Abstract
New work by Bruno et al. (2006) describes a mechanistic switch of the proliferation-promoting Che-1 activator of E2F-target genes into a cell-cycle inhibitor in response to DNA damage, through Che-1 relocalization to, and activation of, the p53 tumor suppressor gene.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Apoptosis Regulatory Proteins / metabolism*
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Carrier Proteins / metabolism*
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Cyclin-Dependent Kinase Inhibitor p21 / metabolism
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DNA Damage*
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Humans
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Models, Biological
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Phosphoproteins / metabolism*
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Promoter Regions, Genetic*
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Repressor Proteins / metabolism*
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Signal Transduction
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Transcription Factors / metabolism*
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Tumor Suppressor Protein p53 / genetics*
Substances
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AATF protein, human
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Apoptosis Regulatory Proteins
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CDKN1A protein, human
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Carrier Proteins
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Cyclin-Dependent Kinase Inhibitor p21
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Phosphoproteins
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RNA polymerase II-binding proteins
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Repressor Proteins
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Transcription Factors
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Tumor Suppressor Protein p53