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The p53 molecule is centrally important to the apoptosis pathway, and found in many cell pathways leading to apoptosis. As a tumour suppressor protein, its downstream compounds act to prevent apoptosis and cell death. This is significant in that is makes p35 a strong contender to prevent cancer, because it protects the genome by regulating the cell cycles.
It is called p53, because it is a protein with a mass of 53kDa. It is made up of 7 domains, each comprising of many amino acids – it is these domains that form the sites for interaction with interacting molecules. One of the most well documented p53 interactions is with MDM2 – the interaction negatively regulates p53 by destabilising it.
Potential p53 inhibitors are strong anti-cancer therapeutic targets, and MDM2 is a prime example. A number of MDM2 antagonists have already entered clinical trials, specifically small-molecule inhibitors. However, in some forms of cancer such as melanoma, p53 can actually be seen to promote proliferation, such are the complexities of molecular interactions! But p53 is being tested in animal models as a gene transfer therapy for pre-malignancies, and potentially forming a vaccine for boosting the immune system in ovarian cancer.
With its central role in regulating the cell cycle (through p21 protein) and being influenced by a range of compounds including ras, arf, p53 is of central importance. While it influences the cell cycles through so many mediating proteints such asp21, 14.3.3., fas, Bax and Puma, the impact of modulating the activity of p53 can be significant, making it a prime therapeutic target for oncologists.
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