RU486-induced glucocorticoid receptor agonism is controlled by the receptor N terminus and by corepressor binding

J Biol Chem. 2002 Jul 19;277(29):26238-43. doi: 10.1074/jbc.M203268200. Epub 2002 May 13.

Abstract

Glucocorticoid-induced gene transcription has been shown to be mediated by coactivators bound to the glucocorticoid receptor (GR). The glucocorticoid antagonist RU486 interferes with the steroid-mediated activation and can also exhibit partial agonist activity, a response in which corepressors have been implicated. Here we have shown that deletion of the N terminus of GR totally abolishes the agonist activity of RU486. Furthermore, we have demonstrated that corepressors bind directly to the RU486-bound GR as determined by glutathione S-transferase pull-down, mammalian two-hybrid assay, and coimmunoprecipitation. Fine mapping of the interaction regions within GR and the corepressor NCoR reveals a complex interaction profile that involves a number of domains in each protein. Notably, the N and the C termini of GR are both involved in corepressor binding. Thus, the N terminus of GR is a major determinant for RU486-dependent NCoR interaction as well as for RU486-mediated agonist activity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cells, Cultured
  • Dexamethasone / metabolism
  • Glutathione Transferase / metabolism
  • Hormone Antagonists / pharmacology*
  • Humans
  • Mifepristone / pharmacology*
  • Nuclear Proteins / metabolism
  • Nuclear Receptor Co-Repressor 1
  • Protein Binding
  • Protein Conformation
  • Receptors, Glucocorticoid / agonists*
  • Repressor Proteins / metabolism
  • Structure-Activity Relationship
  • Transfection

Substances

  • Hormone Antagonists
  • NCOR1 protein, human
  • Nuclear Proteins
  • Nuclear Receptor Co-Repressor 1
  • Receptors, Glucocorticoid
  • Repressor Proteins
  • Mifepristone
  • Dexamethasone
  • Glutathione Transferase