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Related Experiment Videos

A second pathway for modulating glucocorticoid receptor transactivation properties.

Shiyou Chen1, S Stoney Simons

  • 1Steroid Hormones Section, NIDDK/LMCB, National Institutes of Health (NIH), Building 8, Room B2A-07, Bethesda, MD 20892, USA.

Molecular and Cellular Endocrinology
|February 13, 2003
PubMed
Summary
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Glucocorticoid receptor (GR) activity is modulated by a new pathway involving hSur2, a Mediator complex component. This discovery reveals additional cellular mechanisms for controlling gene expression by glucocorticoid hormones.

Area of Science:

  • Molecular Biology
  • Cellular Signaling

Background:

  • Glucocorticoid receptors (GRs) regulate gene expression through dose-response curves and partial agonist activity.
  • Previously identified modulators act at a common rate-limiting step affecting GR activity.

Purpose of the Study:

  • To investigate the mechanism by which the C-terminal fragment of E1A-13S (E1A-133C) modulates GR properties.
  • To identify the cellular factors involved in E1A-133C-mediated GR modulation.

Main Methods:

  • Assessing the impact of saturating GR levels and inhibitors on E1A-133C activity.
  • Investigating the binding interaction between hSur2 and E1A-133C.
  • Analyzing the effect of hSur2 on GR transactivation properties.
  • Utilizing the H160Y mutation to assess the role of hSur2 binding in E1A-133C activity.

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Main Results:

  • E1A-133C modulates GR properties via a distinct pathway downstream of the common rate-limiting step.
  • hSur2 binds to E1A-133C and modulates GR transactivation.
  • hSur2's activity on GR is observed even at saturating GR concentrations.
  • The H160Y mutation, disrupting hSur2 binding, significantly reduces E1A-133C's activity.

Conclusions:

  • E1A-133C's modulatory effects on GR are largely attributed to the recruitment of hSur2, a Mediator complex component.
  • These findings support a novel pathway for modulating GR transactivation.
  • This expands the understanding of cellular mechanisms controlling gene expression by glucocorticoid hormones.