Cellular and Molecular Life Sciences

, Volume 66, Issue 6, pp 981–993

DNA Repair in Mammalian Cells

Base excision repair: the long and short of it
  • A. B. Robertson
  • A. Klungland
  • T. Rognes
  • I. Leiros
Multi-author Review

DOI: 10.1007/s00018-009-8736-z

Cite this article as:
Robertson, A.B., Klungland, A., Rognes, T. et al. Cell. Mol. Life Sci. (2009) 66: 981. doi:10.1007/s00018-009-8736-z

Abstract.

Base excision repair (BER) is the primary DNA repair pathway that corrects base lesions that arise due to oxidative, alkylation, deamination, and depurinatiation/depyrimidination damage. BER facilitates the repair of damaged DNA via two general pathways – short-patch and long-patch. The shortpatch BER pathway leads to a repair tract of a single nucleotide. Alternatively, the long-patch BER pathway produces a repair tract of at least two nucleotides. The BER pathway is initiated by one of many DNA glycosylases, which recognize and catalyze the removal of damaged bases. The completion of the BER pathway is accomplished by the coordinated action of at least three additional enzymes. These downstream enzymes carry out strand incision, gap-filling and ligation. The high degree of BER conservation between E. coli and mammals has lead to advances in our understanding of mammalian BER. This review will provide a general overview of the mammalian BER pathway. (Part of a Multi-author Review)

Keywords.

Base excision repair glycosylase DNA damage alkylation oxidation deamination 

Copyright information

© Birkhäuser Verlag, Basel 2009

Authors and Affiliations

  • A. B. Robertson
    • 1
  • A. Klungland
    • 1
  • T. Rognes
    • 1
    • 2
  • I. Leiros
    • 3
  1. 1.Centre for Molecular Biology and Neuroscience and Institute of Medical Microbiology, Rikshospitalet HFUniversity of OsloOsloNorway
  2. 2.Department of InformaticsUniversity of OsloBlindern, OsloNorway
  3. 3.The Norwegian Structural Biology Centre [NorStruct], Department of Chemistry, Faculty of ScienceUniversity of TromsøTromsøNorway

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