Stress pathway activation induces phosphorylation of retinoid X receptor

J Biol Chem. 2000 Oct 13;275(41):32193-9. doi: 10.1074/jbc.M005490200.

Abstract

Cellular stresses inhibit retinoid signaling, but the molecular basis for this phenomenon has not been revealed. Here, we present evidence that retinoid X receptor (RXR) is a substrate for both mitogen-activated protein kinase kinase-4 (MKK4/SEK1) and its downstream mediator c-Jun N-terminal kinase (JNK). MKK4/SEK1 and JNK recognized distinct features on RXR in the DE and AB regions, respectively. Phosphorylation by MKK4/SEK1 had profound effects on the biochemical properties of RXR, inhibiting the expression of genes activated by RXR-retinoic acid receptor complexes. Tyr-249 in the RXR DE region was required for the inhibitory effect of MKK4/SEK1. These effects were significantly reduced in MKK4/SEK1-null cells, indicating that MKK4/SEK1 is required for the suppression of retinoid signaling by stress. Findings presented here demonstrate that MKK4/SEK1 can directly modulate transcription by phosphorylating RXR, a novel MKK4/SEK1 substrate.

Publication types

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

MeSH terms

  • Animals
  • COS Cells
  • Enzyme Activation
  • Gene Deletion
  • Gene Expression Regulation* / drug effects
  • Genes, Reporter / genetics
  • JNK Mitogen-Activated Protein Kinases
  • Laminin / genetics
  • Ligands
  • MAP Kinase Kinase 4*
  • Mice
  • Mitogen-Activated Protein Kinase 8
  • Mitogen-Activated Protein Kinase 9
  • Mitogen-Activated Protein Kinase Kinases / genetics
  • Mitogen-Activated Protein Kinase Kinases / metabolism*
  • Mitogen-Activated Protein Kinases / genetics
  • Mitogen-Activated Protein Kinases / metabolism*
  • Mutagenesis, Site-Directed
  • Phosphorylation
  • Receptors, Retinoic Acid / chemistry
  • Receptors, Retinoic Acid / genetics
  • Receptors, Retinoic Acid / metabolism*
  • Retinoid X Receptors
  • Signal Transduction / drug effects
  • Transcription Factors / chemistry
  • Transcription Factors / genetics
  • Transcription Factors / metabolism*
  • Transfection
  • Tretinoin / antagonists & inhibitors
  • Tretinoin / pharmacology
  • Tyrosine / genetics
  • Tyrosine / metabolism

Substances

  • Laminin
  • Ligands
  • Receptors, Retinoic Acid
  • Retinoid X Receptors
  • Transcription Factors
  • Tyrosine
  • Tretinoin
  • Mitogen-Activated Protein Kinase 9
  • JNK Mitogen-Activated Protein Kinases
  • Mitogen-Activated Protein Kinase 8
  • Mitogen-Activated Protein Kinases
  • MAP Kinase Kinase 4
  • Map2k4 protein, mouse
  • Mitogen-Activated Protein Kinase Kinases