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UV rays and DNA damage: how to stop them



A study by the University of Milan has identified a family of proteins that helps repair DNA without accumulating chromosomal changes.


by Cristina Da Rold

It is well known that the ultraviolet rays that we expose ourselves to, for example, when we take the sun without adequate protection, damage our DNA. Fortunately, the body is almost always able to quickly repair this damage and transform the damage into a potential tumor. The problem is ̵

1; that we are not always so happy. Sometimes the body is unable to repair these "lesions" in the double helix, which can cause changes in the structure of the chromosomes and can lead to the onset of tumors or cell death.

Understanding why sometimes the repair mechanism does not work and that What went on for long was at the center of biomedical research, and today a study by the University of Milan has for the first time managed to identify a family of proteins involved in DNA repair Helps to accumulate without chromosomal changes and thus prevent cell death and dangerous genomic instability. The research was published in the journal Molecular Cell .

"The first important step was to understand why some body injuries were repaired while others were not – explains OggiScienza Marco Muzi Falconi, among the authors of the study – and we found that the Automatic repair does not happen if we have two lesions close to each other, each on one of the two DNA strands.Usually, the injuries are not so close, but this situation can occur with UV rays, or if the body is chemically drugged The researchers have investigated how the organism interacts with these lesions and how it interacts with these lesions ", said Muzi Falconi

trying in vain to repair them, using at the base a specific protein, EXO1, which begins to destroy the chromosome, and another protein family. How much did the first one decompose? disturbs? In fact, this degradation activity has a positive aspect: it warns the cell of the problem and initiates the repair of DNA damage. On the other hand, when EXO1 is undisturbed, it degrades the DNA uncontrollably and leads to the breakdown of chromosomes.

"We have been able to identify a family of proteins, the DNA polymerase transsection, by limiting the activity of EXO1 allows the cells to repair the lesions without causing chromosome breaks and thus cell death and genomic instability prevent, "explains Muzi Falconi. "We have clearly defined which mechanism predisposes the tumor, and now it will be a question of testing some molecules to understand how to inhibit this process once you discover that this molecule is capable of controlling the effects of these two proteins The goal is to use them in combination with classical therapeutic approaches such as chemotherapy to develop more effective cancer therapies. "

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