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Related Experiment Videos

Oestrogen receptor function at classical and alternative response elements.

P J Kushner1, D Agard, W J Feng

  • 1Metabolic Research Unit, University of California, San Francisco 94143-0540, USA.

Novartis Foundation Symposium
|August 31, 2000
PubMed
Summary
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Oestrogen receptor (ER) structural changes dictate coactivator binding, influencing gene transcription. ER can also activate transcription at alternative sites by interacting with Jun/Fos-bound coactivators.

Area of Science:

  • Molecular Biology
  • Structural Biology
  • Genetics

Background:

  • Oestrogen receptor (ER) regulates gene transcription by binding to oestrogen response elements (EREs) and recruiting coactivators.
  • ER activity is modulated by ligands, including oestrogens and anti-oestrogens, affecting its interaction with coactivator proteins.

Purpose of the Study:

  • To elucidate the structural mechanisms by which oestrogen and anti-oestrogen ligands control ER coactivator recruitment.
  • To investigate the role of ER in transcriptional activation at alternative response elements, such as AP-1 sites.

Main Methods:

  • Structural studies of the oestrogen receptor.
  • Analysis of ER interactions with coactivators like CBP and GRIP1.
  • Investigation of ER-mediated transcription at classical EREs and alternative AP-1 sites.

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Main Results:

  • Oestrogen binding creates a hydrophobic cleft on ER for coactivator docking.
  • Anti-oestrogens occlude this site, blocking coactivator access and inhibiting transcription.
  • ER can activate transcription at AP-1 sites by bridging Jun/Fos proteins to coactivators (CBP, GRIP1).

Conclusions:

  • Ligand-dependent structural changes in ER are critical for coactivator recruitment and transcriptional regulation.
  • ER plays a dual role in transcription: direct activation at EREs and indirect activation at AP-1 sites via coactivator complex formation.