6533b851fe1ef96bd12a9843
RESEARCH PRODUCT
Deregulated repression of c-Jun provides a potential link to its role in tumorigenesis.
Carsten WeissDirk Bohmannsubject
Mitogen-Activated Protein Kinase KinasesTranscriptional ActivationKinaseProtein subunitc-junCell CycleRepressorCell BiologyBiologyHDAC3Histone DeacetylasesMalignant transformationEnzyme ActivationRepressor ProteinsCell Transformation NeoplasticGenes junCancer researchras ProteinsPhosphorylationAnimalsHumansPhosphorylationMolecular BiologyTranscription factorDevelopmental Biologydescription
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.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2004-01-09 |