摘要：The p53 tumor suppressor protein is arguably the most important guardian of the mammalian genome. p53 promotes longevity by reducing somatic mutations or the survival and proliferation of mutant cells. Under normal conditions, this proteins role is inconsequential because of the rapidity of its degradation. But stress signals of almost any form halt the degradation of p53, unleashing an active protein that triggers transient cell cycle arrest, apoptosis, or cellular senescence [1]. Both apoptosis and senescence are potent tumor suppressor mechanisms that irreversibly prevent tumorgenesis [2]. However, both processes also deplete tissues of proliferation-competent progenitor cells, which is a characteristic associated with degenerative aging. Therefore mammalian survival paradoxically lies at the mercy of p53, which oversees a tight balance between tumor suppression and long-term cell proliferation.
