Gene instability often begins with damaged DNA. "Unrepaired DNA strands, particularly DNA double strand breaks, are highly toxic to cells,” says Chunying Du (image left, courtesy UC), PhD, of the UC Department of Cancer Biology. “If left unrepaired, DNA double strand breaks often result in gene mutations which enhance malignant cell growth and tumor development,” she elaborates in a UC press release.
Du and her team worked to find ways to repair broken DNA and discovered their answer in a dynamic duo of proteins.
"In this study, we found a previously unknown function for an apoptotic inhibitor protein called BRUCE—apoptotic inhibitors hinder cell death—and a deubiquitinase called USP8, which controls a number of other metabolic functions in our body. They work together to promote DNA damage repair and prevent genetic instability.”
It turns out that while BRUCE and USP8 don’t actually repair DNA themselves, together they pave the way for another protein, BRIT1, to enter the scene and fix broken strands. BRIT1 is held back by ubiquitin protein chains, and BRUCE and USP8 together remove these chains to unleash the true potential of BRIT1.
(Proteins repair a broken strand of DNA. Image courtesy Wikimedia Commons and Biomedical Beat)
Du hypothesizes that mutations in BRUCE and USP8 lead to diseases associated with genetic instability. She also foresees treatment that focuses on breaking these ubiquitin chains in order to let the body fix more of its DNA immediately.
Funding for this study came from grants from the NSF and NIH. If funding information for the research at UC interests you, consider reading our free University of Cincinnati Funding Stats and Vendor Show Info report, accessible here:
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