{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE329nnn/GSE329318/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE329318"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Effect of interferon-gamma stimulation on the transcriptome of RANKL/M-CSF-induced osteoclasts","description":"Interferon-gamma (IFN-γ) is a pleiotropic cytokine with context-dependent effects on bone homeostasis, capable of both inhibiting and promoting osteoclastogenesis depending on the cellular milieu and stage of differentiation. To delineate the direct transcriptional consequences of IFN-γ exposure during terminal osteoclast differentiation, we performed RNA sequencing on RANKL/M-CSF-induced osteoclasts treated with or without IFN-γ. Differential expression analysis identified a suite of IFN-γ-responsive genes and revealed significant perturbation of pathways governing osteoclast fusion and bone resorption. Notably, we identified Lipocalin-2 (Lcn2) as a key downstream effector whose expression is robustly induced by IFN-γ. These data elucidate the molecular mechanisms by which IFN-γ translates immune signals into pro-osteoclastogenic instructions, highlighting a specific transcriptional program that enhances osteoclast differentiation and may contribute to inflammatory bone loss.","dates":{"publication":"2026/05/02"},"accession":"GSE329318","cross_references":{"GSM":["GSM9701684","GSM9701685","GSM9701688","GSM9701689","GSM9701686","GSM9701687"],"GPL":["34328"],"GSE":["329318"],"taxon":["Mus musculus"]}}