Regulation of NF-κB by Cyclin-Dependent Kinases Associated with the p300 Coactivator
Autor: | David Beach, Neil D. Perkins, Jonathan C. Betts, Lisa K. Felzien, Kwanyee Leung, Gary J. Nabel |
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Rok vydání: | 1997 |
Předmět: |
Cyclin-Dependent Kinase Inhibitor p21
Transcriptional Activation Cyclin A Protein Serine-Threonine Kinases Biology Transfection Cell Line Jurkat Cells Genes Reporter Cyclin-dependent kinase Cyclins Coactivator CDC2-CDC28 Kinases Humans Phosphorylation Transcription factor Multidisciplinary RELA Cell Cycle Cyclin-Dependent Kinase 2 Cyclin-dependent kinase 2 NF-kappa B Transcription Factor RelA Nuclear Proteins Cell cycle Molecular biology Cyclin-Dependent Kinases Trans-Activators biology.protein Tetradecanoylphorbol Acetate Protein Kinases CDK inhibitor Signal Transduction Transcription Factors |
Zdroj: | Science. 275:523-527 |
ISSN: | 1095-9203 0036-8075 |
DOI: | 10.1126/science.275.5299.523 |
Popis: | The nuclear factor kappaB (NF-kappaB) transcription factor is responsive to specific cytokines and stress and is often activated in association with cell damage and growth arrest in eukaryotes. NF-kappaB is a heterodimeric protein, typically composed of 50- and 65-kilodalton subunits of the Rel family, of which RelA(p65) stimulates transcription of diverse genes. Specific cyclin-dependent kinases (CDKs) were found to regulate transcriptional activation by NF-kappaB through interactions with the coactivator p300. The transcriptional activation domain of RelA(p65) interacted with an amino-terminal region of p300 distinct from a carboxyl-terminal region of p300 required for binding to the cyclin E-Cdk2 complex. The CDK inhibitor p21 or a dominant negative Cdk2, which inhibited p300-associated cyclin E-Cdk2 activity, stimulated kappaB-dependent gene expression, which was also enhanced by expression of p300 in the presence of p21. The interaction of NF-kappaB and CDKs through the p300 and CBP coactivators provides a mechanism for the coordination of transcriptional activation with cell cycle progression. |
Databáze: | OpenAIRE |
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