Maintenance of DNA replication fork stability is essential for dividing cells to preserve genomic integrity in the face of endogenous and exogenous DNA damage. To achieve this, cells evoke an intricate network of signal transduction pathways that control the timing of replication origin firing and the stability and repair of individual replicons after damage. Critical to these responses is ATR, the ATM and Rad3 -related phosphoinositide 3-kinase (PI3K)-like protein kinase. ATR is activated during S-phase in response to replication stress and a plethora of DNA lesions including double-strand breaks (DSBs) and interstrand crosslinks.
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