Grundy, Gabrielle J, Moulding, Hayley A, Caldecott, Keith W and Rulten, Stuart L (2014) One ring to bring them all--the role of Ku in mammalian non-homologous end joining. DNA repair, 17. pp. 30-38. ISSN 1568-7856

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Abstract

The repair of DNA double strand breaks is essential for cell survival and several conserved pathways have evolved to ensure their rapid and efficient repair. The non-homologous end joining pathway is initiated when Ku binds to the DNA break site. Ku is an abundant nuclear heterodimer of Ku70 and Ku80 with a toroidal structure that allows the protein to slide over the broken DNA end and bind with high affinity. Once locked into placed, Ku acts as a tool-belt to recruit multiple interacting proteins, forming one or more non-homologous end joining complexes that act in a regulated manner to ensure efficient repair of DNA ends. Here we review the structure and functions of Ku and the proteins with which it interacts during non-homologous end joining.

Item Type:	Article
Schools and Departments:	School of Life Sciences > Sussex Centre for Genome Damage and Stability
Subjects:	Q Science > QP Physiology
Depositing User:	Stuart Rulten
Date Deposited:	18 Sep 2015 12:07
Last Modified:	05 Aug 2016 06:50
URI:	http://srodev.sussex.ac.uk/id/eprint/56818

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