Researchers from Yale University have identified how the molecule DNA2 helps begin the complex process of repairing breaks in DNA that can cause chromosome rearrangements – abnormalities linked to cancer.
Biochemical analysis by James Daley, Adam Miller, and colleagues in the lab of Patrick Sung, professor of molecular biophysics and biochemistry and of therapeutic radiology, identifies a novel role for this enzyme. It shows that DNA2 travels down a single-stranded DNA tail, and then cuts the damaged DNA when it reaches a double-stranded region, an important early step in repair. Daley notes that DNA2 is a potential target for cancer therapeutics because it is overexpressed in many tumors and promotes their proliferation.
The research was published March 23 in the journal Genes and Development.
Publication: Adam S. Miller, et al., “A novel role of the Dna2 translocase function in DNA break resection,” Genes & Dev., 2017; doi:10.1101/gad.295659.116
Source: Bill Hathaway, Yale University
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