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ATR recruitment to some DNA base lesions proceeds through a mismatch repair-dependent mechanism.
Mismatch repair proteins may contribute directly and indirectly to ATR recognition of some times of DNA damage. Direct interactions between the ATR-ATRIP complex and MUTSα and MUTLα proteins may promote activation of ATR independently of RPA and single-stranded DNA. Alternatively, mismatch repair-dependent DNA processing may promote the RPA-dependent canonical ATR signaling pathway.
