1 Ocak 2021 Dergi makalesi Açık Erişim

Huang, Chia-Chi Flora; Lingadahalli, Shreyas; Morova, Tunc; Ozturan, Dogancan; Hu, Eugene; Yu, Ivan Pak Lok; Linder, Simon; Hoogstraat, Marlous; Stelloo, Suzan; Sar, Funda; van der Poel, Henk; Altintas, Umut Berkay; Saffarzadeh, Mohammadali; Le Bihan, Stephane; McConeghy, Brian; Gokbayrak, Bengul; Feng, Felix Y.; Gleave, Martin E.; Bergman, Andries M.; Collins, Colin; Collins, Colin

Dublin Core

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<oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
  <dc:creator>Huang, Chia-Chi Flora</dc:creator>
  <dc:creator>Lingadahalli, Shreyas</dc:creator>
  <dc:creator>Morova, Tunc</dc:creator>
  <dc:creator>Ozturan, Dogancan</dc:creator>
  <dc:creator>Hu, Eugene</dc:creator>
  <dc:creator>Yu, Ivan Pak Lok</dc:creator>
  <dc:creator>Linder, Simon</dc:creator>
  <dc:creator>Hoogstraat, Marlous</dc:creator>
  <dc:creator>Stelloo, Suzan</dc:creator>
  <dc:creator>Sar, Funda</dc:creator>
  <dc:creator>van der Poel, Henk</dc:creator>
  <dc:creator>Altintas, Umut Berkay</dc:creator>
  <dc:creator>Saffarzadeh, Mohammadali</dc:creator>
  <dc:creator>Le Bihan, Stephane</dc:creator>
  <dc:creator>McConeghy, Brian</dc:creator>
  <dc:creator>Gokbayrak, Bengul</dc:creator>
  <dc:creator>Feng, Felix Y.</dc:creator>
  <dc:creator>Gleave, Martin E.</dc:creator>
  <dc:creator>Bergman, Andries M.</dc:creator>
  <dc:creator>Collins, Colin</dc:creator>
  <dc:creator>Collins, Colin</dc:creator>
  <dc:date>2021-01-01</dc:date>
  <dc: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 10-100x 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 constitutively active enhancers. These annotations strongly correlated with enhancer-associated features of both in vitro cell lines and clinical prostate cancer samples. Evaluating the effect of each enhancer class on transcription, we found that AR-regulated enhancers frequently interact with promoters and form central chromosomal loops that are required for transcription. Somatic mutations of these critical AR-regulated enhancers often impact enhancer activity. Conclusions Using a functional map of AR enhancer activity, we demonstrated that AR-regulated enhancers act as a regulatory hub that increases interactions with other AR binding sites and gene promoters.</dc:description>
  <dc:identifier>https://aperta.ulakbim.gov.trrecord/234974</dc:identifier>
  <dc:identifier>oai:aperta.ulakbim.gov.tr:234974</dc:identifier>
  <dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
  <dc:rights>http://www.opendefinition.org/licenses/cc-by</dc:rights>
  <dc:source>GENOME BIOLOGY 22(1)</dc:source>
  <dc:title>Functional mapping of androgen receptor enhancer activity</dc:title>
  <dc:type>info:eu-repo/semantics/article</dc:type>
  <dc:type>publication-article</dc:type>
</oai_dc:dc>