A novel G₁ checkpoint mediated by the p57 CDK inhibitor and p38 SAPK promotes cell survival upon stress

Figures & data

Figure 1. Schematic diagram depicting the mechanism by which p38 SAPK activation promotes G₁ cell cycle arrest through p57^Kip2 phosphorylation. Transition from G₁ to S phase requires Cdk2-cyclinE/A activity. Upon an environmental stress, p38 SAPK becomes transiently activated and phosphorylates the T143 of the CDKi p57^Kip2. p57 phosphorylation increases its affinity toward Cdk2-cyclin E/A complexes, which become inactivated and impose a G₁ delay. Activation of this G₁ checkpoint is essential for proper cell adaptation and survival to stress.