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| Author: Aaron Hall |
The p53 gene, found on chromosome 17, is a tumor-suppressor gene. In the cell, the p53 protein binds DNA at specific locations and stimulates another gene to produce a protein called p21. In turn, p21 suppresses a division-stimulating protein (cdk2) to prevent the cell from passing through to the next stage of cell division. When p53 is mutant and can no longer bind DNA effectively, the p21 protein is not available to act as the 'stop signal' for cell division. Thus cells may divide uncontrollably and form tumors. The p53 gene plays a key role in the pathogenesis or etiology of human cancers and clearly is an important component in a network of events that culminate in tumor formation. Mutations in p53 are found in most tumor types.
Some articles on p53 appear in the May 18, 2001, issue of European Journal of Biochemistry 268 (10). The journal contains several minireviews commissioned and organized by Ettore Appella (NIH National Cancer Institute) and Carl Anderson (Brookhaven National Laboratory). The articles are as follows:
* 'Modulation of p53 Function in Cellular Regulation,' introduction by Appella.
* 'Post-Translational Modifications and Activation of p53 by Genotoxic Stresses,' by Appella and Anderson.
* 'Regulation of p53 Localization,' by Shun-Hsin Liang (Pennsylvania State University) and Michael Clarke (University of Michigan Medical Center).
* 'P300/CBP/p53 Interaction and Regulation of the p53 Response,' by Steven Grossman (Brigham and Women's Hospital and Harvard Medical School).
* 'Regulation of Cellular Senescence by 53,' by Koji Itahan, Goberdhan Dimri, and Judith Campisi (all at Lawrence Berkeley National Laboratory). |
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