Base excision repair fidelity in normal and cancer cells.
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.
Chan
Katie K L
KK
Radiation and Genome Stability Unit, Medical Research Council Harwell, Oxfordshire, UK.
Zhang
Qiu-Mei
QM
Dianov
Grigory L
GL
D000818:Animals; D020137:Base Pair Mismatch; D020029:Base Pairing; D019951:DNA Polymerase beta / Q000378:metabolism; D004260:DNA Repair; D045643:DNA Repair Enzymes / Q000378:metabolism; D004261:DNA Replication; D004259:DNA-Directed DNA Polymerase / Q000378:metabolism*; D042822:Genomic Instability; D006801:Humans; D051379:Mice; D008957:Models, Genetic; D009154:Mutation; D009369:Neoplasms / Q000235:genetics* / Q000378:metabolism; D020033:Protein Isoforms / Q000502:physiology; D011994:Recombinant Proteins / Q000378:metabolism
D020033:Protein Isoforms; D011994:Recombinant Proteins; D019951:DNA Polymerase beta; D004259:DNA-Directed DNA Polymerase; D045643:DNA Repair Enzymes