The Ku-binding motif is a conserved module for recruitment and stimulation of non-homologous end-joining proteins

The Ku-binding motif is a conserved module for recruitment and stimulation of non-homologous end-joining proteins

Werner syndrome is a progeroid disease characterised by genetic instability due to mutations to the WRN helicase/exonuclease. Here the authors define a novel Ku binding motif (KBM) and show that two such motifs facilitate the involvement of WRN in DNA double-strand break repair.

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Detalles Bibliográficos
Autores principales: Gabrielle J. Grundy, Stuart L. Rulten, Raquel Arribas-Bosacoma, Kathryn Davidson, Zuzanna Kozik, Antony W. Oliver, Laurence H. Pearl, Keith W. Caldecott
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2016
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Science
Q
Acceso en línea:https://doaj.org/article/f76baaf3e5cb4dc5b122d503eff9616e
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