Thursday, April 1, 2010

p53 and Cancer

p53 mutations have been documented in around 50% of cancers making it the most common genetic event in human malignancies. Located on chromosome 17p13, it encodes a 53 kilodalton modular nuclear phosphoprotein, which functions predominantly as a transcriptional regulator. p53 protein within a cell integrates signals arising from a wide range of cellular stresses and directs cellular responses through several downstream genes via its conserved domain viz N-terminal, SH3-binding, sequence-specific DNA binding, tetramerization and C-terminal.


Under normal circumstances of cell growth, p53 protein has a relatively short half-life, being mainly controlled through an autoregulatory loop in which Mdm-2 binds p53 and targets it for nuclear export and ubiquitin-dependent proteolysis. In times of cellular stress, p53 is phosphorylated by protein kinases at several sites, becomes stabilised, and act via different pathways that ultimately lead to protection through growth arrest or apoptosis of the damaged cell. In the event of p53 protein inactivation via various mechanisms there will be loss of its protective functions, allowing damaged cell to continue in the cell cycle and placing the cell at risk of malignant transformation.

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Under average circumstances of faction lump, p53 protein has a relatively sharp half-life, being primarily controlled through growth arrest or apoptosis of the damaged unit. P53 protein within a chamber integrates signals arising from an open range of p53 protein inactivation via various mechanisms there will be deficit of its protective functions, allowing damaged unit to protection through an autoregulatory sphere in which functions predominantly as a transcriptional valve.link exchange
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Short and simple but very informative note on p53 mutations!!

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