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Fenofibrate activates Nrf2 through p62-dependent Keap1 degradation

DC FieldValueLanguage
dc.contributor.author박정수-
dc.contributor.author배수한-
dc.date.accessioned2016-02-04T11:44:25Z-
dc.date.available2016-02-04T11:44:25Z-
dc.date.issued2015-
dc.identifier.issn0006-291X-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/141092-
dc.description.abstractPeroxisome proliferator-activated receptor α (PPARα) activates the β-oxidation of fatty acids in the liver. Fenofibrate is a potent agonist of PPARα and is used in the treatment of hyperlipidemia. Fenofibrate treatment often induces the production of intracellular reactive oxygen species (ROS), leading to cell death. The nuclear factor erythroid 2-related factor 2 (Nrf2)-Kelch-like ECH-associated protein 1 (Keap1) pathway is an essential component of the defense mechanism against oxidative stress. However, the molecular mechanism underlying the regulation of the Nrf2-Keap1 pathway in fenofibrate-induced cell death is not known. In this study, we demonstrated that fenofibrate induces Keap1 degradation and Nrf2 activation. This fenofibrate-mediated Keap1 degradation is partly dependent on autophagy. Furthermore, fenofibrate-induced Keap1 degradation followed by Nrf2 activation is mainly mediated by p62, which functions as an adaptor protein in the autophagic pathway. Consistent with these findings, ablation of p62 increased fenofibrate-mediated apoptotic cell death associated with ROS accumulation. These results strongly suggest that p62 plays a crucial role in preventing fenofibrate-induced cell death.-
dc.description.statementOfResponsibilityopen-
dc.format.extent542~547-
dc.relation.isPartOfBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleFenofibrate activates Nrf2 through p62-dependent Keap1 degradation-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Life Science (의생명과학부)-
dc.contributor.googleauthorJeong Su Park-
dc.contributor.googleauthorDong Hoon Kang-
dc.contributor.googleauthorDa Hyun Lee-
dc.contributor.googleauthorSoo Han Bae-
dc.identifier.doi10.1016/j.bbrc.2015.08.056-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA01645-
dc.contributor.localIdA01798-
dc.relation.journalcodeJ00281-
dc.identifier.eissn1090-2104-
dc.identifier.urlhttp://www.sciencedirect.com/science/article/pii/S0006291X15304460-
dc.subject.keywordPPARα-
dc.subject.keywordFenofibrate-
dc.subject.keywordp62-
dc.subject.keywordAutophagy-
dc.subject.keywordNrf2-
dc.subject.keywordKeap1-
dc.contributor.alternativeNamePark, Jeong Su-
dc.contributor.alternativeNameBae, Soo Han-
dc.contributor.affiliatedAuthorPark, Jeong Su-
dc.contributor.affiliatedAuthorBae, Soo Han-
dc.rights.accessRightsnot free-
dc.citation.volume465-
dc.citation.number3-
dc.citation.startPage542-
dc.citation.endPage547-
dc.identifier.bibliographicCitationBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, Vol.465(3) : 542-547, 2015-
Appears in Collections:
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers

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