O-GlcNAcylation enhances FOXO4 transcriptional regulation in response to stress

被引:26
作者
Ho, Shiuh-Rong [1 ]
Wang, Kai [2 ]
Whisenhunt, Thomas R. [1 ]
Huang, Ping [3 ]
Zhu, Xiaolin [1 ]
Kudlow, Jeffrey E. [1 ,2 ,3 ,4 ]
Paterson, Andrew J. [1 ,2 ,4 ]
机构
[1] Univ Alabama, Dept Cell Biol, Birmingham, AL 35294 USA
[2] Univ Alabama, Dept Med, Div Endocrinol Diabet & Metab, Birmingham, AL 35294 USA
[3] Univ Alabama, Dept Pharmacol & Toxicol, Birmingham, AL 35294 USA
[4] Univ Alabama, Dept Physiol & Biophys, Birmingham, AL 35294 USA
来源
FEBS LETTERS | 2010年 / 584卷 / 01期
关键词
OGT; NCOAT; Hydrogen peroxide; O-GlcNAc; p27Kip1; BETA-N-ACETYLGLUCOSAMINE; PROTEIN-KINASE-B; NUCLEOCYTOPLASMIC PROTEINS; P27(KIP1) EXPRESSION; FACTOR AFX; GLCNAC; CELLS; INHIBITION; ACTIVATION;
D O I
10.1016/j.febslet.2009.11.059
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The FOXO4 transcription factor plays an important role in cell survival in response to oxidative stress. The regulation of FOXO4 is orchestrated by post-translational modi. cations including phosphorylation, acetylation, and ubiquitination. Here, we demonstrate that O-GlcNAcylation also contributes to the FOXO4-dependent oxidative stress response. We show that hydrogen peroxide treatment of HEK293 cells increases FOXO4 association with OGT, the enzyme that adds O-GlcNAc to proteins, causing FOXO4 O-GlcNAcylation and enhanced transcriptional activity under acute oxidative stress. O-GlcNAcylation is known to be protective for cells under stress conditions, including oxidative stress. Our data provide a mechanism of FOXO4 anti-oxidative protection through O-GlcNAcylation.
引用
收藏
页码:49 / 54
页数:6
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