Way out/way in: How the relationship between WRN and CDK1 may change the fate of collapsed replication forks

Mol Cell Oncol. 2016 Dec 9;4(1):e1268243. doi: 10.1080/23723556.2016.1268243. eCollection 2017.

Abstract

Replication-dependent double-strand breaks (DSBs) are the main source of genomic instability as their inaccurate repair stimulates chromosomal rearrangements. In a recent work, we uncover a novel regulatory circuit that involves the Werner's syndrome helicase and CDK1, and that is essential for repair pathway choice at replication-dependent DSBs.

Keywords: DNA repair; WRN protein; end-resection.