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Nitric oxide negatively regulates c-Jun N-terminal kinase/stress-activated protein kinase by means of S-nitrosylation.

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dc.contributor.authorPark, HS-
dc.contributor.authorHuh, SH-
dc.contributor.authorKim, MS-
dc.contributor.authorLee, SH-
dc.contributor.authorChoi, EJ-
dc.date.accessioned2011-07-27-
dc.date.available2011-07-27-
dc.date.issued2000-
dc.identifier.issn0027-8424-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/3611-
dc.description.abstractNO, produced from l-arginine in a reaction catalyzed by NO synthase, is an endogenous free radical with multiple functions in mammalian cells. Here, we demonstrate that endogenously produced NO can suppress c-Jun N-terminal kinase (JNK) activation in intact cells. Treatment of BV-2 murine microglial cells with IFN-gamma induced endogenous NO production, concomitantly suppressing JNK1 activation. Similarly, IFN-gamma induced suppression of JNK1 activation in RAW264.7 murine macrophage cells and rat alveolar macrophages. The IFN-gamma-induced suppression of JNK1 activation in BV-2, RAW264.7, or rat alveolar macrophage cells was completely prevented by N(G)-nitro-l-arginine, a NO synthase inhibitor. Interestingly, the IFN-gamma-induced suppression of JNK1 activation was not affected by 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one, an inhibitor of guanylyl cyclase. 8-Bromo-cGMP, a membrane-permeant analogue of cGMP, did not change JNK1 activation in intact cells either. In contrast, S-nitro-N-acetyl-dl-penicillamine (SNAP), a NO donor, inhibited JNK1 activity in vitro. Furthermore, a thiol reducing agent, DTT, reversed not only the in vitro inhibition of JNK1 activity by SNAP but also the in vivo suppression of JNK1 activity by IFN-gamma. Substitution of serine for cysteine-116 in JNK1 abolished the inhibitory effect of IFN-gamma or SNAP on JNK1 activity in vivo or in vitro, respectively. Moreover, IFN-gamma enhanced endogenous S-nitrosylation of JNK1 in RAW264.7 cells. Collectively, our data suggest that endogenous NO mediates the IFN-gamma-induced suppression of JNK1 activation in macrophage cells by means of a thiol-redox mechanism.-
dc.language.isoen-
dc.subject.MESHAnimals-
dc.subject.MESHCell Line-
dc.subject.MESHCells, Cultured-
dc.subject.MESHCyclic GMP-
dc.subject.MESHCysteine-
dc.subject.MESHEnzyme Activation-
dc.subject.MESHHumans-
dc.subject.MESHInterferon-gamma-
dc.subject.MESHJNK Mitogen-Activated Protein Kinases-
dc.subject.MESHMAP Kinase Kinase 4-
dc.subject.MESHMAP Kinase Kinase Kinase 1-
dc.subject.MESHMacrophages-
dc.subject.MESHMale-
dc.subject.MESHMice-
dc.subject.MESHMitogen-Activated Protein Kinase 8-
dc.subject.MESHMitogen-Activated Protein Kinase Kinases-
dc.subject.MESHMitogen-Activated Protein Kinases-
dc.subject.MESHNitric Oxide-
dc.subject.MESHNitric Oxide Donors-
dc.subject.MESHOxidation-Reduction-
dc.subject.MESHPenicillamine-
dc.subject.MESHProtein-Serine-Threonine Kinases-
dc.subject.MESHRats-
dc.subject.MESHRats, Sprague-Dawley-
dc.subject.MESHSulfhydryl Compounds-
dc.titleNitric oxide negatively regulates c-Jun N-terminal kinase/stress-activated protein kinase by means of S-nitrosylation.-
dc.typeArticle-
dc.identifier.pmid11121042-
dc.identifier.urlhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC18927/-
dc.contributor.affiliatedAuthor이, 수환-
dc.type.localJournal Papers-
dc.identifier.doi10.1073/pnas.97.26.14382-
dc.citation.titleProceedings of the National Academy of Sciences of the United States of America-
dc.citation.volume97-
dc.citation.number26-
dc.citation.date2000-
dc.citation.startPage14382-
dc.citation.endPage14387-
dc.identifier.bibliographicCitationProceedings of the National Academy of Sciences of the United States of America, 97(26). : 14382-14387, 2000-
dc.identifier.eissn1091-6490-
dc.relation.journalidJ000278424-
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Journal Papers > School of Medicine / Graduate School of Medicine > Physiology
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