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. Author manuscript; available in PMC: 2014 Sep 19.
Published in final edited form as: Nature. 2013 Dec 18;505(7481):35–36. doi: 10.1038/nature12844

Figure 1. Senescence modules.

Figure 1

Cellular senescence is involved in tumour suppression, tissue repair and, as shown by Muñoz-Espín et al.5 and Storer et al.6, embryogenesis. In all three cases, senescent cells express the protein p21 and proteins associated with the senescence-associated secretory phenotype (SASP); they also exhibit senescence-associated β-galactosidase (SA-β-gal) activity. However, during tumour suppression and tissue repair, senescence depends primarily on the activity of the proteins p53 and p16INK4a, which are often induced as part of the DNA-damage response (DDR). By contrast, senescence during embryogenesis depends on p21, which is switched on by the transcription factors FOXO and SMAD. Senescent cells in the embryo also express p15.