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Inactivation of Sirtuin2 protects mice from acetaminophen-induced liver injury: possible involvement of ER stress and S6K1 activation

Title
Inactivation of Sirtuin2 protects mice from acetaminophen-induced liver injury: possible involvement of ER stress and S6K1 activation
Authors
Lee, Da HyunLee, BuhyunPark, Jeong SuLee, Yu SeolKim, Jin HeeCho, YejinJo, YoonjungKim, Hyun-SeokLee, Yong-hoNam, Ki TaekBae, Soo Han
Ewha Authors
김현석
SCOPUS Author ID
김현석scopus
Issue Date
2019
Journal Title
BMB REPORTS
ISSN
1976-6696JCR Link

1976-670XJCR Link
Citation
BMB REPORTS vol. 52, no. 3, pp. 190 - 195
Keywords
AcetaminophenER stressHepatotoxicityS6K1Sirtuin2
Publisher
KOREAN SOCIETY BIOCHEMISTRY &

MOLECULAR BIOLOGY
Indexed
SCIE; SCOPUS; KCI WOS
Document Type
Article
Abstract
Acetaminophen (APAP) overdose can cause hepatotoxicity by inducing mitochondria! damage and subsequent necrosis in hepatocytes. Sirtuin2 (Sirt2) is an NAD(+)-dependent deacetylase that regulates several biological processes, including hepatic gluconeogenesis, as well as inflammatory pathways. We show that APAP decreases the expression of Sirt2. Moreover, the ablation of Sirt2 attenuates APAP-induced liver injuries, such as oxidative stress and mitochondrial damage in hepatocytes. We found that Sirt2 deficiency alleviates the APAP-mediated endoplasmic reticulum (ER) stress and phosphorylation of the p70 ribosomal S6 kinase 1 (S6K1). Moreover, Sirt2 interacts with and deacetylates S6K1, followed by S6K1 phosphorylation induction. This study elucidates the molecular mechanisms underlying the protective role of Sirt2 inactivation in APAP-induced liver injuries.
DOI
10.5483/BMBRep.2019.52.3.083
Appears in Collections:
일반대학원 > 바이오융합과학과 > Journal papers
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