Damage-induced DNA replication stalling relies on MAPK-activated protein kinase 2 activity

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Abstract
Significance: Our results imply a direct impact of the p38–MAP kinase-activated protein kinase 2 (MK2) kinase pathway on the cellular response to replicative stress. In this situation, MK2 activity determines the decision between replication fork stalling and translesion synthesis. In the absence of MK2 activity, even the otherwise essential checkpoint kinase Chk1 becomes dispensable for S phase progression and cell survival. Moreover, MK2 represents a determinant of cancer cell sensitivity toward nucleoside analogue treatment.

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