Mammalian DNA is constantly being compromised by various endogenous and exogenous insults. This damage can include crosslinks, base modifications, base mismatches, stalled replication forks, single-strand breaks (SSBs), and particularly dangerous double-strand breaks (DSBs). The magnitude of this assault on the genome is conveyed by the fact that a cell can experience at least 10,000 SSBs per day, with unrepaired lesions potentially being converted to DSBs. Fortunately, eukaryotes possess an array of distinct but often interlinked pathways to detect and repair damaged DNA, including base excision repair (BER), nucleotide excision repair (NER), mismatch repair (MMR), single-strand break repair (SSBR), non-homologous end joining (NHEJ), and homologous recombination (HR), among others. In addition to these, checkpoints can arrest cell cycle progression to allow for DNA repair and prevent transmission of damaged DNA to daughter cells. The overriding goal of these mechanisms is the preservation of genomic integrity.
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