{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T13:18:26Z","timestamp":1791206306110,"version":"4.1.0"},"reference-count":53,"publisher":"Oxford University Press (OUP)","issue":"1","license":[{"start":{"date-parts":[[2015,7,14]],"date-time":"2015-07-14T00:00:00Z","timestamp":1436832000000},"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":[[2016,1,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n               <jats:sec>\n                  <jats:title>\u2003<\/jats:title>\n                  <jats:p>Heritable disorders that feature high bone mass (HBM) are rare. The etiology is typically a mutation(s) within a gene that regulates the differentiation and function of osteoblasts (OBs) or osteoclasts (OCs). Nevertheless, the molecular basis is unknown for approximately one-fifth of such entities. NF-\u03baB signaling is a key regulator of bone remodeling and acts by enhancing OC survival while impairing OB maturation and function. The NF-\u03baB transcription complex comprises five subunits. In mice, deletion of the p50 and p52 subunits together causes osteopetrosis (OPT). In humans, however, mutations within the genes that encode the NF-\u03baB complex, including the Rela\/p65 subunit, have not been reported. We describe a neonate who died suddenly and unexpectedly and was found at postmortem to have HBM documented radiographically and by skeletal histopathology. Serum was not available for study. Radiographic changes resembled malignant OPT, but histopathological investigation showed morphologically normal OCs and evidence of intact bone resorption excluding OPT. Furthermore, mutation analysis was negative for eight genes associated with OPT or HBM. Instead, accelerated bone formation appeared to account for the HBM. Subsequently, trio-based whole exome sequencing revealed a heterozygous de novo missense mutation (c.1534_1535delinsAG, p.Asp512Ser) in exon 11 of RELA encoding Rela\/p65. The mutation was then verified using bidirectional Sanger sequencing. Lipopolysaccharide stimulation of patient fibroblasts elicited impaired NF-\u03baB responses compared with healthy control fibroblasts. Five unrelated patients with unexplained HBM did not show a RELA defect. Ours is apparently the first report of a mutation within the NF-\u03baB complex in humans. The missense change is associated with neonatal osteosclerosis from in utero increased OB function rather than failed OC action. These findings demonstrate the importance of the Rela\/p65 subunit within the NF-\u03baB pathway for human skeletal homeostasis and represent a new genetic cause of HBM. \u00a9 2015 American Society for Bone and Mineral Research.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1002\/jbmr.2590","type":"journal-article","created":{"date-parts":[[2015,7,14]],"date-time":"2015-07-14T15:40:25Z","timestamp":1436888425000},"page":"163-172","source":"Crossref","is-referenced-by-count":30,"title":["Neonatal High Bone Mass With First Mutation of the NF-\u03baB Complex: Heterozygous De Novo Missense (p.Asp512Ser) <i>RELA<\/i> (Rela\/p65)"],"prefix":"10.1093","volume":"31","author":[{"given":"Anja L","family":"Frederiksen","sequence":"first","affiliation":[{"name":"Human GeneticsInstitute of Clinical ResearchUniversity of Southern DenmarkOdenseDenmark"},{"name":"Department of Clinical GeneticsOdense University 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Thiis","family":"Knudsen","sequence":"additional","affiliation":[{"name":"Institute of Forensic MedicineUniversity of Southern DenmarkOdenseDenmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Henrik Daa","family":"Schr\u00f8der","sequence":"additional","affiliation":[{"name":"Department of PathologyOdense University HospitalOdenseDenmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Weimin","family":"Qiu","sequence":"additional","affiliation":[{"name":"Molecular Endocrinology Laboratory (KMEB)Department of EndocrinologyOdense University Hospital and University of Southern DenmarkOdenseDenmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christina","family":"Eckhardt","sequence":"additional","affiliation":[{"name":"Department of PediatricsOdense University HospitalOdenseDenmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"William H","family":"McAlister","sequence":"additional","affiliation":[{"name":"Department of Pediatric RadiologyMallinckrodt Institute of RadiologyWashington University School of Medicine at St. Louis Children's HospitalSt. LouisMOUSA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Moustapha","family":"Kassem","sequence":"additional","affiliation":[{"name":"Molecular Endocrinology Laboratory (KMEB)Department of EndocrinologyOdense University Hospital and University of Southern DenmarkOdenseDenmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Steven","family":"Mumm","sequence":"additional","affiliation":[{"name":"Center for Metabolic Bone Disease and Molecular ResearchShriners Hospital for ChildrenSt. LouisMOUSA"},{"name":"Division of Bone and Mineral DiseasesWashington University School of Medicine at Barnes-Jewish HospitalSt. 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