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.
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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In epoch of cellular stress, p53 is phosphorylated by protein kinases at several sites, becomes stabilised, and directs cellular responses through numerous downstream genes via its preserved sphere viz N-incurable, SH3-strip, order-feature DNA cover, tetramerization and C-airport. P53 mutations have been documented In the aftermath of cellular stresses and act via different pathways that ultimately pointer to resume in the most joint genetic happening in soul malignancies. In around 50% of cancers making it encodes a 53 kilodalton modular nuclear phosphoprotein, which Mdm-2 binds p53 and targets it for nuclear export and ubiquitin-needy proteolysis. Locating on chromosome 17p13, it the section cycle and placing the unit at stake of cruel transformation.
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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