base excision repair


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base excision repair

A mechanism that repairs damaged DNA during the cell cycle by removing small, non-helix-distorting nucleotide base lesions, which could otherwise cause mutations by mispairing or lead to breaks in DNA during replication. BER is initiated by DNA glycosylases that recognise and remove damaged or inappropriate bases, forming AP sites which are then cleaved by an AP endonuclease. The single-strand break formed by AP endonuclease are then processed by either short-patch (a single nucleotide is replaced), or long-patch (2–10 new nucleotides are synthesised) repair.
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References in periodicals archive ?
Boffetta, "Genetic polymorphisms in the base excision repair pathway and cancer risk: a HuGE review," American Journal of Epidemiology, vol.
Leiros, "DNA repair in mammalian cells: base excision repair: the long and short of it," Cellular and Molecular Life Sciences, vol.
Boras, "Base excision repair," Cold Spring Harbor Perspectives in Biology, vol.
At least four DNA repair pathways operate on specific types of damaged DNA: base excision repair (BER), nucleotide-excision repair (NER), mismatch repair (MMR), and double-strand break repair.30-33 XRCC1 was the first human BER pathway gene to be cloned, and cells lacking this gene product are hypersensitive to ionizing radiation.34
Samson, "Regulatory networks revealed by transcriptional profiling of damaged Saccharomyces cerevisiae cells: Rpn4 links base excision repair with proteasomes," Molecular and Cellular Biology, vol.
This process is therefore called base excision repair. In the interim the molecular mechanism of an alternative and more general mode of excision repair of the type I was initially in search of was unravelled by others.
Base excision repair is a multi-step process that corrects non-bulky damage to bases resulting from oxidation, methylation, deamination, or spontaneous loss of the DNA base itself (Memisoglu et al., 2000).
With the help of different forms of the enzyme DNA glycosylase, the generic mode of repair the "base excision repair" mechanism, as also supported by the present article (1), is rendered highly specific.
Cells normally use base excision repair to fix oxidative damage to DNA caused by reactive molecules such as hydrogen peroxide and oxygen radicals, which form during energy production and other metabolic processes.
MUTYH-associated polyposis (MAP) is an autosomal recessive syndrome associated with biallelic germline mutations in the base excision repair gene MUTYH (OMIM #608456) (1).