{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE315nnn/GSE315744/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Genomics"],"species":["Mus musculus"],"gds_type":["Genome binding/occupancy profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE315744"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Steroid hormone antagonism affords vascular protection in a mouse model of Vascular Ehlers-Danlos Syndrome","description":"Aortic dissection is a significant cause of mortality in vascular Ehlers-Danlos syndrome (VEDS), a disorder caused by mutations in the COL3A1 gene. Col3a1G938D/+ mice recapitulate features of VEDS, including high risk of aortic rupture, and aortic risk in this model accelerates at the onset of puberty, especially in males. We identify developmentally regulated gene programs associated with this vulnerability and targeted by treatments that mitigate it, including androgen receptor (AR) and mineralocorticoid receptor (MR) antagonism. We provide ATAC-seq data from aortic nuclei collected at postnatal day 60 from Col3a1G938D/+ (vEDS model) and Col3a1+/+ (WT) mice. For each genotype, aortic tissue from two age- and sex-matched animals was pooled prior to nuclei isolation. Downstream sequence and motif analyses (gkm-SVM/gkmPWM/mapTF) were performed to characterize sequence features and transcription factor binding site enrichment differences between genotypes.","dates":{"publication":"2026/04/16"},"accession":"GSE315744","cross_references":{"GSM":["GSM9436137","GSM9436138","GSM9436139","GSM9436140"],"GPL":["24247"],"GSE":["315744"],"taxon":["Mus musculus"]}}