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Related Experiment Videos

RelB forms transcriptionally inactive complexes with RelA/p65.

Ralf Marienfeld1, Michael J May, Ingolf Berberich

  • 1Section of Immunobiology and Department of Molecular Biophysics and Biochemistry, Yale University Medical School, New Haven, Connecticut 06520, USA. rmarienfeld@hotmail.com

The Journal of Biological Chemistry
|March 27, 2003
PubMed
Summary
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RelB acts as a repressor by forming inactive RelA-RelB dimers that cannot bind DNA. This mechanism explains how RelB inhibits NF-kappaB-dependent gene expression.

Area of Science:

  • Molecular Biology
  • Cellular Signaling
  • Transcription Factor Regulation

Background:

  • RelB is a unique NF-kappaB family member with dual activator/repressor roles.
  • The mechanisms underlying RelB's repressive function on NF-kappaB are not fully understood.

Purpose of the Study:

  • To elucidate the molecular mechanisms by which RelB represses NF-kappaB-dependent gene expression.
  • To investigate the formation and function of RelA-RelB heterodimers.

Main Methods:

  • Reporter gene assays to assess transcriptional activity.
  • Electrophoretic mobility shift assays (EMSA) to evaluate DNA binding.
  • Analysis of RelA.RelB heterodimer formation and localization in murine embryonic fibroblasts.

Main Results:

Related Experiment Videos

  • RelB represses NF-kappaB activity at the level of RelA.
  • RelB inhibits the DNA binding of RelA through the formation of transcriptionally inactive RelA.RelB heterodimers.
  • These heterodimers are not regulated by IkappaB proteins and are found in both cytoplasm and nucleus.

Conclusions:

  • Sequestration of RelA within inactive RelA.RelB complexes is a key mechanism for RelB-mediated repression of NF-kappaB.
  • This finding provides a molecular basis for RelB's inhibitory role in NF-kappaB signaling pathways.