BRCA2, a key tumor suppressor that helps repair and protect DNA during replication, is often mutated in cancer cells. Normally, BRCA2 interacts with another protein, RAD51, to suppress genomic instability by fixing damage at DNA breaks or by protecting DNA at stalled replication forks, which can occur during DNA replication. By examining the protein structure of a specific region of BRCA2, known as the C-terminal end, researchers led by Katharina Schlacher, Ph.D., and John Tainer, Ph.D., uncovered a...










