Lehmann, Alan R (2009) DNA damage tolerance and translesions synthesis. In: Khanna, Kum Kum and Shiloh, Yosef (eds.) The DNA damage response: implications on cancer formation and treatment. Springer, Dordrecht, pp. 209-234. ISBN 9789048125609

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Abstract

When the replication machinery encounters a DNA lesion, it is able to continue to replicate the DNA either by damage avoidance processes involving switching templates, or by translesion synthesis past the lesion using specialized DNA polymerases. Most of these polymerases are in the Y-family and have open structures that enable them to accommodate particular damaged bases in their active sites. Translesion synthesis can be error-free or error-prone and defective DNA polymerase η results in the variant form of the highly skin-cancer prone disorder xeroderma pigmentosum. Single-stranded regions of DNA exposed at sites of stalled replication forks trigger the ubiquitination of the sliding clamp protein proliferating cell nuclear antigen (PCNA). This increases the affinity of the Y-family polymerases for PCNA, as they all contain ubiquitin-binding domains, and provides a mechanism for the recruitment of these enzymes to stalled replication forks.

Item Type:	Book Section
Additional Information:	GDSC304
Schools and Departments:	School of Life Sciences > Sussex Centre for Genome Damage and Stability
Research Centres and Groups:	Genome Damage and Stability Centre
Depositing User:	Gee Wheatley
Date Deposited:	08 Apr 2010
Last Modified:	16 Mar 2018 14:56
URI:	http://srodev.sussex.ac.uk/id/eprint/2301

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