Regulation of SIRT1 by MicroRNAs

被引：99

作者：

Choi, Sung-E ^{[1
,2
]}

Kemper, Jongsook Kim ^{[1
]}

机构：

[1] Univ Illinois, Dept Mol & Integrat Physiol, Urbana, IL 61801 USA

[2] Ajou Univ, Chron Inflammatory Dis Res Ctr, Suwon 442749, South Korea

来源：

MOLECULES AND CELLS | 2013年 / 36卷 / 05期

基金：

新加坡国家研究基金会;

关键词：

METABOLISM; EXPRESSION; NAD(+); GENE; SIRTUINS; MIR-34A; PROTEIN; HOMOLOG; PATHWAY; HEALTH;

D O I：

10.1007/s10059-013-0297-1

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

Sirtuin 1 (SIRT1) is an NAD(+)-dependent deacetylase that connects cellular energy levels to homeostatic responses by deacetylating and modulating the activities of many transcriptional regulators. Discovered as a longevity protein in yeast, the mammalian SIRT1 has been intensively studied because of its great potential as a therapeutic target to benefit human health by preventing and improving many age-related diseases. There has been, therefore, substantial interest in developing agents that upregulate SIRT1 expression and activity. SIRT1 is regulated at multiple levels, including post-transcriptionally by microRNAs (miRs), powerful regulators of diverse biological pathways. Here we discuss how expression and activity of SIRT1 and other sirtuins are inhibited by miRs and further discuss the therapeutic potential of targeting miRs for age-related diseases that involve SIRT1 dysfunction, focusing on obesityrelated diseases.

引用

页码：385 / 392

页数：8

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