Base excision repair fidelity in normal and cancer cells | Zendy

Karen K. L. Chan | Zendy; Q.-M. Zhang | Zendy; Grigory L. Dianov | Zendy

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Base excision repair fidelity in normal and cancer cells

Author(s) -

Karen K. L. Chan,

Q.-M. Zhang,

Grigory L. Dianov

Publication year - 2006

Publication title -

mutagenesis

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.723

H-Index - 91

eISSN - 1464-3804

pISSN - 0267-8357

DOI - 10.1093/mutage/gel020

Subject(s) - base excision repair , nucleotide excision repair , dna repair , dna polymerase beta , microbiology and biotechnology , dna polymerase , dna mismatch repair , dna , biology , base pair , nucleotide , chemistry , genetics , cancer research , gene

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.

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