Cited 156 times in
Differential role of glutaredoxin and thioredoxin in metabolic oxidative stress-induced activation of apoptosis signal-regulating kinase 1
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 송재진 | - |
dc.date.accessioned | 2015-07-15T17:17:50Z | - |
dc.date.available | 2015-07-15T17:17:50Z | - |
dc.date.issued | 2003 | - |
dc.identifier.issn | 0264-6021 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/114625 | - |
dc.description.abstract | Redox-sensing molecules such as thioredoxin (TRX) and glutaredoxin (GRX) bind to apoptosis signal-regulating kinase 1 (ASK1) and suppress its activation. Glucose deprivation disrupted the interaction between TRX/GRX and ASK1 and subsequently activated the ASK1-stress-activated protein kinase/extracellular-signal-regulated kinase kinase-c-Jun N-terminal kinase 1 (JNK1) signal-transduction pathway. L-Buthionine-( S, R )-sulphoximine, which decreases intracellular glutathione content, enhanced glucose deprivation-induced activation of JNK1 by promoting the dissociation of TRX, but not GRX, from ASK1. Treatment of cells with exogenous glutathione disulphide ester resulted in the dissociation of GRX, but not TRX, from ASK1 and the subsequent activation of JNK1. Nonetheless, overexpression of calatase, an H(2)O(2) scavenger, inhibited JNK1 activation and cytotoxicity as well as the dissociation of TRX and GRX from ASK1 during combined glucose deprivation and L-buthionine-( S, R )-sulphoximine treatment. Taken together, glucose deprivation-induced metabolic oxidative stress may activate ASK1 through two different pathways: glutathione-dependent GRX-ASK1 and glutathione-independent TRX-ASK1 pathways. | - |
dc.description.statementOfResponsibility | open | - |
dc.format.extent | 845~853 | - |
dc.relation.isPartOf | BIOCHEMICAL JOURNAL | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.subject.MESH | Adenoviridae/genetics | - |
dc.subject.MESH | Buthionine Sulfoximine/pharmacology | - |
dc.subject.MESH | Catalase/metabolism | - |
dc.subject.MESH | Enzyme Activation | - |
dc.subject.MESH | Genetic Vectors | - |
dc.subject.MESH | Glucose/metabolism | - |
dc.subject.MESH | Glutaredoxins | - |
dc.subject.MESH | Humans | - |
dc.subject.MESH | MAP Kinase Kinase Kinase 5 | - |
dc.subject.MESH | MAP Kinase Kinase Kinases/metabolism* | - |
dc.subject.MESH | Male | - |
dc.subject.MESH | Oxidative Stress* | - |
dc.subject.MESH | Oxidoreductases* | - |
dc.subject.MESH | Proteins/physiology* | - |
dc.subject.MESH | Thioredoxins/metabolism* | - |
dc.subject.MESH | Tumor Cells, Cultured | - |
dc.title | Differential role of glutaredoxin and thioredoxin in metabolic oxidative stress-induced activation of apoptosis signal-regulating kinase 1 | - |
dc.type | Article | - |
dc.contributor.college | Researcher Institutes (부설 연구소) | - |
dc.contributor.department | Institute for Cancer Research (암연구소) | - |
dc.contributor.googleauthor | Jae J Song | - |
dc.contributor.googleauthor | Yong J Lee | - |
dc.identifier.doi | 10.1042/BJ20030275 | - |
dc.admin.author | false | - |
dc.admin.mapping | false | - |
dc.contributor.localId | A02056 | - |
dc.relation.journalcode | J00282 | - |
dc.identifier.eissn | 1470-8728 | - |
dc.identifier.pmid | 12723971 | - |
dc.subject.keyword | apoptosis signal-regulating kinase 1 | - |
dc.subject.keyword | glucose deprivation | - |
dc.subject.keyword | glutaredoxin | - |
dc.subject.keyword | glutathione | - |
dc.subject.keyword | metabolic oxidative stress | - |
dc.subject.keyword | thioredoxin | - |
dc.contributor.alternativeName | Song, Jae Jin | - |
dc.contributor.affiliatedAuthor | Song, Jae Jin | - |
dc.rights.accessRights | free | - |
dc.citation.volume | 373 | - |
dc.citation.number | Pt.3 | - |
dc.citation.startPage | 845 | - |
dc.citation.endPage | 853 | - |
dc.identifier.bibliographicCitation | BIOCHEMICAL JOURNAL, Vol.373(Pt.3) : 845-853, 2003 | - |
dc.identifier.rimsid | 40076 | - |
dc.type.rims | ART | - |
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.