Doing the right thing: feedback control and p53.
Recent evidence suggests that exposure of cells to DNA-damaging agents causes a rise in the levels of the p53 tumor suppressor protein and arrest of progression through the cell cycle. p53 may therefore resemble a member of the RAD gene class identified in yeast, RAD9, which allows cells to repair DNA before continuation of the cell cycle. The evidence that p53 is a sequence-specific, DNA-binding protein that can regulate transcription suggests several ways in which p53 might effect this growth cessation.
Prives
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Department of Biological Sciences, Columbia University, New York, New York 10027.
D004260:DNA Repair; D004261:DNA Replication / Q000187:drug effects; D004268:DNA-Binding Proteins; D005246:Feedback; D006801:Humans; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000502:physiology*
D004268:DNA-Binding Proteins; D016159:Tumor Suppressor Protein p53