{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,29]],"date-time":"2026-10-29T16:31:46Z","timestamp":1793291506445,"version":"4.5.0"},"reference-count":52,"publisher":"The Endocrine Society","issue":"6","license":[{"start":{"date-parts":[[2019,12,10]],"date-time":"2019-12-10T00:00:00Z","timestamp":1575936000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"name":"KACST Biotech","award":["13-MED1765-20"],"award-info":[{"award-number":["13-MED1765-20"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2020,6,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Context<\/jats:title>\n                  <jats:p>Hypophosphatemic rickets (HR) is a group of rare hereditary renal phosphate wasting disorders caused by mutations in PHEX, FGF23, DMP1, ENPP1, CLCN5, SLC9A3R1, SLC34A1, or SLC34A3.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Objective<\/jats:title>\n                  <jats:p>A large kindred with 5 HR patients was recruited with dominant inheritance. The study was undertaken to investigate underlying genetic defects in HR patients.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Design<\/jats:title>\n                  <jats:p>Patients and their family members were initially analyzed for PHEX and FGF23 mutations using polymerase chain reaction sequencing and copy number analysis. Exome sequencing was subsequently performed to identify novel candidate genes.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>PHEX and FGF23 mutations were not detected in the patients. No copy number variation was observed in the genome using CytoScan HD array analysis. Mutations in DMP1, ENPP1, CLCN5, SLC9A3R1, SLC34A1, or SLC34A3 were also not found by exome sequencing. A novel c.979\u201396 T&amp;gt;A mutation in the SGK3 gene was found to be strictly segregated in a heterozygous pattern in patients and was not present in normal family members. The mutation is located 1 bp downstream of a highly conserved adenosine branch point, resulted in exon 13 skipping and in-frame deletion of 29 amino acids, which is part of the protein kinase domain and contains a Thr-320 phosphorylation site that is required for its activation. Protein tertiary structure modelling showed significant structural change in the protein kinase domain following the deletion.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusions<\/jats:title>\n                  <jats:p>The c.979\u201396 T&amp;gt;A splice mutation in the SGK3 gene causes exon 13 skipping and deletion of 29 amino acids in the protein kinase domain. The SGK3 mutation may cause autosomal dominant HR.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1210\/clinem\/dgz260","type":"journal-article","created":{"date-parts":[[2019,12,10]],"date-time":"2019-12-10T15:57:16Z","timestamp":1575993436000},"page":"1840-1850","source":"Crossref","is-referenced-by-count":15,"title":["Mutation of SGK3, a Novel Regulator of Renal Phosphate Transport, Causes Autosomal Dominant Hypophosphatemic Rickets"],"prefix":"10.1210","volume":"105","author":[{"given":"Ay\u015fe Nurcan","family":"Cebeci","sequence":"first","affiliation":[{"name":"Department of Pediatric Endocrinology, Istanbul Bilim University, Istanbul, Turkey"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Minjing","family":"Zou","sequence":"additional","affiliation":[{"name":"Department of Genetics, King Faisal Specialist Hospital & Research Centre, Riyadh, Saudi Arabia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Huda A","family":"BinEssa","sequence":"additional","affiliation":[{"name":"Department of Genetics, King Faisal Specialist Hospital & Research Centre, Riyadh, Saudi Arabia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ali S","family":"Alzahrani","sequence":"additional","affiliation":[{"name":"Department of Medicine King Faisal Specialist Hospital & Research Centre, Riyadh, Saudi Arabia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Roua A","family":"Al-Rijjal","sequence":"additional","affiliation":[{"name":"Department of Genetics, King Faisal Specialist Hospital & Research Centre, Riyadh, Saudi Arabia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anwar F","family":"Al-Enezi","sequence":"additional","affiliation":[{"name":"Department of Genetics, King Faisal Specialist Hospital & Research Centre, Riyadh, Saudi Arabia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Futwan A","family":"Al-Mohanna","sequence":"additional","affiliation":[{"name":"Department of Cell Biology, King Faisal Specialist Hospital & Research Centre, Riyadh, Saudi Arabia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Etienne","family":"Cavalier","sequence":"additional","affiliation":[{"name":"Department of Clinical Chemistry, University of Li\u00e8ge, CHU de Li\u00e8ge, Li\u00e8ge, Belgium"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brian F","family":"Meyer","sequence":"additional","affiliation":[{"name":"Department of Genetics, King Faisal Specialist Hospital & Research Centre, Riyadh, Saudi Arabia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6999-0191","authenticated-orcid":false,"given":"Yufei","family":"Shi","sequence":"additional","affiliation":[{"name":"Department of Genetics, King Faisal Specialist Hospital & Research Centre, Riyadh, Saudi Arabia"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"80","published-online":{"date-parts":[[2019,12,10]]},"reference":[{"issue":"3","key":"2021122105220404700_CIT0001","doi-asserted-by":"crossref","first-page":"491","DOI":"10.1530\/EJE-08-0818","article-title":"Incidence and prevalence of nutritional and hereditary rickets in southern Denmark","volume":"160","author":"Beck-Nielsen","year":"2009","journal-title":"Eur J Endocrinol."},{"issue":"7","key":"2021122105220404700_CIT0002","doi-asserted-by":"crossref","first-page":"435","DOI":"10.1038\/s41581-019-0152-5","article-title":"Clinical practice recommendations for the diagnosis and management of X-linked hypophosphataemia","volume":"15","author":"Haffner","year":"2019","journal-title":"Nat Rev Nephrol."},{"issue":"2","key":"2021122105220404700_CIT0003","doi-asserted-by":"crossref","first-page":"443","DOI":"10.1016\/S0031-3955(05)70485-5","article-title":"New perspectives on the biology and treatment of X-linked hypophosphatemic rickets","volume":"44","author":"Carpenter","year":"1997","journal-title":"Pediatr Clin North Am."},{"key":"2021122105220404700_CIT0004","first-page":"88","article-title":"Genetic causes of rickets","volume":"9","author":"Acar","year":"2017","journal-title":"J Clin Res Pediatr Endocrinol."},{"issue":"1","key":"2021122105220404700_CIT0005","doi-asserted-by":"crossref","first-page":"1","DOI":"10.1007\/s00774-011-0340-2","article-title":"The expanding family of hypophosphatemic syndromes","volume":"30","author":"Carpenter","year":"2012","journal-title":"J Bone Miner Metab."},{"issue":"2","key":"2021122105220404700_CIT0006","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. 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