Abstract
The cellular NAD(+)/NADH level controls Sir2 (silent information regulator 2) deacetylase activity in regulating aging in lower species. Much work has been put forth to identify ways to activate SIRT1, the mammalian ortholog of Sir2. The identification of p53 as a bona fide substrate of SIRT1 deacetylation has linked SIRT1 to a role in tumorigenesis. Here, we review the various SIRT1 endogenous and small molecular activators and inhibitors that regulate p53 acetylation and subsequent activation of p53 tumor suppression activity.