PAXX promotes KU accumulation at DNA breaks and is essential for end-joining in XLF-deficient mice
Non-homologous end-joining is the key pathway for repairing double-stranded DNA breaks in mammalian cells. Here the authors show that PAXX promotes the accumulation of KU at DNA breaks and is essential for end-joining in cells lacking XLF.
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| Autores principales: | , , , , |
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| Formato: | article |
| Lenguaje: | EN |
| Publicado: |
Nature Portfolio
2017
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| Materias: | |
| Acceso en línea: | https://doaj.org/article/b22beddb938e4935afca7966266c756f |
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| Sumario: | Non-homologous end-joining is the key pathway for repairing double-stranded DNA breaks in mammalian cells. Here the authors show that PAXX promotes the accumulation of KU at DNA breaks and is essential for end-joining in cells lacking XLF. |
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