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Regulation of ERK1 gene expression by coactivator proteins

Beanca Y Chu1, Kim Tran, Tony K S Ku

  • 1Center for Craniofacial Molecular Biology, University of Southern California, 2250 Alcazar Street, Los Angeles, CA 90033, USA.

The Biochemical Journal
|July 30, 2005
PubMed

Insights

Retinoic acid receptors (RARs) regulate gene expression. This study reveals how coactivators CBP and PCAF control ERK1 expression, impacting cell proliferation and retinoic acid response.

Area of Science:

  • Molecular Biology
  • Gene Regulation
  • Cellular Signaling

Background:

  • Retinoic acid receptors (RARs) mediate retinoic acid (RA) effects on gene expression.
  • RA inhibits cellular proliferation partly by decreasing ERK1 expression.
  • The mechanism of RA-mediated ERK1 regulation is not well understood.

Purpose of the Study:

  • To characterize coactivator-mediated regulation of RA target gene expression.
  • To analyze ERK1 promoter activation by coactivators CBP and PCAF.
  • To elucidate the role of CBP and PCAF in RA's control of ERK1.

Main Methods:

  • Analysis of ERK1 promoter activity in stable cell clones.
  • Co-immunoprecipitation and yeast two-hybrid assays to study protein interactions.
  • Assessment of mRNA stability and protein levels.

Main Results:

  • CBP and PCAF differentially regulate ERK1 expression and cell proliferation.
  • CBP clones show higher ERK1, faster growth, and RA resistance; PCAF clones show lower ERK1 and slower growth.
  • RA treatment decreases CBP and PCAF binding to the ERK1 promoter, with PCAF affecting mRNA stability.

Conclusions:

  • CBP and PCAF coactivators play distinct roles in regulating ERK1 expression.
  • Regulation occurs at both transcriptional and post-transcriptional levels.
  • Understanding this mechanism provides insight into RA-mediated cellular processes.

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