heart hypertrophy in sickle cell disease.
prolonged exposure to high apical calcium and calcium hyperabsorption were sensed by CaSR (show CASR Antibodies), which, in turn, increased FGF-23 expression to suppress calcium transport
In a Canadian Asian population with CKD, FGF23 levels obtained at 6-monthly intervals for 3 years predicted ESRD and mortality suggesting that it is also a risk marker in Asians
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