DNA repair in mammalian cells: Base excision repair: the long and short of it

Cell Mol Life Sci. 2009 Mar;66(6):981-93. doi: 10.1007/s00018-009-8736-z.


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).

Publication types

  • Review

MeSH terms

  • Alkylation
  • Amino Acid Sequence
  • Animals
  • Bacterial Proteins / chemistry
  • Bacterial Proteins / genetics
  • Bacterial Proteins / metabolism
  • DNA Breaks, Single-Stranded
  • DNA Damage / physiology*
  • DNA Glycosylases / chemistry
  • DNA Glycosylases / genetics
  • DNA Glycosylases / metabolism*
  • DNA Repair / physiology*
  • DNA Repair Enzymes / chemistry
  • DNA Repair Enzymes / genetics
  • DNA Repair Enzymes / metabolism*
  • Fungal Proteins / chemistry
  • Fungal Proteins / genetics
  • Fungal Proteins / metabolism
  • Humans
  • Models, Molecular*
  • Molecular Sequence Data
  • Oxidation-Reduction
  • Protein Conformation


  • Bacterial Proteins
  • Fungal Proteins
  • DNA Glycosylases
  • DNA Repair Enzymes