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. 2009 Mar 15;100(5):792–797. doi: 10.1111/j.1349-7006.2009.01123.x

Figure 2.

Figure 2

Molecular mechanisms of cellular senescence. Oncogenic stress induces p16 and the p53‐target p21. When protein retinoblastoma (pRb) is fully activated by high‐level expression of p16INK4a, mitogenic signals, in turn, increase the level of reactive oxygen species (ROS) and elicit a positive feedback activation of the ROS–PKC‐δ signaling pathway. Elevated levels of p16INK4a therefore establish the autonomous activation of ROS–PKC‐δ signaling, leading to an irrevocable block to cytokinesis in human senescent cells. CDK, cyclin‐dependent kinase.