Base excision repair (Homo sapiens)

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Base excision repair is a cellular mechanism that repairs damaged DNA throughout the cell cycle. It is primarily responsible for removing small, non-helix-distorting base lesions from the genome.

Base excision repair is important for removing damaged bases that could otherwise cause mutations by mispairing, or could lead to breaks in DNA during replication.

BER is initiated by DNA glycosylases, which recognize and remove specific damaged or inappropriate bases, forming AP sites. These are then cleaved by an AP endonuclease. The resulting single-strand break can then be processed by either short-patch (where a single nucleotide is replaced) or long-patch BER (where 2-10 new nucleotides are synthesized). The choice between short- and long-patch repair is currently under investigation. Various factors are thought to influence this decision, including the type of lesion, the cell cycle stage, and whether the cell is terminally differentiated or actively dividing. Some lesions, such as oxidized or reduced AP sites, are resistant to pol β lyase activity and therefore must be processed by long-patch BER.

This pathway is based on information from REPAIRtoire (http://repairtoire.genesilico.pl/Pathway/4/), Wikipedia (https://en.wikipedia.org/wiki/Base_excision_repair) and KEGG (https://www.genome.jp/dbget-bin/www_bget?map03410). The description was adapted from REPAIRtoire, layout is based on KEGG.