Nuclear retinoid receptors and the transcription of retinoid-target genes

Gene. 2004 Mar 17;328:1-16. doi: 10.1016/j.gene.2003.12.005.

Abstract

The pleiotropic effects of retinoids are mediated by nuclear retinoid receptors (RARs and RXRs) which are ligand-activated transcription factors. In response to retinoid binding, RAR/RXR heterodimers undergo major conformational changes and orchestrate the transcription of specific gene networks, through binding to specific DNA response elements and recruiting cofactor complexes that act to modify local chromatin structure and/or engage the basal transcription machinery. Then the degradation of RARs and RXRs by the ubiquitin-proteasome controls the magnitude and the duration of the retinoid response. RARs and RXRs also integrate a variety of signaling pathways through phosphorylation events which cooperate with the ligand for the control of retinoid-target genes transcription. These different modes of regulation reveal unexpected levels of complexity in the dynamics of retinoid-dependent transcription.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Base Sequence
  • Binding Sites / genetics
  • Cysteine Endopeptidases / metabolism
  • Gene Expression Regulation
  • Humans
  • Models, Genetic
  • Multienzyme Complexes / metabolism
  • Phosphorylation
  • Proteasome Endopeptidase Complex
  • Receptors, Retinoic Acid / metabolism*
  • Retinoids / pharmacology*
  • Transcription, Genetic / drug effects*
  • Transcription, Genetic / genetics
  • Ubiquitin / metabolism

Substances

  • Multienzyme Complexes
  • Receptors, Retinoic Acid
  • Retinoids
  • Ubiquitin
  • Cysteine Endopeptidases
  • Proteasome Endopeptidase Complex