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ArticleVolume 45, Issue 7117664Open access Affiliations & Notes 1Division of Biological Sciences, University of California, La Jolla, San Diego, CA, USA 2Department of Pediatrics, University of California, San Diego, San Diego School of Medicine, La Jolla, San Diego, CA, USA 3Infectious Disease and Microbiome Program, The Broad Institute, Cambridge, MA, USA 4Department of Immunology and Infectious Diseases, Harvard T.H. Chan School of Public Health, Boston, MA, USA 5Department of Microbiology...
Abstract Human gene expression is controlled from distance via enhancers, which can form longer "super-enhancer"-regions of intense regulatory activity. Whether super-enhancers constitute a separate regulatory paradigm remains unclear, largely due to the difficulty of dissecting the contributions and interactions of individual elements within their natural chromosomal context.
Abstract Mutagenic outcomes of CRISPR/Cas9-generated double-stranded breaks depend on both the sequence flanking the cut and cellular DNA damage repair. The interaction of these features has been largely unexplored, limiting our ability to understand and manipulate the outcomes. Here, we measured how the absence of 18 repair genes changed frequencies of 83,680 unique mutational outcomes generated by Cas9 double-stranded breaks at 2,838 synthetic target sequences in mouse embryonic stem cells.
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