<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Jaffery H</submitter><funding>Versus Arthritis</funding><funding>Wellcome Trust</funding><pagination>2148-2160</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10952620</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>75(12)</volume><pubmed_abstract>&lt;h4>Objective&lt;/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.&lt;h4>Methods&lt;/h4>To assess the contribution of BCL3 to skeletal homeostasis, neonatal mice (n = 6-14) lacking BCL3 (Bcl3&lt;sup>-/-&lt;/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&lt;sup>-/-&lt;/sup> mice, transcriptomic analysis of early osteogenic differentiation </pubmed_abstract><journal>Arthritis &amp; rheumatology (Hoboken, N.J.)</journal><pubmed_title>IĸB Protein BCL3 as a Controller of Osteogenesis and Bone Health.</pubmed_title><pmcid>PMC10952620</pmcid><funding_grant_id>099786/Z/12/A</funding_grant_id><funding_grant_id>22072</funding_grant_id><funding_grant_id>22858</funding_grant_id><funding_grant_id>099786/Z/12/Z</funding_grant_id><pubmed_authors>McInnes IB</pubmed_authors><pubmed_authors>van 't Hof RJ</pubmed_authors><pubmed_authors>Jaffery H</pubmed_authors><pubmed_authors>Huesa C</pubmed_authors><pubmed_authors>Chilaka S</pubmed_authors><pubmed_authors>Doonan J</pubmed_authors><pubmed_authors>Akbar M</pubmed_authors><pubmed_authors>Dunning L</pubmed_authors><pubmed_authors>Carmody RJ</pubmed_authors><pubmed_authors>Goodyear CS</pubmed_authors><pubmed_authors>Cole J</pubmed_authors><pubmed_authors>Tanner KE</pubmed_authors></additional><is_claimable>false</is_claimable><name>IĸB Protein BCL3 as a Controller of Osteogenesis and Bone Health.</name><description>&lt;h4>Objective&lt;/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.&lt;h4>Methods&lt;/h4>To assess the contribution of BCL3 to skeletal homeostasis, neonatal mice (n = 6-14) lacking BCL3 (Bcl3&lt;sup>-/-&lt;/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&lt;sup>-/-&lt;/sup> mice, transcriptomic analysis of early osteogenic differentiation </description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Dec</publication><modification>2026-06-02T19:53:57.289Z</modification><creation>2024-11-20T03:29:23.011Z</creation></dates><accession>S-EPMC10952620</accession><cross_references><pubmed>37410754</pubmed><doi>10.1002/art.42639</doi></cross_references></HashMap>