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http://purl.uniprot.org/citations/17495071http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/17495071http://www.w3.org/2000/01/rdf-schema#comment"The aim of the present study was to investigate whether K(V)3.4 channel subunits are involved in neuronal death induced by neurotoxic beta-amyloid peptides (Abeta). In particular, to test this hypothesis, three main questions were addressed: 1) whether the Abeta peptide can up-regulate both the transcription/translation and activity of K(V)3.4 channel subunit and its accessory subunit, MinK-related peptide 2 (MIRP2); 2) whether the increase in K(V)3.4 expression and activity can be mediated by the nuclear factor-kappaB (NF-kappaB) family of transcriptional factors; and 3) whether the specific inhibition of K(V)3.4 channel subunit reverts the Abeta peptide-induced neurodegeneration in hippocampal neurons and nerve growth factor (NGF)-differentiated PC-12 cells. We found that Abeta(1-42) treatment induced an increase in K(V)3.4 and MIRP2 transcripts and proteins, detected by reverse transcription-polymerase chain reaction and Western blot analysis, respectively, in NGF-differentiated PC-12 cells and hippocampal neurons. Patch-clamp experiments performed in whole-cell configuration revealed that the Abeta peptide caused an increase in I(A) current amplitude carried by K(V)3.4 channel subunits, as revealed by their specific blockade with blood depressing substance-I (BDS-I) in both hippocampal neurons and NGF-differentiated PC-12 cells. The inhibition of NF-kappaB nuclear translocation with the cell membrane-permeable peptide SN-50 prevented the increase in K(V)3.4 protein and transcript expression. In addition, the SN-50 peptide was able to block Abeta(1-42)-induced increase in K(V)3.4 K(+) currents and to prevent cell death caused by Abeta(1-42) exposure. Finally, BDS-I produced a similar neuroprotective effect by inhibiting the increase in K(V)3.4 expression. As a whole, our data indicate that K(V)3.4 channels could be a novel target for Alzheimer's disease pharmacological therapy."xsd:string
http://purl.uniprot.org/citations/17495071http://purl.org/dc/terms/identifier"doi:10.1124/mol.107.034868"xsd:string
http://purl.uniprot.org/citations/17495071http://purl.uniprot.org/core/author"Adornetto A."xsd:string
http://purl.uniprot.org/citations/17495071http://purl.uniprot.org/core/author"Annunziato L."xsd:string
http://purl.uniprot.org/citations/17495071http://purl.uniprot.org/core/author"Boscia F."xsd:string
http://purl.uniprot.org/citations/17495071http://purl.uniprot.org/core/author"Scorziello A."xsd:string
http://purl.uniprot.org/citations/17495071http://purl.uniprot.org/core/author"Taglialatela M."xsd:string
http://purl.uniprot.org/citations/17495071http://purl.uniprot.org/core/author"Castaldo P."xsd:string
http://purl.uniprot.org/citations/17495071http://purl.uniprot.org/core/author"Di Renzo G.F."xsd:string
http://purl.uniprot.org/citations/17495071http://purl.uniprot.org/core/author"Pannaccione A."xsd:string
http://purl.uniprot.org/citations/17495071http://purl.uniprot.org/core/author"Sirabella R."xsd:string
http://purl.uniprot.org/citations/17495071http://purl.uniprot.org/core/date"2007"xsd:gYear
http://purl.uniprot.org/citations/17495071http://purl.uniprot.org/core/name"Mol Pharmacol"xsd:string
http://purl.uniprot.org/citations/17495071http://purl.uniprot.org/core/pages"665-673"xsd:string
http://purl.uniprot.org/citations/17495071http://purl.uniprot.org/core/title"Up-regulation and increased activity of KV3.4 channels and their accessory subunit MinK-related peptide 2 induced by amyloid peptide are involved in apoptotic neuronal death."xsd:string
http://purl.uniprot.org/citations/17495071http://purl.uniprot.org/core/volume"72"xsd:string
http://purl.uniprot.org/citations/17495071http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/17495071
http://purl.uniprot.org/citations/17495071http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/17495071
http://purl.uniprot.org/uniprot/#_A6HUU1-mappedCitation-17495071http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/17495071
http://purl.uniprot.org/uniprot/#_Q63734-mappedCitation-17495071http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/17495071
http://purl.uniprot.org/uniprot/#_Q2N1I1-mappedCitation-17495071http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/17495071
http://purl.uniprot.org/uniprot/#_Q6IAE6-mappedCitation-17495071http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/17495071
http://purl.uniprot.org/uniprot/#_Q9Y6H6-mappedCitation-17495071http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/17495071
http://purl.uniprot.org/uniprot/A6HUU1http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/17495071