ATR-Chk1 activation mitigates replication stress caused by mismatch repair-dependent processing of DNA damage

G/T lesion recognition by MMR initiates mismatch excision, the reinsertion of a mismatched thymidine during resynthesis could initiate futile repair cycles. One consequence of futile repair cycles might be a disruption of overall DNA replication in the affected cell. Herein, we show that in MMR-prof... View More