Abstract
Double-stranded DNA breaks (DSBs) that arise during replication are particularly severe form of damage that are repaired by homologous recombination (HR) machinery. Unrepaired DSBs lead to gross chromosomal rearrangements and is a key driver of genomic instability. HR is a complex process orchestrated by over two dozen protein complexes, and mutations in HR-proteins (BRCA2, RAD51, and RAD52) are associated with genetic diseases and cancers. RAD51 is the recombinase that binds to single-stranded DNA (ssDNA), forms a filament, and is the enzymatic engine that drives the search for homology.
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