{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T22:28:56Z","timestamp":1790720936090,"version":"4.1.0"},"reference-count":53,"publisher":"Oxford University Press (OUP)","issue":"6","license":[{"start":{"date-parts":[[2013,1,16]],"date-time":"2013-01-16T00:00:00Z","timestamp":1358294400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2013,6,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n               <jats:sec>\n                  <jats:title>\u2003<\/jats:title>\n                  <jats:p>Fibroblast growth factor 23 (FGF23) plays a crucial role in renal phosphate regulation, exemplified by the causal role of PHEX and DMP1 mutations in X-linked hypophosphatemic rickets and autosomal recessive rickets type 1, respectively. Using whole exome sequencing we identified compound heterozygous mutations in family with sequence similarity 20, member C (FAM20C) in two siblings referred for hypophosphatemia and severe dental demineralization disease. FAM20C mutations were not found in other undiagnosed probands of a national Norwegian population of familial hypophosphatemia. Our results demonstrate that mutations in FAM20C provide a putative new mechanism in human subjects leading to dysregulated FGF23 levels, hypophosphatemia, hyperphosphaturia, dental anomalies, intracerebral calcifications and osteosclerosis of the long bones in the absence of rickets.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1002\/jbmr.1850","type":"journal-article","created":{"date-parts":[[2013,1,16]],"date-time":"2013-01-16T16:12:03Z","timestamp":1358352723000},"page":"1378-1385","source":"Crossref","is-referenced-by-count":155,"title":["Exome sequencing reveals FAM20c mutations associated with fibroblast growth factor 23\u2013related hypophosphatemia, dental anomalies, and ectopic calcification"],"prefix":"10.1093","volume":"28","author":[{"given":"Silje Hjorth","family":"Rafaelsen","sequence":"first","affiliation":[{"name":"Center for Medical Genetics and Molecular MedicineHaukeland University HospitalBergenNorway"},{"name":"Department of Clinical MedicineUniversity of BergenBergenNorway"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Helge","family":"R\u00e6der","sequence":"additional","affiliation":[{"name":"Department of PediatricsHaukeland University HospitalBergenNorway"},{"name":"Department of Clinical MedicineUniversity of BergenBergenNorway"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anne Kristine","family":"Fagerheim","sequence":"additional","affiliation":[{"name":"Medical DepartmentNordland County HospitalBod\u00f8Norway"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Per","family":"Knappskog","sequence":"additional","affiliation":[{"name":"Center for Medical Genetics and Molecular MedicineHaukeland University HospitalBergenNorway"},{"name":"Department of Clinical MedicineUniversity of BergenBergenNorway"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas O","family":"Carpenter","sequence":"additional","affiliation":[{"name":"Departments of Pediatrics (Endocrinology) and Orthopaedics and RehabilitationYale University School of MedicineNew HavenCTUSA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stefan","family":"Johansson","sequence":"additional","affiliation":[{"name":"Department of BiomedicineUniversity of BergenBergenNorway"},{"name":"Center for Medical Genetics and Molecular MedicineHaukeland University HospitalBergenNorway"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert","family":"Bjerknes","sequence":"additional","affiliation":[{"name":"Department of PediatricsHaukeland University HospitalBergenNorway"},{"name":"Department of Clinical MedicineUniversity of BergenBergenNorway"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2013,1,16]]},"reference":[{"issue":"12","key":"2024020318385423100_jbmr1850-bib-0001","doi-asserted-by":"crossref","first-page":"3820","DOI":"10.1172\/JCI36479","article-title":"Endocrine functions of bone in mineral metabolism regulation","volume":"118","author":"Quarles","year":"2008","journal-title":"J Clin Invest."},{"issue":"11","key":"2024020318385423100_jbmr1850-bib-0002","doi-asserted-by":"crossref","first-page":"6500","DOI":"10.1073\/pnas.101545198","article-title":"Cloning characterization of FGF23 as a causative factor of tumor-induced osteomalacia","volume":"98","author":"Shimada","year":"2001","journal-title":"Proc Natl Acad Sci U.S.A."},{"issue":"5","key":"2024020318385423100_jbmr1850-bib-0003","doi-asserted-by":"crossref","first-page":"1305","DOI":"10.1681\/ASN.2005111185","article-title":"Fibroblast growth factor 23 is a counter-regulatory phosphaturic hormone for vitamin D","volume":"17","author":"Liu","year":"2006","journal-title":"J Am Soc Nephrol."},{"issue":"2","key":"2024020318385423100_jbmr1850-bib-0004","doi-asserted-by":"crossref","first-page":"130","DOI":"10.1038\/ng1095-130","article-title":"A gene (PEX) with homologies to endopeptidases is mutated in patients with X-linked hypophosphatemic rickets","volume":"11","author":"Francis","year":"1995","journal-title":"The HYP Consortium. 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