Bcl-2 relieves the trans-repressive function of the glucocorticoid receptor and inhibits the activation of CPP32-like cysteine proteases

Biochemical and Biophysical Research Communications
T MiyashitaM Yamada

Abstract

Glucocorticoid induces apoptosis in immature lymphocytes which is inhibitable by Bcl-2. Although glucocorticoid-mediated signal transduction is well understood, the mechanism of the induction of apoptosis by the activated glucocorticoid receptor as well as the inhibition of apoptosis by Bcl-2 remains enigmatic. Here we report that overexpressed Bcl-2 relieves the glucocorticoid receptor-mediated repressive function on the AP-1 activity and completely inhibits the activation of CPP32-like cysteine proteases. In contrast, glucocorticoid receptor-mediated transactivation was not affected by Bcl-2. This suggests that glucocorticoid may induce apoptosis by repressing transactivation by AP-1 which is relieved by Bcl-2. Furthermore, we report evidence that, in contrast with CPP32-like proteases, ICE-like proteases are not involved in this apoptotic pathway.

References

Mar 25, 1989·Nucleic Acids Research·G R MacGregor, C T Caskey
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Nov 3, 1995·The Journal of Biological Chemistry·T MiyashitaJ C Reed
Jun 21, 1994·Proceedings of the National Academy of Sciences of the United States of America·J J RyanM F Clarke
Sep 13, 1994·Proceedings of the National Academy of Sciences of the United States of America·Y Shen, T Shenk

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Citations

Nov 20, 1997·The Journal of Biological Chemistry·T MiyashitaM Yamada
Jun 11, 1998·The Journal of Biological Chemistry·M KullmannA C Cato
Apr 20, 1999·Biochemical and Biophysical Research Communications·T MiyashitaM Yamada
Sep 3, 1998·European Journal of Pharmacology·T NittohK Ohuchi
Oct 16, 1999·Brain Research. Molecular Brain Research·C Bossenmeyer-PouriéJ L Daval

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