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Tigar or how p53 controls glycolysis
Catalan researchers of the Institute for Biomedical Research of Bellvitge in Barcelona and the Beatson Institute for Cancer Research in Glasgow, published in Cell the discovery of Tigar, the first gene involved in the antioxidant cellular mechanism associated with the prevention of tumor formation. This paper shows that low concentrations of p53 protein are sufficient to activate the gene Tigar.
Researchers have found that this gene acts as a reducer of glycolysis. p53 is operated against cellular stress. When the damage caused by cell stress is relatively mild, the p53 protein activates the mechanism of cell cycle arrest, resulting in the repair of DNA damage. If the damage is substantial or irreparable, p53 initiates the process of apoptosis.
One of the main agents that cause mutations in the DNA of cells are molecules called reactive oxygen species (ROS), which include the known free radicals. In case of mild cellular stress, p53 activates the gene Tigar, which decreases the rate of glycolysis and hence the presence of ROS in the cell. However, if cell stress is irreparable, it produces the opposite strategy and p53 induces a greater presence of ROS molecules to trigger apoptosis or cell death, preventing the proliferation of cells with altered DNA.
The authors have shown how, in the event of loss of Tigar, cells rapidly entered apoptosis with minimal stress. And propose a model of p53 function, whereby at first, after oxidative stress, this protein activated the antioxidant gene Tigar to gain control of ROS molecules and facilitate DNA repair before they increase the stress and will trigger a possible tumor proliferation.
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