دورية أكاديمية
Sestrins Activate Nrf2 by Promoting p62-Dependent Autophagic Degradation of Keap1 and Prevent Oxidative Liver Damage
| العنوان: | Sestrins Activate Nrf2 by Promoting p62-Dependent Autophagic Degradation of Keap1 and Prevent Oxidative Liver Damage |
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| المساهمون: | Soo Han Bae, Su Haeng Sung, Sue Young Oh, Jung Mi Lim, Se Kyoung Lee, Young Nyun Park, Hye Eun Lee, Dongmin Kang, Sue Goo Rhee, Rhee, Sue Goo, Park, Young Nyun, Bae, Soo Han, Sung, Su Haeng |
| المصدر: | T201305659.pdf |
| سنة النشر: | 2013 |
| مصطلحات موضوعية: | Adaptor Proteins, Signal Transducing/metabolism, Animals, Autophagy, Carrier Proteins/metabolism, Cell Cycle Proteins/metabolism, Cytoskeletal Proteins/metabolism, HCT116 Cells, HEK293 Cells, HeLa Cells, Humans, Kelch-Like ECH-Associated Protein 1, Liver/metabolism, Liver/physiopathology, Male, Mice, Inbred C57BL, NF-E2-Related Factor 2/metabolism, Nuclear Proteins, Oxidative Stress, Protein Binding, Proteins/metabolism, Transcription Factors/metabolism, Transfection, Up-Regulation |
| الوصف: | Sestrins (Sesns) protect cells from oxidative stress. The mechanism underlying the antioxidant effect of Sesns has remained unknown, however. The Nrf2-Keap1 pathway provides cellular defense against oxidative stress by controlling the expression of antioxidant enzymes. We now show that Sesn1 and Sesn2 interact with the Nrf2 suppressor Keap1, the autophagy substrate p62, and the ubiquitin ligase Rbx1 and that the antioxidant function of Sesns is mediated through activation of Nrf2 in a manner reliant on p62-dependent autophagic degradation of Keap1. Sesn2 was upregulated in the liver of mice subjected to fasting or subsequent refeeding with a high-carbohydrate, fat-free diet, whereas only refeeding promoted Keap1 degradation and Nrf2 activation, because only refeeding induced p62 expression. Ablation of Sesn2 blocked Keap1 degradation and Nrf2 activation induced by refeeding and thereby increased the susceptibility of the liver to oxidative damage resulting from the acute stimulation of lipogenesis associated with refeeding. ; open |
| نوع الوثيقة: | article in journal/newspaper |
| اللغة: | unknown |
| تدمد: | 1550-4131 1932-7420 23274085 |
| العلاقة: | CELL METABOLISM; J00486; OAK-2013-03052; https://ir.ymlib.yonsei.ac.kr/handle/22282913/89166Test; T201305659; CELL METABOLISM, Vol.17(1) : 73-84, 2013 |
| DOI: | 10.1016/j.cmet.2012.12.002 |
| الإتاحة: | https://doi.org/10.1016/j.cmet.2012.12.002Test https://ir.ymlib.yonsei.ac.kr/handle/22282913/89166Test |
| حقوق: | CC BY-NC-ND 2.0 KR ; https://creativecommons.org/licenses/by-nc-nd/2.0/krTest/ ; free |
| رقم الانضمام: | edsbas.360A74B4 |
| قاعدة البيانات: | BASE |
Full Text Finder | تدمد: | 15504131 19327420 23274085 |
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| DOI: | 10.1016/j.cmet.2012.12.002 |