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10.1038/ki.2014.316

http://scihub22266oqcxt.onion/10.1038/ki.2014.316
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C4246422!4246422!25427080
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suck abstract from ncbi


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pmid25427080      Kidney+Int 2014 ; 86 (6): 1072-4
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  • Molecular interactions of FGF23 and PTH in phosphate regulation #MMPMID25427080
  • Lanske B; Razzaque MS
  • Kidney Int 2014[Dec]; 86 (6): 1072-4 PMID25427080show ga
  • 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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