<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>22(1)</volume><submitter>Huang CF</submitter><funding>Canadian Network for Research and Innovation in Machining Technology, Natural Sciences and Engineering Research Council of Canada</funding><funding>Türkiye Bilimsel ve Teknolojik Araştirma Kurumu</funding><funding>KWF Kankerbestrijding</funding><pubmed_abstract>&lt;h4>Background&lt;/h4>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.&lt;h4>Results&lt;/h4>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</pubmed_abstract><journal>Genome biology</journal><pagination>149</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8112059</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Functional mapping of androgen receptor enhancer activity.</pubmed_title><pmcid>PMC8112059</pmcid><pubmed_authors>van der Poel H</pubmed_authors><pubmed_authors>Altintas UB</pubmed_authors><pubmed_authors>Hach F</pubmed_authors><pubmed_authors>Huang CF</pubmed_authors><pubmed_authors>Hoogstraat M</pubmed_authors><pubmed_authors>Stelloo S</pubmed_authors><pubmed_authors>Gleave ME</pubmed_authors><pubmed_authors>Bergman AM</pubmed_authors><pubmed_authors>Ozturan D</pubmed_authors><pubmed_authors>Hu E</pubmed_authors><pubmed_authors>Feng FY</pubmed_authors><pubmed_authors>Zwart W</pubmed_authors><pubmed_authors>Sar F</pubmed_authors><pubmed_authors>Lack NA</pubmed_authors><pubmed_authors>Collins C</pubmed_authors><pubmed_authors>Morova T</pubmed_authors><pubmed_authors>Le Bihan S</pubmed_authors><pubmed_authors>Lingadahalli S</pubmed_authors><pubmed_authors>Gokbayrak B</pubmed_authors><pubmed_authors>Yu IPL</pubmed_authors><pubmed_authors>Linder S</pubmed_authors><pubmed_authors>Saffarzadeh M</pubmed_authors><pubmed_authors>McConeghy B</pubmed_authors><pubmed_authors>Emberly E</pubmed_authors></additional><is_claimable>false</is_claimable><name>Functional mapping of androgen receptor enhancer activity.</name><description>&lt;h4>Background&lt;/h4>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.&lt;h4>Results&lt;/h4>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</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 May</publication><modification>2026-05-09T09:48:20.076Z</modification><creation>2025-04-03T21:33:41.185Z</creation></dates><accession>S-EPMC8112059</accession><cross_references><pubmed>33975627</pubmed><doi>10.1186/s13059-021-02339-6</doi></cross_references></HashMap>