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Human FGF23 ELISA Kit für Sandwich ELISA - ABIN416862
Oikonomou, Orfanidou, Vlychou, Kapsoritakis, Tsezou, Malizos, Potamianos: Lower fibroblast growth factor 23 levels in young adults with Crohn disease as a possible secondary compensatory effect on the disturbance of bone and mineral metabolism. in Journal of clinical densitometry : the official journal of the International Society for Clinical Densitometry 2014
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Human FGF23 ELISA Kit für Sandwich ELISA - ABIN368019
Xu, Yang, Sun, Yuan, Cheng, Wei, Li, Cheng, Brann, Wang: A new antifibrotic target of Ac-SDKP: inhibition of myofibroblast differentiation in rat lung with silicosis. in PLoS ONE 2012
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Rat (Rattus) FGF23 ELISA Kit für Sandwich ELISA - ABIN367437
Lind, Sundqvist, Hu, Pejler, Andersson, Jacobson, Melhus: Vitamin a is a negative regulator of osteoblast mineralization. in PLoS ONE 2013
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Mouse (Murine) FGF23 ELISA Kit für Sandwich ELISA - ABIN415718
Chen, Feng, Bao, Li, Zhang, Shen, Zhao, Guo, Jing, Lin, Zong: Adverse Effects of Osteocytic Constitutive Activation of ß-Catenin on Bone Strength and Bone Growth. in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research 2015
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FGF23 functions as a hypocalcemic hormone in zebrafish.
This study showed that stanniocalcin 1 (stc1 (zeige STC1 ELISA Kits))modulates cation levels in trpm7 (zeige TRPM7 ELISA Kits) mutants and in the wild type; levels of cations are restored to normal in trpm7 (zeige TRPM7 ELISA Kits) mutants when stc1 (zeige STC1 ELISA Kits) 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 (zeige KL ELISA Kits) 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 (zeige IL6 ELISA Kits), C-reactive protein (zeige CRP ELISA Kits), 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 (zeige SOST ELISA Kits) levels in KTR are normal and influenced more by bone turnover than by eGFR (zeige EGFR ELISA Kits). Its involvement with other hormones of mineral homeostasis (FGF23/Klotho (zeige KL ELISA Kits) 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 (zeige FTL ELISA Kits), resulting in increased usages of iron supplementation in HD patients
There might be a strong correlation between FGF-23 and ghrelin (zeige GHRL ELISA Kits) 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 (zeige PHEX ELISA Kits), independent of its role in phosphate homeostasis
FGF23 augments pro-fibrotic signalling cascades in injury-primed renal fibroblasts via activation of FGFR4 (zeige FGFR4 ELISA Kits)
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 (zeige PTH ELISA Kits) signaling in bone and kidney.
EPO (zeige EPO ELISA Kits) dependent regulation pathway of FGF23 gene expression
Klotho (zeige KL ELISA Kits) in bone is crucial for inducing FGF23 production upon renal failure
dietary iron content and chronic kidney disease affected FGF23 production and metabolism
Dmp1 (zeige DMP1 ELISA Kits) 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 (zeige ANXA7 ELISA Kits) deficiency upregulates FGF23 plasma levels, an effect paralleled by increased corticosterone plasma levels, as well as decreased 1,25(OH)2 D3 and PTH (zeige PTH ELISA Kits) 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