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Sestrins Activate Nrf2 by Promoting p62-Dependent Autophagic Degradation of Keap1 and Prevent Oxidative Liver Damage

DC Field Value Language
dc.contributor.author이서구-
dc.contributor.author박영년-
dc.contributor.author배수한-
dc.contributor.author성수행-
dc.date.accessioned2014-12-18T09:58:00Z-
dc.date.available2014-12-18T09:58:00Z-
dc.date.issued2013-
dc.identifier.issn1550-4131-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/89166-
dc.description.abstractSestrins (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.-
dc.description.statementOfResponsibilityopen-
dc.relation.isPartOfCELL METABOLISM-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAdaptor Proteins, Signal Transducing/metabolism*-
dc.subject.MESHAnimals-
dc.subject.MESHAutophagy-
dc.subject.MESHCarrier Proteins/metabolism-
dc.subject.MESHCell Cycle Proteins/metabolism-
dc.subject.MESHCytoskeletal Proteins/metabolism*-
dc.subject.MESHHCT116 Cells-
dc.subject.MESHHEK293 Cells-
dc.subject.MESHHeLa Cells-
dc.subject.MESHHumans-
dc.subject.MESHKelch-Like ECH-Associated Protein 1-
dc.subject.MESHLiver/metabolism*-
dc.subject.MESHLiver/physiopathology-
dc.subject.MESHMale-
dc.subject.MESHMice-
dc.subject.MESHMice, Inbred C57BL-
dc.subject.MESHNF-E2-Related Factor 2/metabolism*-
dc.subject.MESHNuclear Proteins-
dc.subject.MESHOxidative Stress-
dc.subject.MESHProtein Binding-
dc.subject.MESHProteins/metabolism*-
dc.subject.MESHTranscription Factors/metabolism*-
dc.subject.MESHTransfection-
dc.subject.MESHUp-Regulation-
dc.titleSestrins Activate Nrf2 by Promoting p62-Dependent Autophagic Degradation of Keap1 and Prevent Oxidative Liver Damage-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Pathology (병리학)-
dc.contributor.googleauthorSoo Han Bae-
dc.contributor.googleauthorSu Haeng Sung-
dc.contributor.googleauthorSue Young Oh-
dc.contributor.googleauthorJung Mi Lim-
dc.contributor.googleauthorSe Kyoung Lee-
dc.contributor.googleauthorYoung Nyun Park-
dc.contributor.googleauthorHye Eun Lee-
dc.contributor.googleauthorDongmin Kang-
dc.contributor.googleauthorSue Goo Rhee-
dc.identifier.doi10.1016/j.cmet.2012.12.002-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA02847-
dc.contributor.localIdA01563-
dc.contributor.localIdA01798-
dc.contributor.localIdA01948-
dc.relation.journalcodeJ00486-
dc.identifier.eissn1932-7420-
dc.identifier.pmid23274085-
dc.subject.keywordAdaptor Proteins, Signal Transducing/metabolism*-
dc.subject.keywordAnimals-
dc.subject.keywordAutophagy-
dc.subject.keywordCarrier Proteins/metabolism-
dc.subject.keywordCell Cycle Proteins/metabolism-
dc.subject.keywordCytoskeletal Proteins/metabolism*-
dc.subject.keywordHCT116 Cells-
dc.subject.keywordHEK293 Cells-
dc.subject.keywordHeLa Cells-
dc.subject.keywordHumans-
dc.subject.keywordKelch-Like ECH-Associated Protein 1-
dc.subject.keywordLiver/metabolism*-
dc.subject.keywordLiver/physiopathology-
dc.subject.keywordMale-
dc.subject.keywordMice-
dc.subject.keywordMice, Inbred C57BL-
dc.subject.keywordNF-E2-Related Factor 2/metabolism*-
dc.subject.keywordNuclear Proteins-
dc.subject.keywordOxidative Stress-
dc.subject.keywordProtein Binding-
dc.subject.keywordProteins/metabolism*-
dc.subject.keywordTranscription Factors/metabolism*-
dc.subject.keywordTransfection-
dc.subject.keywordUp-Regulation-
dc.contributor.alternativeNameRhee, Sue Goo-
dc.contributor.alternativeNamePark, Young Nyun-
dc.contributor.alternativeNameBae, Soo Han-
dc.contributor.alternativeNameSung, Su Haeng-
dc.contributor.affiliatedAuthorRhee, Sue Goo-
dc.contributor.affiliatedAuthorPark, Young Nyun-
dc.contributor.affiliatedAuthorBae, Soo Han-
dc.contributor.affiliatedAuthorSung, Su Haeng-
dc.rights.accessRightsfree-
dc.citation.volume17-
dc.citation.number1-
dc.citation.startPage73-
dc.citation.endPage84-
dc.identifier.bibliographicCitationCELL METABOLISM, Vol.17(1) : 73-84, 2013-
dc.identifier.rimsid34416-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Pathology (병리학교실) > 1. Journal Papers

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