Linking p53, p21, and mTOR in Aging and Regeneration

The p53 protein is a pivot point between aging and cancer: suppressing cancer at the cost of faster aging. p21 has a similar role, and is also a regulator of regeneration: p21-deficient mice are capable of regenerating injuries that normally don't heal in mammals. mTOR is a calorie restriction associated protein that when manipulated can extend life in mammals. These proteins influence many aspects of cell growth and other important metabolic processes, and are all tied together in the mechanisms of the cell: "The mechanism(s) by which p53 chooses between outcomes of senescence or quiescence has remained elusive. ... Recent studies [have] shown that [gene expression] of p21, a key p53 downstream target that is required for both senescence and quiescence, drives [cancer cells] into senescence ... Notably, rapamycin, a classical inhibitor of the mTOR pathway, can also suppress p21-mediated senescence suggesting the possibility that p53 might supress senescence by inhibiting mTOR signalling. Several key components of the mTOR pathway are, in fact, down-regulated by p53. ... Collectively, these analyses pinpoint p53-mediated inhibition of the mTOR pathway as a major effector in suppressing senescence, depending on whether p53 levels are above or below a critical threshold." This isn't all abstract low-level research: sophisticated manipulation of p53 can extend life in mice by 50%, and better understanding should mean better results.


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