Adhesion Molecules-28

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Channels and Transporters-79

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Circadian Rhythms-13

Coagulation-14

Cytokines/Growth Factors-52

Development-223

DNA-56

DNA Surveillance and Repair-42

Drug Design-17

Endocrine-66

Evolution-33

Extracellular Matrix-30

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Gene Expression-178

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Heart-61

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Protein-12

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RNA-152

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Viruses-85

Chapter category: DNA Surveillance and Repair

Mammalian Base Excision Repair

Chapter authors:
Grigory L. Dianov, Sarah L. Allinson, Helen Budworth and Kate Sleeth

In living cells DNA base lesions are formed continuously as a consequence of normal me tabolism and are also generated by a number of external factors. Simple base damages are repaired by base excision repair that includes two major pathways. These two pathways involve different subsets of enzymes and result in replacement of one (short-patch pathway) or more (long-patch pathway) nucleotides. Both pathways are initiated by a damage specific DNA glycosylase, which removes the damaged base creating an abasic site (apurinic/apyrimidinic, AP site). AP endonuclease then cleaves the phosphodiester bond 5' to the AP site and then DNA polymerase b adds the first nucleotide to the 3'-end of the incised AP site. Normally, the reaction continues through the short-patch repair pathway where Pol b removes the 5'-sugar phosphate residue and DNA ligase complete the repair. However, if the 5'-sugar phosphate is resistant to b-elimination, catalyzed by DNA polymerase b, then additional DNA synthesis is required to displace the 5'-sugar phosphate as part of a flap. This flap is then removed by flap endonuclease, and DNA ligase completes long-patch repair by ligating the DNA ends. These processes are directed and coordinated by multiple protein-protein interactions.

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