Contact: Rita Sullivan King
Rockefeller University Press
Caption: A JCB study determined how BRCA1-deficient cells protect themselves from genomic instability. The cells can accumulate fused and broken chromosomes (see image) because they canít use homologous recombination to repair their DNA. But the cells can resume proliferation by cranking up their output of cathepsin L, which destroys 53BP1, a protein that prods the cells to use alternative, sloppier repair mechanisms.
Credit: Susana Gonzalo
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