Bone as a source of FGF23: regulation by phosphate?
Author:
Publisher
Elsevier BV
Subject
Histology,Physiology,Endocrinology, Diabetes and Metabolism
Reference31 articles.
1. Autosomal dominant hypophosphataemic rickets is associated with mutations in FGF23;Nat. Genet.,2000
2. Increased circulatory level of biologically active full-length FGF-23 in patients with hypophosphatemic rickets/osteomalacia;Yamazaki;J. Clin. Endocrinol. Metab.,2002
3. The autosomal dominant hypophosphatemic rickets (ADHR) gene is a secreted polypeptide overexpressed by tumors that cause phosphate wasting;White;J. Clin. Endocrinol. Metab.,2001
4. Clinical case seminar: fibroblast growth factor 23: a new clinical marker for oncogenic osteomalacia;Nelson;J. Clin. Endocrinol. Metab.,2003
5. A gene (PEX) with homologies to endopeptidases is mutated in patients with X-linked hypophosphatemic rickets;The HYP Consortium;Nat. Genet.,1995
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