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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 (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
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
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.
AN69ST-continuous hemodiafiltration can be a novel FGF-23 lowering therapy for acute illnesses requiring acute blood purification.
FGF23 and its co-receptor klotho (show KL Antibodies) play an important role in bone mineral and vitamin D metabolism. In chronic kidney disease, disturbances in bone metabolism increase cardiovascular risk. FGF23 levels are very high in chronic kidney disease and may contribute to vascular calcification and other cardiovascular problems. Review.
Elevated levels of interleukin-6 (show IL6 Antibodies), C-reactive protein (show CRP Antibodies), and FGF23 are independent risk factors for mortality in chronic kidney disease.
Main demonstrable effect of FGF23 in the setting of preserved renal function is suppression of 1,25-dihydroxyvitamin D3 rather than stimulation of renal phosphate excretion.
An overview of FGF23 biology and physiology is provided, clinical outcomes that have been associated with FGF23 are summarized, potential mechanisms for these observations are discussed.
Sclerostin (show SOST Antibodies) levels in KTR are normal and influenced more by bone turnover than by eGFR (show EGFR Antibodies). Its involvement with other hormones of mineral homeostasis (FGF23/Klotho (show KL Antibodies) and Vitamin D) is part of the sophisticated cross-talk between bone and the kidney
High serum FGF23 expression is associated with acute decompensated heart failure.
High FGF-23 expression is associated with cardiovascular disease.
high i-FGF23 levels may be associated with prolongation of low levels of ferritin (show FTL Antibodies), resulting in increased usages of iron supplementation in HD patients
There might be a strong correlation between FGF-23 and ghrelin (show GHRL Antibodies) levels irrespective of the stage of chronic kidney disease and the dialysis modality
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
Klotho (show KL Antibodies) in bone is crucial for inducing FGF23 production upon renal failure
dietary iron content and chronic kidney disease affected FGF23 production and metabolism
Dmp1 (show DMP1 Antibodies) mutation creates a lower set point for extracellular phosphate and maintains it through the regulation of Fgf23 cleavage and expression
Although FGF23 is present in the fetal circulation at levels that may equal adult values, and there is robust expression of FGF23 target genes in placenta and fetal kidneys, FGF23 itself is not an important regulator of fetal phosphorous metabolism.
Annexin A7 (show ANXA7 Antibodies) deficiency upregulates FGF23 plasma levels, an effect paralleled by increased corticosterone plasma levels, as well as decreased 1,25(OH)2 D3 and PTH (show PTH Antibodies) plasma levels.
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