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Chemical Senses 20: 251-255,
© 1995

research-article

The Glucocorticoid Receptor Synergizes with Jun Homodimers to Activate AP-1-regulated Promoters Lacking GR Binding Sites

Sibylle Teurich and Peter Angel

Forschungszentrum Karlsruhe, Institut für Genetik Postfach 3640, 76021 Karlsruhe, Germany

Correspondence to be sent to: P. Angel, Forschungszentrum Karlsruhe, Institut für Genetik, Postfach 3640, 76021 Karlsruhe, Germany

Jun/Fos (AP-1) and steroid hormone receptors (SHR) are distinct families of transcription factors that convert extracellular signals into long-term genetic responses. Despite clear differences in their modes of activation and DNA binding specificities, a regulatory cross-talk between AP-1 and SHR such as the glucocorticoid receptor (GR), has been established. Here, we show that the hormone-activated GR negatively or positively modulates the expression of AP-1-dependent genes, depending on the subunits of the dimeric AP-1 complex. This type of regulation does not depend on the presence of a GR binding site in the promoter and is mediated through the DNA binding domain of Jun. Since individual subunits of AP-1 exhibit small differences in sequence specificity, specific subsets of AP-1-dependent genes may be regulated by steroid hormones in different directions.


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