Estradiol (E2)- and tamoxifen (Tmx)-bound ER-alpha (ERα) interact differentially with histone deacetylases 1 and 3 (HDACs 1 and 3)

Dharmendra Sharma, Yuan Liu, Rosalie Maire Uht

Research output: Contribution to journalArticle

Abstract

Although ERα activation properties have been intensively studied, this is not the case for their repressive properties. In this report, the ERα ligand binding domain (LBD) is shown to interact both with a deacetylase function and with HDAC1 and HDAC3. Ligands do not affect binding to the deacetylase activity or to HDAC1. In distinction, E2 reduced LBD binding to HDAC3, whereas Tmx had no effect. Knock-down of either HDAC1 or 3 led to increased transcriptional activity by both HDACs, presumably by decreased repression. In distinction, only HDAC3 knock-down led to increased activity in the presence of Tmx. In summary, ERα differentially interacts with HDACs 1 and 3 to regulate transcriptional activity.

Original languageEnglish
Pages (from-to)128-132
Number of pages5
JournalJournal of Steroid Biochemistry and Molecular Biology
Volume174
DOIs
Publication statusPublished - 1 Nov 2017

    Fingerprint

Keywords

  • Repression
  • Steroid receptor
  • Transcription

Cite this