Publication: Molecular interactions of FGF23 and PTH in phosphate regulation
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Date
2014
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Lanske, Beate, and Mohammed S. Razzaque. 2014. “Molecular interactions of FGF23 and PTH in phosphate regulation.” Kidney international 86 (6): 1072-1074. doi:10.1038/ki.2014.316. http://dx.doi.org/10.1038/ki.2014.316.
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Abstract
Bone-derived fibroblast growth factor-23 (FGF23) plays an important role in systemic phosphate turnover. Increased FGF23 activity results in hypophosphatemic, while reduced activity is linked to hyperphosphatemic disorders. FGF23, together with klotho as co-factor, can activate FGF-receptors in its target tissues to exert its functions. However, molecular regulation of FGF23 synthesis is not clearly defined, and recent studies have found that PTH can activate the nuclear receptor-associated protein-1 (Nurr1) to induce FGF23 transcription in bone cells.
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Keywords
Kidney, Bone, transcription, regulation
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