Role of in Replicative Senescence and DNA Damage-Induced Premature Senescence in p53-Deficient Human Cells
Figure 2
Model illustrating the involvement of the p16, p53, and p21 tumor suppressors in senescence of human fibroblast cultures [42]. In p53-proficient (normal) fibroblasts, telomerase shortening (e.g., as a function of culture age) or exposure to DNA-damaging agents results in activation of p53, which represses p16 and transcriptionally activates p21. The latter protein suppresses apoptosis and triggers senescence. On the other hand, p53-deficient (Li-Fraumeni syndrome) fibroblasts respond to stress by upregulating p16 which suppresses apoptosis and triggers senescence.
