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http://hdl.handle.net/10261/59393
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Campo DC | Valor | Lengua/Idioma |
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dc.contributor.author | Rubio, Alicia | - |
dc.contributor.author | Sánchez-Mut, José V. | - |
dc.contributor.author | García, Esther | - |
dc.contributor.author | Velasquez, Zahady D. | - |
dc.contributor.author | Oliver de la Cruz, Jorge | - |
dc.contributor.author | Esteller, Manel | - |
dc.contributor.author | Ávila, Jesús | - |
dc.date.accessioned | 2012-11-02T13:12:51Z | - |
dc.date.available | 2012-11-02T13:12:51Z | - |
dc.date.issued | 2011 | - |
dc.identifier.citation | Journal of Neuroscience Research 90 (1): 13-20 (2011) | es_ES |
dc.identifier.issn | 1097-4547 | - |
dc.identifier.uri | http://hdl.handle.net/10261/59393 | - |
dc.description.abstract | Beta Amyloid, present in senile plaques, has been related largely to neuronal loss in the brain of patients with Alzheimer’s disease. However, how neurons respond to b amyloid insults is still poorly understood. Here we show that b amyloid increases somatostatin and cortistatin gene expression mainly through an increase in histone 3 lysine 4 methylation (H3K4me3), a modification associated with transcriptional activation. Somatostatin and cortistatin partially decreased b amyloid toxicity in primary cortical neurons in culture. Thus we suggest that neurons respond to b amyloid insults by releasing somatostatin and cortistatin, which will act as a protective agent against b amyloid toxicity. Our results suggest a relevant function for both neuropeptides against b amyloid toxicity, providing new insights into Alzheimer’s disease | es_ES |
dc.description.sponsorship | b Amyloid, present in senile plaques, has been related largely to neuronal loss in the brain of patients with Alzheimer’s disease. However, how neurons respond to b amyloid insults is still poorly understood. Here we show that b amyloid increases somatostatin and cortistatin gene expression mainly through an increase in histone 3 lysine 4 methylation (H3K4me3), a modification associated with transcriptional activation. Somatostatin and cortistatin partially decreased b amyloid toxicity in primary cortical neurons in culture. Thus we suggest that neurons respond to b amyloid insults by releasing somatostatin and cortistatin, which will act as a protective agent against b amyloid toxicity. Our results suggest a relevant function for both neuropeptides against b amyloid toxicity, providing new insights into Alzheimer’s disease | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | John Wiley & Sons | es_ES |
dc.rights | closedAccess | es_ES |
dc.subject | Somatostatin | es_ES |
dc.subject | Amyloid | es_ES |
dc.subject | Neurons | es_ES |
dc.subject | GSK3 | es_ES |
dc.subject | Alzheimer’s disease | es_ES |
dc.subject | Histone methylation | es_ES |
dc.title | Epigenetic Control of Somatostatin and Cortistatin Expression by Beta Amyloid Peptide | es_ES |
dc.type | artículo | es_ES |
dc.identifier.doi | 10.1002/jnr.22731 | - |
dc.description.peerreviewed | Peer reviewed | es_ES |
dc.relation.publisherversion | http://dx.doi.org/10.1002/jnr.22731 | es_ES |
dc.type.coar | http://purl.org/coar/resource_type/c_6501 | es_ES |
item.openairetype | artículo | - |
item.cerifentitytype | Publications | - |
item.languageiso639-1 | en | - |
item.grantfulltext | none | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.fulltext | No Fulltext | - |
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