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

Abstract

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.