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The Base Excision Repair (BER) pathway is a critical cellular DNA repair mechanism that corrects small, non-helix-distorting base lesions throughout the cell cycle. These lesions are typically caused by deamination, oxidation, or alkylation of DNA bases and can arise from spontaneous decay or exposure to environmental agents such as chemicals and radiation. BER operates in both the nucleus and mitochondria, often utilizing different isoforms of key proteins in each compartment. Defects in BER components increase susceptibility to cancer and neurodegenerative diseases due to accumulation of mutations from unrepaired base damage. The pathway's role makes it a target for therapeutic intervention strategies.
Targeting components of the BER pathway to inhibit DNA repair in cancer cells, leading to increased sensitivity to chemotherapeutic agents or radiation.
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