{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Jaffery H"],"funding":["Versus Arthritis","Wellcome Trust"],"pagination":["2148-2160"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10952620"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["75(12)"],"pubmed_abstract":["<h4>Objective</h4>IĸB protein B cell lymphoma 3-encoded protein (BCL3) is a regulator of the NF-κB family of transcription factors. NF-κB signaling fundamentally influences the fate of bone-forming osteoblasts and bone-resorbing osteoclasts, but the role of BCL3 in bone biology has not been investigated. The objective of this study was to evaluate BCL3 in skeletal development, maintenance, and osteoarthritic pathology.<h4>Methods</h4>To assess the contribution of BCL3 to skeletal homeostasis, neonatal mice (n = 6-14) lacking BCL3 (Bcl3<sup>-/-</sup> ) and wild-type (WT) controls were characterized for bone phenotype and density. To reveal the contribution to bone phenotype by the osteoblast compartment in Bcl3<sup>-/-</sup> mice, transcriptomic analysis of early osteogenic differentiation "],"journal":["Arthritis & rheumatology (Hoboken, N.J.)"],"pubmed_title":["IĸB Protein BCL3 as a Controller of Osteogenesis and Bone Health."],"pmcid":["PMC10952620"],"funding_grant_id":["099786/Z/12/A","22072","22858","099786/Z/12/Z"],"pubmed_authors":["McInnes IB","van 't Hof RJ","Jaffery H","Huesa C","Chilaka S","Doonan J","Akbar M","Dunning L","Carmody RJ","Goodyear CS","Cole J","Tanner KE"],"additional_accession":[]},"is_claimable":false,"name":"IĸB Protein BCL3 as a Controller of Osteogenesis and Bone Health.","description":"<h4>Objective</h4>IĸB protein B cell lymphoma 3-encoded protein (BCL3) is a regulator of the NF-κB family of transcription factors. NF-κB signaling fundamentally influences the fate of bone-forming osteoblasts and bone-resorbing osteoclasts, but the role of BCL3 in bone biology has not been investigated. The objective of this study was to evaluate BCL3 in skeletal development, maintenance, and osteoarthritic pathology.<h4>Methods</h4>To assess the contribution of BCL3 to skeletal homeostasis, neonatal mice (n = 6-14) lacking BCL3 (Bcl3<sup>-/-</sup> ) and wild-type (WT) controls were characterized for bone phenotype and density. To reveal the contribution to bone phenotype by the osteoblast compartment in Bcl3<sup>-/-</sup> mice, transcriptomic analysis of early osteogenic differentiation ","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Dec","modification":"2026-06-02T19:53:57.289Z","creation":"2024-11-20T03:29:23.011Z"},"accession":"S-EPMC10952620","cross_references":{"pubmed":["37410754"],"doi":["10.1002/art.42639"]}}