{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["22(1)"],"submitter":["Huang CF"],"funding":["Canadian Network for Research and Innovation in Machining Technology, Natural Sciences and Engineering Research Council of Canada","Türkiye Bilimsel ve Teknolojik Araştirma Kurumu","KWF Kankerbestrijding"],"pubmed_abstract":["Background
Androgen receptor (AR) is critical to the initiation, growth, and progression of prostate cancer. Once activated, the AR binds to cis-regulatory enhancer elements on DNA that drive gene expression. Yet, there are 10-100× more binding sites than differentially expressed genes. It is unclear how or if these excess binding sites impact gene transcription.Results
To characterize the regulatory logic of AR-mediated transcription, we generated a locus-specific map of enhancer activity by functionally testing all common clinical AR binding sites with Self-Transcribing Active Regulatory Regions sequencing (STARRseq). Only 7% of AR binding sites displayed androgen-dependent enhancer activity. Instead, the vast majority of AR binding sites were either inactive or constitut"],"journal":["Genome biology"],"pagination":["149"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8112059"],"repository":["biostudies-literature"],"pubmed_title":["Functional mapping of androgen receptor enhancer activity."],"pmcid":["PMC8112059"],"pubmed_authors":["van der Poel H","Altintas UB","Hach F","Huang CF","Hoogstraat M","Stelloo S","Gleave ME","Bergman AM","Ozturan D","Hu E","Feng FY","Zwart W","Sar F","Lack NA","Collins C","Morova T","Le Bihan S","Lingadahalli S","Gokbayrak B","Yu IPL","Linder S","Saffarzadeh M","McConeghy B","Emberly E"],"additional_accession":[]},"is_claimable":false,"name":"Functional mapping of androgen receptor enhancer activity.","description":"Background
Androgen receptor (AR) is critical to the initiation, growth, and progression of prostate cancer. Once activated, the AR binds to cis-regulatory enhancer elements on DNA that drive gene expression. Yet, there are 10-100× more binding sites than differentially expressed genes. It is unclear how or if these excess binding sites impact gene transcription.Results
To characterize the regulatory logic of AR-mediated transcription, we generated a locus-specific map of enhancer activity by functionally testing all common clinical AR binding sites with Self-Transcribing Active Regulatory Regions sequencing (STARRseq). Only 7% of AR binding sites displayed androgen-dependent enhancer activity. Instead, the vast majority of AR binding sites were either inactive or constitut","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 May","modification":"2026-05-09T09:48:20.076Z","creation":"2025-04-03T21:33:41.185Z"},"accession":"S-EPMC8112059","cross_references":{"pubmed":["33975627"],"doi":["10.1186/s13059-021-02339-6"]}}