Phosphorylated ETS1 and ETS2 stimulate p16INK4A transcription, resulting in cell cycle arrest with arrested cells exhibiting high p16INK4A level and senescence-associated beta-galactosidase activity. It is possible that ETS2 is the main transmitter of RAS signaling to p16INK4A at the initiation of the senescence program, and that ETS1 maintains high p16INK4A level once the senescence is already established (Ohtani et al. 2001).
Sharrocks, AD, Peters, G, Ohashi, Y, Sugimoto, M, Zebedee, Z, Ohtani, N, Huot, TJ, Hara, E, Stinson, JA
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