<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>30(1)</volume><submitter>Lee S</submitter><pubmed_abstract>&lt;h4>Background&lt;/h4>Bone remodeling is a critical process that maintains skeletal integrity, orchestrated by the balanced activities of osteoclasts, which resorb bone, and osteoblasts, which form bone. Osteoclastogenesis, the formation of osteoclasts, is primarily driven by NFATc1, a process activated through c-Fos and NF-κB signaling pathways in response to receptor activator of nuclear factor κB ligand (RANKL). Dysregulation of RANKL signaling is a key contributor to pathological bone loss, as seen in conditions such as osteoporosis.&lt;h4>Methods&lt;/h4>We investigated the effects of denatonium, a known bitter compound, on RANKL-induced osteoclast differentiation. We used RNA sequencing (RNA-seq) to analyze gene expression profiles in osteoclast precursors treated with denatonium. Transcriptio</pubmed_abstract><journal>Molecular medicine (Cambridge, Mass.)</journal><pagination>248</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11660935</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Denatonium inhibits RANKL-induced osteoclast differentiation and rescues the osteoporotic phenotype by blocking p65 signaling pathway.</pubmed_title><pmcid>PMC11660935</pmcid><pubmed_authors>Lee S</pubmed_authors><pubmed_authors>Kim JM</pubmed_authors><pubmed_authors>Park JI</pubmed_authors><pubmed_authors>Kim HJ</pubmed_authors><pubmed_authors>Kim K</pubmed_authors><pubmed_authors>Lee K</pubmed_authors><pubmed_authors>Lee H</pubmed_authors><pubmed_authors>Lee JY</pubmed_authors><pubmed_authors>Park S</pubmed_authors><pubmed_authors>Jang YJ</pubmed_authors><pubmed_authors>Yi SJ</pubmed_authors><pubmed_authors>Hyun TK</pubmed_authors><pubmed_authors>Song JS</pubmed_authors><pubmed_authors>Lee JH</pubmed_authors></additional><is_claimable>false</is_claimable><name>Denatonium inhibits RANKL-induced osteoclast differentiation and rescues the osteoporotic phenotype by blocking p65 signaling pathway.</name><description>&lt;h4>Background&lt;/h4>Bone remodeling is a critical process that maintains skeletal integrity, orchestrated by the balanced activities of osteoclasts, which resorb bone, and osteoblasts, which form bone. Osteoclastogenesis, the formation of osteoclasts, is primarily driven by NFATc1, a process activated through c-Fos and NF-κB signaling pathways in response to receptor activator of nuclear factor κB ligand (RANKL). Dysregulation of RANKL signaling is a key contributor to pathological bone loss, as seen in conditions such as osteoporosis.&lt;h4>Methods&lt;/h4>We investigated the effects of denatonium, a known bitter compound, on RANKL-induced osteoclast differentiation. We used RNA sequencing (RNA-seq) to analyze gene expression profiles in osteoclast precursors treated with denatonium. Transcriptio</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Dec</publication><modification>2025-04-22T10:40:26.645Z</modification><creation>2025-04-05T23:42:01.028Z</creation></dates><accession>S-EPMC11660935</accession><cross_references><pubmed>39701944</pubmed><doi>10.1186/s10020-024-01031-2</doi></cross_references></HashMap>