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p62/SQSTM1 is required for the protection against endoplasmic reticulum stress-induced apoptotic cell death

DC Field Value Language
dc.contributor.author박정수-
dc.contributor.author배수한-
dc.contributor.author이서구-
dc.contributor.author이용호-
dc.contributor.author이다현-
dc.date.accessioned2017-10-26T07:58:49Z-
dc.date.available2017-10-26T07:58:49Z-
dc.date.issued2016-
dc.identifier.issn1071-5762-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/152774-
dc.description.abstractEndoplasmic reticulum (ER) stress is triggered by various cellular stresses that disturb protein folding or calcium homeostasis in the ER. To cope with these stresses, ER stress activates the unfolded protein response (UPR) pathway, but unresolved ER stress induces reactive oxygen species (ROS) accumulation leading to apoptotic cell death. However, the mechanisms that underlie protection from ER stress-induced cell death are not clearly defined. The nuclear factor erythroid 2-related factor 2 (Nrf2)-Kelch-like ECH-associated protein 1 (Keap1) pathway plays a crucial role in the protection of cells against ROS-mediated oxidative damage. Keap1 acts as a negative regulator of Nrf2 activation. In this study, we investigated the role of the Nrf2-Keap1 pathway in protection from ER stress-induced cell death using tunicamycin (TM) as an ER stress inducer. We found that Nrf2 is an essential protein for the prevention from TM-induced apoptotic cell death and its activation is driven by autophagic Keap1 degradation. Furthermore, ablation of p62, an adapter protein in the autophagy process, attenuates the Keap1 degradation and Nrf2 activation that was induced by TM treatment, and thereby increases susceptibility to apoptotic cell death. Conversely, reinforcement of p62 alleviated TM-induced cell death in p62-deficient cells. Taken together, these results demonstrate that p62 plays an important role in protecting cells from TM-induced cell death through Nrf2 activation.-
dc.description.statementOfResponsibilityrestriction-
dc.languageEnglish-
dc.publisherInforma Healthcare-
dc.relation.isPartOfFREE RADICAL RESEARCH-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAnimals-
dc.subject.MESHApoptosis/physiology-
dc.subject.MESHAutophagy/drug effects-
dc.subject.MESHAutophagy/physiology-
dc.subject.MESHCell Death/physiology-
dc.subject.MESHEndoplasmic Reticulum Stress/physiology-
dc.subject.MESHHEK293 Cells-
dc.subject.MESHHumans-
dc.subject.MESHKelch-Like ECH-Associated Protein 1/metabolism-
dc.subject.MESHMice-
dc.subject.MESHNF-E2-Related Factor 2/metabolism-
dc.subject.MESHOxidative Stress/physiology-
dc.subject.MESHRNA-Binding Proteins/metabolism*-
dc.subject.MESHSequestosome-1 Protein/metabolism*-
dc.subject.MESHTunicamycin/pharmacology-
dc.titlep62/SQSTM1 is required for the protection against endoplasmic reticulum stress-induced apoptotic cell death-
dc.typeArticle-
dc.publisher.locationEngland-
dc.contributor.collegeCollege of Medicine-
dc.contributor.departmentDept. of Life Science-
dc.contributor.googleauthorJeong Su Park-
dc.contributor.googleauthorSue Young Oh-
dc.contributor.googleauthorDa Hyun Lee-
dc.contributor.googleauthorYu Seol Lee-
dc.contributor.googleauthorSu Haeng Sung-
dc.contributor.googleauthorHye Won Ji-
dc.contributor.googleauthorMoon Joo Lee-
dc.contributor.googleauthorYong-ho Lee-
dc.contributor.googleauthorSue Goo Rhee-
dc.contributor.googleauthorSoo Han Bae-
dc.identifier.doi10.1080/10715762.2016.1253073-
dc.contributor.localIdA01645-
dc.contributor.localIdA01798-
dc.contributor.localIdA02847-
dc.contributor.localIdA02989-
dc.relation.journalcodeJ00907-
dc.identifier.eissn1029-2470-
dc.identifier.pmid27780373-
dc.identifier.urlhttp://www.tandfonline.com/doi/abstract/10.1080/10715762.2016.1253073-
dc.subject.keywordER stress-
dc.subject.keywordKeap1-
dc.subject.keywordNrf2-
dc.subject.keywordTunicamycin-
dc.subject.keywordautophagy-
dc.subject.keywordp62-
dc.contributor.alternativeNamePark, Jeong Su-
dc.contributor.alternativeNameBae, Soo Han-
dc.contributor.alternativeNameRhee, Sue Goo-
dc.contributor.alternativeNameLee, Yong Ho-
dc.contributor.affiliatedAuthorPark, Jeong Su-
dc.contributor.affiliatedAuthorBae, Soo Han-
dc.contributor.affiliatedAuthorRhee, Sue Goo-
dc.contributor.affiliatedAuthorLee, Yong Ho-
dc.citation.volume50-
dc.citation.number12-
dc.citation.startPage1408-
dc.citation.endPage1421-
dc.identifier.bibliographicCitationFREE RADICAL RESEARCH, Vol.50(12) : 1408-1421, 2016-
dc.date.modified2017-10-24-
dc.identifier.rimsid39782-
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 Internal Medicine (내과학교실) > 1. Journal Papers

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