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In mammalian cells, base excision repair (BER) is the major repair pathway involved in the removal of non-bulky damaged nucleotides. The fidelity of BER is dependent on the polymerization step, where the major BER DNA polymerase (Pol beta) must incorporate the correct Watson-Crick base paired nucleotide into the one nucleotide repair gap. Recent studies have indicated that expression of some Pol beta variants or changes in expression of wild-type Pol beta protein, frequently found in cancer cells, can lead to DNA repair synthesis errors and confers to cells a mutator phenotype.

Original publication

DOI

10.1093/mutage/gel020

Type

Journal article

Journal

Mutagenesis

Publication Date

05/2006

Volume

21

Pages

173 - 178

Keywords

Animals, Base Pair Mismatch, Base Pairing, DNA Polymerase beta, DNA Repair, DNA Repair Enzymes, DNA Replication, DNA-Directed DNA Polymerase, Genomic Instability, Humans, Mice, Models, Genetic, Mutation, Neoplasms, Protein Isoforms, Recombinant Proteins