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• W2912162884 abstract "Chronic hepatitis B is a severe liver disease caused by hepatitis B virus (HBV) infection. Covalently closed circular DNA (cccDNA), a super-spiralized, double-stranded form of the HBV genome, is the major determinant of viral persistence. CRISPR/Cas9 nucleases have been recently shown to introduce double-stranded DNA breaks into HBV cccDNA. The inflicted damage results predominantly in erroneous repair of cccDNA by non-homologous end-joining (NHEJ). NHEJ has been suggested to enhance anti-HBV activity of CRISPR/Cas9 and increase cccDNA mutation. In this study, we assessed anti-HBV activity of CRISPR/Cas9 and cccDNA repair outcomes in an altered NHEJ/HR environment. NU7026, a strong inhibitor of NHEJ, prevented CRISPR/Cas9-mediated degradation of cccDNA and resulted in frequent on-target deletions. We conclude that CRISPR/Cas9 is a highly effective tool to degrade cccDNA and first demonstrate that inhibiting NHEJ impairs cccDNA degradation." @default.
• W2912162884 created "2019-02-21" @default.
• W2912162884 creator A5000031944 @default.
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• W2912162884 date "2019-02-12" @default.
• W2912162884 modified "2023-10-13" @default.
• W2912162884 title "Suppressing the NHEJ pathway by DNA-PKcs inhibitor NU7026 prevents degradation of HBV cccDNA cleaved by CRISPR/Cas9" @default.
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• W2912162884 doi "https://doi.org/10.1038/s41598-019-38526-6" @default.
• W2912162884 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6372644" @default.
• W2912162884 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30755668" @default.
• W2912162884 hasPublicationYear "2019" @default.
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