Deregulated repression of c-Jun provides a potential link to its role in tumorigenesis

The transcription factor c-Jun cooperates with oncogenic alleles of ras in malignant transformation. Constitutively active Ras causes, via activation of mitogen activated protein kinases, phosphorylation of c-Jun which is essential for subsequent target gene activation and tumorigenesis. Studying th...

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Bibliographic Details
Published in:Cell cycle (Georgetown, Tex.) Tex.), 2004-02, Vol.3 (2), p.111
Main Authors: Weiss, Carsten, Bohmann, Dirk
Format: Article
Language:English
Subjects:
Animals
Cell Cycle
Cell Transformation, Neoplastic - metabolism
Enzyme Activation - physiology
Genes, jun - physiology
Histone Deacetylases - metabolism
Humans
Mitogen-Activated Protein Kinase Kinases - metabolism
Phosphorylation
ras Proteins - metabolism
Repressor Proteins - metabolism
Transcriptional Activation - genetics
Transcriptional Activation - physiology
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Summary:The transcription factor c-Jun cooperates with oncogenic alleles of ras in malignant transformation. Constitutively active Ras causes, via activation of mitogen activated protein kinases, phosphorylation of c-Jun which is essential for subsequent target gene activation and tumorigenesis. Studying the mechanisms controlling c-Jun activity we found that its transcription activation function is actively repressed by a presumably multimeric repressor complex that includes histone deacetylase 3 as a critical subunit. Suppression of c-Jun is relieved by MAP kinase-mediated phosphorylation and/or titration of inhibitor components. The viral tumorigenic counterpart of c-Jun, v-Jun, escapes this inhibition, suggesting deregulated transcriptional activity of c-Jun as a relevant cause for carcinogenesis.
ISSN:1538-4101