Lee James T, Gu Wei
Psychogenics Inc., Montvale, NJ, USA.
Genes Cancer. 2013 Mar;4(3-4):112-7. doi: 10.1177/1947601913484496.
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.
细胞内NAD(+)/NADH水平在调控低等生物衰老过程中控制Sir2(沉默信息调节因子2)脱乙酰酶活性。人们已开展大量工作来寻找激活SIRT1(Sir2在哺乳动物中的同源物)的方法。p53被鉴定为SIRT1脱乙酰化的真正底物,这将SIRT1与肿瘤发生联系起来。在此,我们综述了各种调控p53乙酰化及随后p53肿瘤抑制活性激活的SIRT1内源性和小分子激活剂及抑制剂。