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O-GlcNAcylation of SIRT1 enhances its deacetylase activity and promotes cytoprotection under stress.

Abstract：

:SIRT1 is the most evolutionarily conserved mammalian sirtuin, and it plays a vital role in the regulation of metabolism, stress responses, genome stability, and ageing. As a stress sensor, SIRT1 deacetylase activity is significantly increased during stresses, but the molecular mechanisms are not yet fully clear. Here, we show that SIRT1 is dynamically modified with O-GlcNAc at Ser 549 in its carboxy-terminal region, which directly increases its deacetylase activity both in vitro and in vivo. The O-GlcNAcylation of SIRT1 is elevated during genotoxic, oxidative, and metabolic stress stimuli in cellular and mouse models, thereby increasing SIRT1 deacetylase activity and protecting cells from stress-induced apoptosis. Our findings demonstrate a new mechanism for the activation of SIRT1 under stress conditions and suggest a novel potential therapeutic target for preventing age-related diseases and extending healthspan.

journal_name

Nat Commun

journal_title

Nature communications

authors

Han C,Gu Y,Shan H,Mi W,Sun J,Shi M,Zhang X,Lu X,Han F,Gong Q,Yu W

doi

10.1038/s41467-017-01654-6

subject

Has Abstract

pub_date

2017-11-14 00:00:00

pages

1491

issue

1

issn

2041-1723

pii

10.1038/s41467-017-01654-6

journal_volume

8

pub_type

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