Missense and nonsense mutations in the CDKN2A gene that result in amino acid substitutions in p16INK4A or p16INK4A truncations, impairing its ability to bind to CDK4 and CDK6, interfere with p16INK4A-mediated induction of cellular senescence in response to oncogenic signaling (Haferkamp et al. 2008).Loss-of-function mutations in p16INK4A can also contribute to cancer by interfering with p16INK4A-mediated inhibition of NFKB signaling (Becker et al. 2005).
Becker, TM, Rizos, H, Haferkamp, S, Kefford, RF, Scurr, LL
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