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Some patients with\n                    <jats:italic>FAM20C<\/jats:italic>\n                    mutations as well as\n                    <jats:italic>Fam20C<\/jats:italic>\n                    KO mice develop hypophosphatemia due to elevated levels of the phosphate-regulating hormone FGF23. In this paper, we show that Fam20C phosphorylates FGF23 on a Ser-x-Glu motif that lies within a critical region of the hormone. The phosphorylation promotes FGF23 proteolysis by furin by blocking O-glycosylation by polypeptide\n                    <jats:italic>N<\/jats:italic>\n                    -acetylgalactosaminyltransferase 3. Our results have important implications for patients with abnormalities in phosphate homeostasis.\n                  <\/jats:p>","DOI":"10.1073\/pnas.1402218111","type":"journal-article","created":{"date-parts":[[2014,3,27]],"date-time":"2014-03-27T00:32:49Z","timestamp":1395880369000},"page":"5520-5525","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":303,"title":["Dynamic regulation of FGF23 by Fam20C phosphorylation, GalNAc-T3 glycosylation, and furin proteolysis"],"prefix":"10.1073","volume":"111","author":[{"given":"Vincent S.","family":"Tagliabracci","sequence":"first","affiliation":[{"name":"Departments of aPharmacology,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James L.","family":"Engel","sequence":"additional","affiliation":[{"name":"Departments of aPharmacology,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sandra 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