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Inhibition of apoptosis signal-regulating kinase 1 by nitric oxide through a thiol redox mechanism

DC Field Value Language
dc.contributor.author유제욱-
dc.date.accessioned2015-07-14T17:30:00Z-
dc.date.available2015-07-14T17:30:00Z-
dc.date.issued2004-
dc.identifier.issn0021-9258-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/113006-
dc.description.abstractNitric oxide is an endogenous thiol-reactive molecule that modulates the functions of many regulatory proteins by a thiol-redox mechanism. NO has now been shown to inhibit the activation of apoptosis signal-regulating kinase 1 (ASK1) in murine fibrosarcoma L929 cells through such a mechanism. Exposure of L929 cells to interferon-gamma resulted in the endogenous production of NO and in inhibition of the activation of ASK1 by hydrogen peroxide. The interferon-gamma-induced inhibition of ASK1 activity was blocked by N(G)-nitro-l-arginine, an inhibitor of NO synthase. Furthermore, the NO donor S-nitro-N-acetyl-dl-penicillamine (SNAP) inhibited ASK1 activity in vitro, and this inhibition was reversed by thiol-reducing agents such as dithiothreitol and beta-mercaptoethanol. SNAP did not inhibit the kinase activities of MKK3, MKK6, or p38 in vitro. The inhibition of ASK1 by interferon-gamma was not changed by 1H- (1,2,4)oxadiazolo[4,3-alpha]quinoxalin-1-one, an inhibitor of guanylyl cyclase nor was it mimicked by 8-bromo-cyclic GMP. Site-directed mutagenesis revealed that replacement of cysteine 869 of ASK1 by serine rendered this protein resistant to the inhibitory effects both of interferon-gamma in intact cells and of SNAP in vitro. Co-immunoprecipitation data showed that NO production inhibited a binding of ASK1, but not ASK1(C869S), to MKK3 or MKK6. Moreover, interferon-gamma induced the S-nitrosylation of endogenous ASK1 in L929 cells. Together, these results suggest that NO mediates the interferon-gamma-induced inhibition of ASK1 in L929 cells through a thiolredox mechanism.-
dc.description.statementOfResponsibilityopen-
dc.format.extent7584~7590-
dc.relation.isPartOfJOURNAL OF BIOLOGICAL CHEMISTRY-
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.MESHCell Line-
dc.subject.MESHCysteine-
dc.subject.MESHEnzyme Activation/drug effects-
dc.subject.MESHEnzyme Inhibitors/pharmacology*-
dc.subject.MESHFibrosarcoma-
dc.subject.MESHHumans-
dc.subject.MESHHydrogen Peroxide/pharmacology-
dc.subject.MESHInterferon-gamma/pharmacology-
dc.subject.MESHMAP Kinase Kinase Kinase 5-
dc.subject.MESHMAP Kinase Kinase Kinases/antagonists & inhibitors*-
dc.subject.MESHMAP Kinase Kinase Kinases/chemistry-
dc.subject.MESHMAP Kinase Kinase Kinases/genetics-
dc.subject.MESHMice-
dc.subject.MESHMutagenesis, Site-Directed-
dc.subject.MESHNitric Oxide/pharmacology*-
dc.subject.MESHNitric Oxide Donors/pharmacology-
dc.subject.MESHNitric Oxide Synthase/antagonists & inhibitors-
dc.subject.MESHNitroarginine/pharmacology-
dc.subject.MESHOxidation-Reduction-
dc.subject.MESHPenicillamine/analogs & derivatives*-
dc.subject.MESHPenicillamine/pharmacology-
dc.subject.MESHStructure-Activity Relationship-
dc.subject.MESHSulfhydryl Compounds/metabolism*-
dc.subject.MESHTransfection-
dc.subject.MESHTumor Cells, Cultured-
dc.titleInhibition of apoptosis signal-regulating kinase 1 by nitric oxide through a thiol redox mechanism-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Microbiology (미생물학)-
dc.contributor.googleauthorHee-Sae Park-
dc.contributor.googleauthorJe-Wook Yu-
dc.contributor.googleauthorEui-Ju Choi-
dc.contributor.googleauthorKanghyun Ryoo-
dc.contributor.googleauthorSung-Ho Huh-
dc.contributor.googleauthorMi-Sung Kim-
dc.contributor.googleauthorJun-Ho Cho-
dc.identifier.doi10.1074/jbc.M304183200-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA02508-
dc.relation.journalcodeJ01258-
dc.identifier.eissn1083-351X-
dc.identifier.pmid14668338-
dc.contributor.alternativeNameYu, Je Wook-
dc.contributor.affiliatedAuthorYu, Je Wook-
dc.rights.accessRightsfree-
dc.citation.volume279-
dc.citation.number9-
dc.citation.startPage7584-
dc.citation.endPage7590-
dc.identifier.bibliographicCitationJOURNAL OF BIOLOGICAL CHEMISTRY, Vol.279(9) : 7584-7590, 2004-
dc.identifier.rimsid36850-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Microbiology (미생물학교실) > 1. Journal Papers

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