{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Lehle JD"],"funding":["Eunice Kennedy Shriver National Institute of Child Health and Human Development","NICHD NIH HHS","The Robert J. Kleberg, Jr. and Helen C. Kleberg Foundation","NIDA NIH HHS","NCI NIH HHS","National Institute on Drug Abuse","Nancy Hurd Smith Foundation","NIH HHS","NIGMS NIH HHS"],"pagination":["RP93975"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11449486"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13"],"pubmed_abstract":["Endocrine disrupting chemicals (EDCs) such as bisphenol S (BPS) are xenobiotic compounds that can disrupt endocrine signaling due to steric similarities to endogenous hormones. EDCs have been shown to induce disruptions in normal epigenetic programming (epimutations) and differentially expressed genes (DEGs) that predispose disease states. Most interestingly, the prevalence of epimutations following exposure to many EDCs persists over multiple generations. Many studies have described direct and prolonged effects of EDC exposure in animal models, but many questions remain about molecular mechanisms by which EDC-induced epimutations are introduced or subsequently propagated, whether there are cell type-specific susceptibilities to the same EDC, and whether this correlates with differential e"],"journal":["eLife"],"pubmed_title":["An in vitro approach reveals molecular mechanisms underlying endocrine disruptor-induced epimutagenesis."],"pmcid":["PMC11449486"],"funding_grant_id":["U01 DA054179","P50 HD98593","R25 GM060655","P50 HD098593","P30 CA054174","S10 OD030311"],"pubmed_authors":["Chavez L","McCarrey JR","Lin YH","Lehle JD","Gomez A"],"additional_accession":[]},"is_claimable":false,"name":"An in vitro approach reveals molecular mechanisms underlying endocrine disruptor-induced epimutagenesis.","description":"Endocrine disrupting chemicals (EDCs) such as bisphenol S (BPS) are xenobiotic compounds that can disrupt endocrine signaling due to steric similarities to endogenous hormones. EDCs have been shown to induce disruptions in normal epigenetic programming (epimutations) and differentially expressed genes (DEGs) that predispose disease states. Most interestingly, the prevalence of epimutations following exposure to many EDCs persists over multiple generations. Many studies have described direct and prolonged effects of EDC exposure in animal models, but many questions remain about molecular mechanisms by which EDC-induced epimutations are introduced or subsequently propagated, whether there are cell type-specific susceptibilities to the same EDC, and whether this correlates with differential e","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Oct","modification":"2026-06-07T08:06:46.279Z","creation":"2025-04-04T19:38:37.411Z"},"accession":"S-EPMC11449486","cross_references":{"pubmed":["39361026"],"doi":["10.7554/eLife.93975"]}}