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Ca2+-mediated activation of c-Jun N-terminal kinase and nuclear factor kappa B by NMDA in cortical cell cultures.

DC Field Value Language
dc.contributor.authorKo, HW-
dc.contributor.authorPark, KY-
dc.contributor.authorKim, H-
dc.contributor.authorHan, PL-
dc.contributor.authorKim, YU-
dc.contributor.authorGwag, BJ-
dc.contributor.authorChoi, EJ-
dc.date.accessioned2011-08-22T05:56:14Z-
dc.date.available2011-08-22T05:56:14Z-
dc.date.issued1998-
dc.identifier.issn0022-3042-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/3885-
dc.description.abstractWe examined the possibility that c-Jun N-terminal kinase (JNK) and nuclear factor kappaB (NF-kappaB) might be involved in intracellular signaling cascades that mediate NMDA-initiated neuronal events. Exposure of cortical neurons to 100 microM NMDA induced activation of JNK within 1 min. Activity of JNK was further increased over the next 5 min and then declined by 30 min. Similarly, ionomycin, a selective Ca2+ ionophore, induced activation of JNK. The NMDA-induced activation of JNK was abrogated in the absence of extracellular Ca2+, suggesting that Ca2+ entry is necessary and sufficient for the JNK activation. Immunohistochemistry with anti-NF-kappaB antibody demonstrated nuclear translocation of NF-kappaB within 5 min following NMDA treatment. NMDA treatment also enhanced the DNA binding activity of nuclear NF-kappaB in a Ca2+-dependent manner. Treatment with 3 mM aspirin blocked the NMDA-induced activation of JNK and NF-kappaB. Neuronal death following a brief exposure to 100 microM NMDA was Ca2+ dependent and attenuated by addition of aspirin or sodium salicylate. The present study suggests that Ca2+ influx is required for NMDA-induced activation of JNK and NF-kappaB as well as NMDA neurotoxicity. This study also implies that aspirin may exert its neuroprotective action against NMDA through blocking the NMDA-induced activation of NF-kappaB and JNK.-
dc.language.isoen-
dc.subject.MESHAnimals-
dc.subject.MESHAspirin-
dc.subject.MESHCalcium-
dc.subject.MESHCalcium-Calmodulin-Dependent Protein Kinases-
dc.subject.MESHCells, Cultured-
dc.subject.MESHCerebral Cortex-
dc.subject.MESHEnzyme Activation-
dc.subject.MESHFetus-
dc.subject.MESHJNK Mitogen-Activated Protein Kinases-
dc.subject.MESHMice-
dc.subject.MESHMitogen-Activated Protein Kinases-
dc.subject.MESHN-Methylaspartate-
dc.subject.MESHNF-kappa B-
dc.titleCa2+-mediated activation of c-Jun N-terminal kinase and nuclear factor kappa B by NMDA in cortical cell cultures.-
dc.typeArticle-
dc.identifier.pmid9751169-
dc.identifier.urlhttp://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0022-3042&date=1998&volume=71&issue=4&spage=1390-
dc.contributor.affiliatedAuthor곽, 병주-
dc.type.localJournal Papers-
dc.citation.titleJournal of neurochemistry-
dc.citation.volume71-
dc.citation.number4-
dc.citation.date1998-
dc.citation.startPage1390-
dc.citation.endPage1395-
dc.identifier.bibliographicCitationJournal of neurochemistry, 71(4). : 1390-1395, 1998-
dc.identifier.eissn1471-4159-
dc.relation.journalidJ000223042-
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Journal Papers > School of Medicine / Graduate School of Medicine > Pharmacology
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