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pubmed-article:15755516pubmed:abstractTextNF-kappaB is a nuclear transcription factor involved in the control of fundamental cellular functions including cell survival. Among the many target genes of this factor, both pro- and anti-apoptotic genes have been described. To evaluate the contribution of NF-kappaB activation to excitotoxic insult, we analysed the effect of IkappaBalpha (IkappaBalpha) phosphorylation blockade on glutamate-induced toxicity in adult mouse hippocampal slices. By using immunocytochemical and EMSA techniques, we found that (i) acute exposure of hippocampal slices to NMDA induced nuclear translocation of NF-kappaB, (ii) NMDA-mediated activation of NF-kappaB was prevented by BAY 11-7082, an inhibitor of IkappaBalpha phosphorylation and degradation, and (iii) BAY 11-7082-mediated inhibition of NF-kappaB activation was associated with neuroprotection.lld:pubmed
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pubmed-article:15755516pubmed:dateRevised2006-11-15lld:pubmed
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pubmed-article:15755516pubmed:articleTitleThe inhibitor of I kappa B alpha phosphorylation BAY 11-7082 prevents NMDA neurotoxicity in mouse hippocampal slices.lld:pubmed
pubmed-article:15755516pubmed:affiliationDivision of Pharmacology, Department of Biomedical Sciences and Biotechnologies, Viale Europa, 11, 25123 Brescia, Italy.lld:pubmed
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