The nuclear protein kinase ATR controls S-phase progression in response to DNA damage
and replication fork stalling, including damage caused by ultraviolet irradiation, hyperoxia,
and replication inhibitors like aphidicolin and hydroxyurea. ATR activation and substrate
specificity require the presence of adapter and mediator molecules, ultimately resulting in
the downstream inhibition of the S-phase kinases that function to initiate DNA replication at
origins of replication. The data reviewed strongly support the hypothesis that ATR is …