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Contact: Karen Kreeger
karen.kreeger@uphs.upenn.edu
215-349-5658
University of Pennsylvania School of Medicine

Changes to DNA On-Off Switches

Caption: This is a model showing that TIP60/NuA4-dependent acetylation limits 53BP1 binding to histone H4 when present on the same histone H4 tail with the mark H4K20Me2, a recognition mark for 53BP1. A TIP60 deficiency would result in reduced H4 acetylation, and increased 53BP1 binding, thus blocking BRCA1 function at DNA double-strand breaks.

Credit: Roger A. Greenberg, M.D., Ph.D., Perelman School of Medicine, University of Pennsylvania

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Related news release: Changes to DNA on-off switches affect cells' ability to repair breaks, respond to chemotherapy


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