title: Molecular interactions of FGF23 and PTH in phosphate regulation.
abstract: Bone-derived fibroblast growth factor-23 (FGF23) plays an important role in systemic phosphate turnover. Increased FGF23 activity results in hypophosphatemic disorders, 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, the molecular regulation of FGF23 synthesis is not clearly defined, and recent studies have found that parathyroid hormone (PTH) can activate the nuclear receptor-associated protein-1 (Nurr1) to induce FGF23 transcription in bone cells.
authors.affiliation: Department of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine, Boston, Massachusetts, USA.
authors.forename: Beate
authors.initials: B
authors.lastname: Lanske
authors.affiliation: Department of Applied Oral Sciences, The Forsyth Institute, Cambridge, Massachusetts, USA.
authors.forename: Mohammed S
authors.initials: MS
authors.lastname: Razzaque
mesh_terms: D000818:Animals; D005346:Fibroblast Growth Factors / Q000235:genetics*; D008297:Male; D057126:Nuclear Receptor Subfamily 4, Group A, Member 2 / Q000235:genetics* / Q000378:metabolism*; D010281:Parathyroid Hormone / Q000494:pharmacology*; D012333:RNA, Messenger / Q000378:metabolism*; D014158:Transcription, Genetic / Q000187:drug effects*
chemical_list: D057126:Nuclear Receptor Subfamily 4, Group A, Member 2; D010281:Parathyroid Hormone; D012333:RNA, Messenger; D005346:Fibroblast Growth Factors