Journal
EMBO JOURNAL
Volume 22, Issue 14, Pages 3686-3695Publisher
OXFORD UNIV PRESS
DOI: 10.1093/emboj/cdg364
Keywords
c-Jun transcription factor; HDAC; MAP kinase; phosphorylation; repression of transcription; signaling
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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.
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