JNK phosphorylation relieves HDAC3-dependent suppression of the transcriptional activity of c-Jun
Open Access
- 15 July 2003
- journal article
- research article
- Published by Springer Science and Business Media LLC in The EMBO Journal
- Vol. 22 (14), 3686-3695
- https://doi.org/10.1093/emboj/cdg364
Abstract
The AP‐1 transcription factor c‐Jun is a prototypical nuclear effector of the JNK signal transduction pathway. The integrity of JNK phosphorylation sites at serines 63/73 and at threonines 91/93 in c‐Jun is essential for signal‐dependent target gene activation. We show that c‐Jun phosphorylation mediates dissociation of an inhibitory complex, which is associated with histone deacetylase 3 (HDAC3). The subsequent events that ultimately cause increased mRNA synthesis are independent of c‐Jun phosphorylation and its interaction with JNK. These findings provide an ‘activation by de‐repression’ model as an explanation for the stimulatory function of JNK on c‐Jun.Keywords
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