{"database":"biostudies-arrayexpress","file_versions":[],"scores":null,"additional":{"submitter":["Ubaid Ullah Kalim"],"organism":["Mus musculus"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/E-MTAB-17644"],"description":["We induced EAE in mice carrying a gene-trap disruption of Cip2a (hereafter referred to as knockout [KO] mice) and wild-type (WT) control C57BL/6J male and female mice, aged 8-12 weeks. We performed scRNA-seq analysis of lymph node cells from five WT and five KO mice at the peak of EAE. The goal was to see if there are differences in cell type abundance and gene expression between WT and KO mice. The samples were sequenced in two technical replicates, rep1 and rep2.  Using cell multiplexing oligo (CMO) by 10X, 5 KO mice lymph nodes (CMO301-305) and 5 WT tagged (CMO306-310) processed as 1 sample for 10X chromium. Same sample ran twice on two lanes of Chromium chip as technical replicate for capturing more single cells for analysis."],"repository":["biostudies-arrayexpress"],"sample_protocol":["Sample Collection - Lymph nodes were extracted at the peak of EAE and single cell suspensions were prepared.","Library Construction - The PCR steps were carried out using a Bio-Rad C1000 Touch instrument, using 12 cycles for cDNA pre-amplification and 13 cycles for the sample index PCR.","Nucleic Acid Extraction - For the lymph node samples, the CellPlex-labelled pools were processed using Chromium Next GEM Single Cell 3’ Reagent Kit v3.1 with Feature Barcode technology for Cell Multiplexing and the Chromium X instrument, targeting 30,000 cells per pool.","Sequencing - For the lymph node samples, the CellPlex-labelled pools were processed using Chromium Next GEM Single Cell 3’ Reagent Kit v3.1 with Feature Barcode technology for Cell Multiplexing and the Chromium X instrument, targeting 30,000 cells per pool. The sequencing was performed at Finnish Functional Genomics Centre, Turku, Finland."],"figure_sub":["Organization","MINSEQE Score","Assays and Data","Processed Data","MAGE-TAB Files"],"data_protocol":["Data Transformation - The data was analyzed using Seurat (v4.2.0) (26) in R (v4.2). For lymph node data cells with more than 10% mitochondrial reads, less than 200 expressed genes or more than 7000 expressed genes were filtered out. Normalization, identification of highly variable features, scaling, dimensionality reduction with PCA, integration, and clustering were performed per Seurat’s instructions. Uniform manifold approximation and projection (UMAP) was used for data visualization. The clusters were annotated using a reference annotation with SingleR (v1.10.0)(27) and manual annotation. Mouse atlas data was used for the reference annotation. For differential expression analysis between KO and WT, cell-level counts were aggregated into sample-level counts in each cell type using muscat"],"omics_type":["Metabolomics","Unknown","Transcriptomics","Genomics","Proteomics"],"instrument_platform":["Illumina NovaSeq 6000"],"pubmed_abstract":["<h4>ABSTRACT</h4>  Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system (CNS) driven by pathogenic T cell-mediated inflammation. Fingolimod (FTY720), an approved therapy for MS, is an established activator of protein phosphatase 2A (PP2A). However the contribution of PP2A in autoimmune neuroinflammation remains incompletely understood. Here, we addressed this question using experimental autoimmune encephalomyelitis (EAE), a murine model of MS, in mice carrying a genetic disruption of the locus encoding cancerous inhibitor of protein phosphatase 2A (CIP2A), an endogenous inhibitor of PP2A. Mice with disruption of the CIP2A locus, the knock out (KO) mice, exhibited attenuated EAE severity compared with wild-type (WT) controls. Histological and flow-cytometric"],"study_type":["RNA-seq of coding RNA from single cells"],"species":["Mus musculus"],"pubmed_title":["Genetic Disruption at the CIP2A Locus Modulates T Cell Responses and Attenuates Experimental Autoimmune Encephalomyelitis"],"pubmed_authors":["Mohd Moin Khan, Inna Starskaia, Emilie Rydgren, Sini Junttila, Johannes Smolander, Meraj Hasan Khan, Rahul Biradar, Roosa Kattelus, Anne Ahtikoski, Maria Gardberg, Mudassir Meraj Banday, Uzma Riyaz, Joonas Khabbal, Emrah Yatkin,  Li Tian, Peggy P. Ho, Tapio Lönnberg, Laura L. Elo, Lawrence Steinman, Jukka Westermarck, Omid Rasool, Riitta Lahesmaa, and Ubaid Ullah Kalim","Ubaid Ullah Kalim"],"additional_accession":[]},"is_claimable":false,"name":"scRNA-seq of lymph node of mice where Cip2a locus has been disrupted and wild-type control mice at the peak of Experimental Autoimmune Encephalomyelis","description":"We induced EAE in mice carrying a gene-trap disruption of Cip2a (hereafter referred to as knockout [KO] mice) and wild-type (WT) control C57BL/6J male and female mice, aged 8-12 weeks. We performed scRNA-seq analysis of lymph node cells from five WT and five KO mice at the peak of EAE. The goal was to see if there are differences in cell type abundance and gene expression between WT and KO mice. The samples were sequenced in two technical replicates, rep1 and rep2.  Using cell multiplexing oligo (CMO) by 10X, 5 KO mice lymph nodes (CMO301-305) and 5 WT tagged (CMO306-310) processed as 1 sample for 10X chromium. Same sample ran twice on two lanes of Chromium chip as technical replicate for capturing more single cells for analysis.","dates":{"release":"2026-09-30T00:00:00Z","modification":"2026-09-30T01:01:02.516Z","creation":"2026-09-17T15:18:40.389Z"},"accession":"E-MTAB-17644","cross_references":{"ENA":["ERP206555"],"EFO":["EFO_0002944","EFO_0004170","EFO_0005684","EFO_0005518","EFO_0003816","EFO_0004184"],"doi":["10.64898/2026.08.28.746989"]}}