ENAapplication/xmlftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR233/054/SRR23301954/SRR23301954.fastq.gzprimaryOK200GenomicsThe Univ of Tokyohttps://www.ebi.ac.uk/ena/browser/view/PRJNA930352Mus musculusxref:PubMed:39080781In rheumatoid arthritis (RA), inflammation and joint destruction are exacerbated by a complicated interaction among immune cells, synovial fibroblasts and bone cells. It remains to be elucidated which cell-cell interaction critically drives the pathogenesis of RA and serves as a therapeutic target for synthetic disease modifying antirheumatic drugs (DMARDs) such as janus kinase (JAK) inhibitors. we performed a scRNA-seq analysis of the synovium of collagen-induced arthritis (CIA) mice treated with JAK inhibitor, followed by a computational analysis to identify the drug target cells and signaling pathways in vivo Overall design: scRNA-seq analysis was performed on synovial cells which were isolated from the knee joints of CIA mice treated with a JAK inhibitor, upadacitinib (n=6). Alignment, quantitation and aggregation of the sample count matrices were performed using the 10x Genomics Cell Ranger pipeline (v.3.0) according to the manufacturer’s protocol (GENEWIZ).ENAfalseTranscriptomic analysis of synovial cells derived from collagen-induced arthritis mice treated with a JAK inhibitor, upadacitinibTranscriptomic analysis of synovial cells derived from collagen-induced arthritis mice treated with a JAK inhibitor, upadacitinib2025-09-242024-08-26PRJNA930352GSE2242211009039080781