ROCHESTER, Minn. — Damage to DNA is a daily occurrence but one that human cells have evolved to manage. Now, in a new paper published in Nature Structural & Molecular Biology, Mayo researchers have determined how one DNA repair protein gets to the site of DNA damage. The authors say they hope this discovery research will help identify new therapies for ovarian cancer.
While the human genome is constantly damaged, cells have proteins that detect and repair the damage. One of those proteins is called 53BP1. It is involved in the repair of DNA when both strands break. In the publication, Georges Mer, Ph.D., a Mayo Clinic structural biologist, and his team report on how 53BP1 relocates to chromosomes to do its job.
Dr. Mer explains that, in the absence of DNA damage, 53BP1 is inactive — blocked by a protein called “TIRR.” Using a visualization technique called X-ray crystallography, the authors show that TIRR obstructs an area on 53BP1 that 53BP1 uses to bind chromosomes. But what shifts TIRR away from 53BP1, so the repair protein can work?
The authors theorized that a type of nucleic acid called RNA was responsible for this shift. To test their theory,
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