Fibrous Dysplasia and Fibroblast Growth Factor-23 Regulation View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2013-06

AUTHORS

Alison M. Boyce, Nisan Bhattacharyya, Michael T. Collins

ABSTRACT

Fibrous dysplasia (FD) is a skeletal disorder caused by activating mutations in Gsα that result in elevations in cAMP. A feature of FD is elevated blood levels of the bone cell-derived phosphaturic hormone, fibroblast growth factor-23 (FGF23). FGF23 regulates serum phosphorus and active vitamin D levels by action on proximal renal tubule cells. An essential step in the production of biologically active FGF23 is glycosylation by the UDP-N-acetyl-α-D-galactosamine:polypeptide N-acetylgalactosaminyl transferase (ppGalNAc-T3). In the absence of glycosylation, FGF23 is processed into inactive N- and C-terminal proteins by a subtilisin proprotein convertase, probably furin. Normally, most if not all circulating FGF23 is intact. In FD, C-terminal levels are elevated, suggesting altered FGF23 processing. Altered processing in FD is the result of a cAMP-dependent, coordinated decrease in ppGalNAc-T3 and an increase in furin enzyme activity. These findings, and emerging data from other diseases, suggest regulation of FGF23 processing may be a physiologically important process. More... »

PAGES

65-71

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s11914-013-0144-5

DOI

http://dx.doi.org/10.1007/s11914-013-0144-5

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1047480924

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/23532406


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