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Cells undergo DNA damage constantly from exogenous and endogenous sources. Some of these sources include UV-light, ionizing radiation, alkylating agents and other environmental DNA damaging agents, as well as other sources derived spontaneously from cellular metabolism, such as reactive oxygen species. DNA damaging agents can cause a number of DNA lesions, including adducts, apurinic/apyrimidinic sites (AP sites), single-strand and double-strand DNA breaks. Left unrepaired, these DNA lesions could result in mutations, senescence, or induction of cell death which could lead to the development of neurodegeneration, cancer and other diseases.

In order to maintain genomic integrity, cells have developed the DNA damage response (DDR) pathway which allows cells to recognize the DNA damage and facilitate recruitment and activation of DNA repair proteins. Members of the phosphatidyl-inositol 3-kinase like protein kinase (PIKK) family, such as ATM, ATR and DNA-PK, are involved in this response, as well as a few members of the poly (ADP-ribose) polymerase (PARP) family.

Several DNA repair pathways exist to correct the DNA lesions depending on the particular form of DNA damage. For instance, the base excision repair (BER) and the mismatch repair (MMR) pathways mend damaged or mispaired DNA bases by excising the damaged base or by replacing mispaired bases with correct ones. Nucleotide excision repair (NER) fixes DNA lesions such as intrastrand crosslinks by removing a larger oligonucleotide DNA fragment; while double-strand breaks are generally repaired by non-homology end-joining (NHEJ) or by homology-directed repair (HDR).

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