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- W2155602479 startingPage "2185" @default.
- W2155602479 abstract "The product of the human p53 tumor suppressor gene is a 393 amino acid polypeptide that functions primarily as a homotetrameric transcription factor. p53 regulates the expression of genes that control cell cycle progression, the induction of apoptosis or senescence, DNA repair, and other functions that involve cellular responses to stress. Approximately 50 percent of all tumors harbor a p53 mutation, and loss of p53 function, either directly through mutation or indirectly through several mechanisms, plays a central role in the development of cancer. The p53 protein has been highly conserved during evolution, and orthologs have been found in the sequenced genomes of most multi-cellular organisms from the animal kingdom including zebrafish, Drosophila, and Caenorhabditis elegans , but not in unicellular yeasts. The p53 protein normally is short lived and is present at low levels in unstressed mammalian cells; however, in response to both genotoxic and non-genotoxic stresses it accumulates in the nucleus where it binds to specific DNA sequences. A fundamental question that remains only partially answered is what mechanism(s) contribute to the ability of different cells to interpret p53 activation in different ways. The activation of p53 by hypoxia or oncogenes clearly induces different effects than do responses to genotoxic stresses. p53 protein forms complexes with many other cellular components and with particular nuclear structures. This characteristic may influence the degree of p53 activation and contribute to the heterogeneity of p53 dependent responses observed within a specific tissue." @default.
- W2155602479 created "2016-06-24" @default.
- W2155602479 creator A5022226465 @default.
- W2155602479 creator A5036354240 @default.
- W2155602479 date "2010-01-01" @default.
- W2155602479 modified "2023-09-25" @default.
- W2155602479 title "Signaling to the p53 Tumor Suppressor through Pathways Activated by Genotoxic and Non-Genotoxic Stresses" @default.
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