{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE319nnn/GSE319550/"]},"type":"primary"},"statusCodeValue":200,"statusCode":"OK"}],"scores":null,"additional":{"omics_type":["Genomics"],"species":["Homo sapiens"],"gds_type":["Genome binding/occupancy profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE319550"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Chromatin accessibility in human colonic fibroblasts","description":"We investigated genome-wide chromatin accessibility changes associated with replicative senescence in human colonic fibroblasts (HCoFs). A replicative senescence model was established by serial passaging of HCoFs, and cells at different stages of aging were collected: young (passage 6), mid-old (passage 15), and old (passage 23). To characterize age-associated alterations in chromatin structure, Assay for Transposase-Accessible Chromatin with high-throughput sequencing (ATAC-seq) was performed. Comprehensive epigenomic profiling revealed progressive remodeling of chromatin accessibility during replicative aging. Comparative analysis across young, mid-old, and old cells enabled identification of senescence-associated regulatory regions and dynamic changes in accessible chromatin landscapes. These data provide a valuable resource for understanding the epigenetic mechanisms underlying replicative senescence in human colonic fibroblasts and offer insight into how age-dependent chromatin reorganization contributes to transcriptional regulation during cellular aging.","dates":{"publication":"2026/07/01"},"accession":"GSE319550","cross_references":{"GSM":["GSM9519652","GSM9519653","GSM9519650","GSM9519651","GSM9519646","GSM9519654","GSM9519649","GSM9519647","GSM9519648"],"GPL":["34284"],"GSE":["319550"],"taxon":["Homo sapiens"]}}