Base Excision Repair (BER)

Base excision repair (BER) is a fundamental cellular mechanism responsible for repairing small, non-helix-distorting lesions in DNA. These lesions are typically caused by oxidation, deamination, or alkylation. BER operates throughout the cell cycle and is essential for maintaining genomic stability by preventing mutations that could arise from damaged bases. The pathway involves recognition and removal of damaged bases by DNA glycosylases, incision at abasic (AP) sites by AP endonucleases, gap filling by DNA polymerase, and ligation by DNA ligase. BER is crucial for preventing mutagenesis due to endogenous metabolic processes as well as environmental insults. Defects in this pathway can lead to increased susceptibility to cancer and other diseases related to genome instability such as neurodegenerative disorders. There are two main sub-pathways: Short-patch BER (replaces one nucleotide) and Long-patch BER (replaces two to ten nucleotides; uses additional proteins).

Inhibiting or enhancing BER pathway components to modulate DNA repair efficiency in cancer cells or protect against DNA damage in healthy cells.