{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE339nnn/GSE339077/"]},"type":"primary"},"statusCodeValue":200,"statusCode":"OK"}],"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=GSE339077"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Fibronectin inhibition restores myelination in endothelial TNFR2-depedent non-remitting Experimental Autoimmune Encephalomyelitis [RNA-seq]","description":"Multiple Sclerosis (MS) is characterized by impaired remyelination and progressive neurodegeneration. Here, we investigated the mechanisms underlying remyelination failure in Experimental Autoimmune Encephalomyelitis (EAE), a murine model of MS. Tumor Necrosis Factor Receptor 2 (TNFR2) deletion causes a severe non-remitting disease after EAE induction. To delineate the TNFR2-dependent effect on remyelination, we assessed the transcriptional profiles of mice expressing TNFR2 (TNFR2FF) and TNFR2-deleted mice (TNFR2KO) at key EAE stages. Our study highlights the key role of TNFR2 at the non-remitting stage of the disease.","dates":{"publication":"2026/09/07"},"accession":"GSE339077","cross_references":{"GSM":["GSM9888093","GSM9888094","GSM9888091","GSM9888092","GSM9888097","GSM9888086","GSM9888087","GSM9888098","GSM9888095","GSM9888085","GSM9888096","GSM9888090","GSM9888099","GSM9888088","GSM9888100","GSM9888089"],"GPL":["16331"],"GSE":["339077"],"taxon":["Mus musculus"]}}