Deacetylation by SIRT1 Reprograms Inflammation and Cancer.
Deacetylation by SIRT1 Reprograms Inflammation and Cancer.
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DOI：
10.1177/1947601913476948
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发表时间：
2013-03-01
期刊：
影响因子：
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通讯作者：
McCall, Charles E
中科院分区：
文献类型：
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作者：
Liu, Tie Fu;McCall, Charles E
NAD（+）依赖性去乙酰化酶SIRT1是核小体定位和染色质结构的主要调控因子，从而对基因表达进行重编程。在急性炎症中，染色质以有序的顺序离开和恢复稳态。该序列依赖于SIRT1激活和信号蛋白去乙酰化的NAD（+）可用性的变化，这在急性炎症期间通过在常染色质和异染色质之间切换来支持有序的基因重编程。相反，在慢性炎症和癌症中，NAD（+）的有限可用性和SIRT1表达的减少可能维持异常的染色质结构和功能。SIRT1还通过直接去乙酰化靶如NFkappaB p65和p53来影响炎症和癌症。在这里，我们回顾了SIRT1在炎症和癌症中的作用。
NAD(+)-dependent deacetylase SIRT1 is a master regulator of nucleosome positioning and chromatin structure, thereby reprogramming gene expression. In acute inflammation, chromatin departs from, and returns to, homeostasis in an orderly sequence. This sequence depends on shifts in NAD(+) availability for SIRT1 activation and deacetylation of signaling proteins, which support orderly gene reprogramming during acute inflammation by switching between euchromatin and heterochromatin. In contrast, in chronic inflammation and cancer, limited availability of NAD(+) and reduced expression of SIRT1 may sustain aberrant chromatin structure and functions. SIRT1 also influences inflammation and cancer by directly deacetylating targets like NFkappaB p65 and p53. Here, we review SIRT1 in the context of inflammation and cancer.