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. 2011 Feb 24;135(3):263–280. doi: 10.1007/s00418-011-0793-3

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© The Author(s) 2011

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Fig. 2 — A model for the hydroxyurea-induced checkpoint signaling and modulation by caffeine, 2-aminopurine, staurosporine and sodium metavanadate. The mechanisms connected with the S-phase checkpoints are set in motion under the conditions of replication stress [under the influence of hydroxyurea (HU), an inhibitor of ribonucleotide reductase (RNR)], which results in the phosphorylation of Chk1 kinase by superior kinases: ATM and ATR. The activated Chk1 can inactivate Cdc25C phosphatase by phosphorylation on Ser216, which results in the inhibition of Cdc2 activation and G2/M passages (orange pathway). Caffeine (CF), 2-aminopurine (2-AP), staurosporine (ST) and sodium metavanadate (Van) induce the premature condensation of chromosomes (PCC), most probably by omitting the mechanism that blocks Cdc25 phosphatase and Cdk1/cyclin B complex (red and blue pathways)