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DNA damage tolerance and translesions synthesis

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posted on 2023-06-07, 15:17 authored by Alan LehmannAlan Lehmann
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 ? 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.

History

Publication status

  • Published

Publisher

Springer

Page range

209-234

Pages

449.0

Book title

The DNA damage response: implications on cancer formation and treatment

Place of publication

Dordrecht

ISBN

9789048125609

Department affiliated with

  • Sussex Centre for Genome Damage Stability Publications

Research groups affiliated with

  • Genome Damage and Stability Centre Publications

Notes

GDSC304

Full text available

  • No

Peer reviewed?

  • Yes

Editors

Kum Kum Khanna, Yosef Shiloh

Legacy Posted Date

2010-04-08

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