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. Author manuscript; available in PMC: 2019 Mar 1.
Published in final edited form as: Radiother Oncol. 2017 Oct 18;126(3):450–464. doi: 10.1016/j.radonc.2017.09.043

Fig. 2.

Fig. 2

ATR/CHK1 suppresses oncogene-induced RS. Oncogene activation causes replication stress via uncoordinated origin firing, a reduction in licensed replication origins and inappropriate re-licensing of newly replicated DNA. Increased CDK activity leads to not only dysregulated replication initiation but also a deceased number of licensed replication origins, leading to under-replicated DNA. ATR/CHK1 signaling inhibits oncogene-induced replication stress via CDKs. Although it has been demonstrated that ATR/CHK1 suppresses replication stress via inhibition of CDK-induced replication initiation, it is not clear if ATR/CHK1 suppress CDK-mediated regulation of the number of licensed replication origins. CDK signaling suppressed by ATR/CHK1 is presented by gray arrows.