Grundy, Gabrielle J., Moulding, Hayley ![]() |
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 |
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Date Type: | Publication |
Status: | Published |
Schools: | Medicine MRC Centre for Neuropsychiatric Genetics and Genomics (CNGG) |
Subjects: | Q Science > QH Natural history > QH426 Genetics |
Uncontrolled Keywords: | Non-homologous end joining; Ku; Double-strand break; APLF; WRN |
Publisher: | Elsevier |
ISSN: | 1568-7864 |
Date of Acceptance: | 25 February 2014 |
Last Modified: | 19 Oct 2022 06:47 |
URI: | https://orca.cardiff.ac.uk/id/eprint/87904 |
Citation Data
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