Promoter hypermethylation of the phosphatase DUSP22 mediates PKA-dependent TAU phosphorylation and CREB activation in Alzheimer's disease

Genetic screening in Alzheimer's disease (AD) has identified only a handful of genes that are mutated in the disorder. Thus, for a very large proportion of patients, the biology of their disease is poorly understood. Epigenetic alterations may provide an explanation in these cases. Using DNA me...

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Detalles Bibliográficos
Autores: Sanchez-Mut, Jose Vicente, Aso Pérez, Ester, Heyn, Holger, Matsuda, Tadashi, Bock, Christoph, Ferrer, Isidro (Ferrer Abizanda), Esteller, Manel
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2014
País:España
Institución:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
Repositorio:Recercat. Dipósit de la Recerca de Catalunya
OAI Identifier:oai:recercat.cat:2445/111024
Acceso en línea:https://hdl.handle.net/2445/111024
Access Level:acceso abierto
Palabra clave:Epigènesi
Metilació
ADN
Hipocamp (Cervell)
Malaltia d'Alzheimer
Malalties neurodegeneratives
Epigenesis
Methylation
DNA
Hippocampus (Brain)
Alzheimer's disease
Neurodegenerative Diseases
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spelling Promoter hypermethylation of the phosphatase DUSP22 mediates PKA-dependent TAU phosphorylation and CREB activation in Alzheimer's diseaseSanchez-Mut, Jose VicenteAso Pérez, EsterHeyn, HolgerMatsuda, TadashiBock, ChristophFerrer, Isidro (Ferrer Abizanda)Esteller, ManelEpigènesiMetilacióADNHipocamp (Cervell)Malaltia d'AlzheimerMalalties neurodegenerativesEpigenesisMethylationDNAHippocampus (Brain)Alzheimer's diseaseNeurodegenerative DiseasesGenetic screening in Alzheimer's disease (AD) has identified only a handful of genes that are mutated in the disorder. Thus, for a very large proportion of patients, the biology of their disease is poorly understood. Epigenetic alterations may provide an explanation in these cases. Using DNA methylation profiles of human hippocampus from controls and patients, we have identified the presence of promoter hypermethylation of the dual-specificity phosphatase 22 (DUSP22) gene in AD. DUSP22 is a likely candidate gene for involvement in the pathogenesis of the disorder since, as we demonstrate here, it inhibits PKA activity and thereby determines TAU phosphorylation status and CREB signaling.Wiley2017201720142017info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersion6 p.application/pdfhttps://hdl.handle.net/2445/111024Articles publicats en revistes (Ciències Fisiològiques)reponame:Recercat. Dipósit de la Recerca de Catalunyainstname:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)InglésReproducció del document publicat a: https://doi.org/10.1002/hipo.22245Hippocampus, 2014, vol. 24, num. 4, p. 363-368https://doi.org/10.1002/hipo.22245cc by-nc-nd (c) Sánchez-Mut et al., 2014http://creativecommons.org/licenses/by-nc-nd/3.0/info:eu-repo/semantics/openAccessoai:recercat.cat:2445/1110242026-05-29T05:05:01Z
dc.title.none.fl_str_mv Promoter hypermethylation of the phosphatase DUSP22 mediates PKA-dependent TAU phosphorylation and CREB activation in Alzheimer's disease
title Promoter hypermethylation of the phosphatase DUSP22 mediates PKA-dependent TAU phosphorylation and CREB activation in Alzheimer's disease
spellingShingle Promoter hypermethylation of the phosphatase DUSP22 mediates PKA-dependent TAU phosphorylation and CREB activation in Alzheimer's disease
Sanchez-Mut, Jose Vicente
Epigènesi
Metilació
ADN
Hipocamp (Cervell)
Malaltia d'Alzheimer
Malalties neurodegeneratives
Epigenesis
Methylation
DNA
Hippocampus (Brain)
Alzheimer's disease
Neurodegenerative Diseases
title_short Promoter hypermethylation of the phosphatase DUSP22 mediates PKA-dependent TAU phosphorylation and CREB activation in Alzheimer's disease
title_full Promoter hypermethylation of the phosphatase DUSP22 mediates PKA-dependent TAU phosphorylation and CREB activation in Alzheimer's disease
title_fullStr Promoter hypermethylation of the phosphatase DUSP22 mediates PKA-dependent TAU phosphorylation and CREB activation in Alzheimer's disease
title_full_unstemmed Promoter hypermethylation of the phosphatase DUSP22 mediates PKA-dependent TAU phosphorylation and CREB activation in Alzheimer's disease
title_sort Promoter hypermethylation of the phosphatase DUSP22 mediates PKA-dependent TAU phosphorylation and CREB activation in Alzheimer's disease
dc.creator.none.fl_str_mv Sanchez-Mut, Jose Vicente
Aso Pérez, Ester
Heyn, Holger
Matsuda, Tadashi
Bock, Christoph
Ferrer, Isidro (Ferrer Abizanda)
Esteller, Manel
author Sanchez-Mut, Jose Vicente
author_facet Sanchez-Mut, Jose Vicente
Aso Pérez, Ester
Heyn, Holger
Matsuda, Tadashi
Bock, Christoph
Ferrer, Isidro (Ferrer Abizanda)
Esteller, Manel
author_role author
author2 Aso Pérez, Ester
Heyn, Holger
Matsuda, Tadashi
Bock, Christoph
Ferrer, Isidro (Ferrer Abizanda)
Esteller, Manel
author2_role author
author
author
author
author
author
dc.subject.none.fl_str_mv Epigènesi
Metilació
ADN
Hipocamp (Cervell)
Malaltia d'Alzheimer
Malalties neurodegeneratives
Epigenesis
Methylation
DNA
Hippocampus (Brain)
Alzheimer's disease
Neurodegenerative Diseases
topic Epigènesi
Metilació
ADN
Hipocamp (Cervell)
Malaltia d'Alzheimer
Malalties neurodegeneratives
Epigenesis
Methylation
DNA
Hippocampus (Brain)
Alzheimer's disease
Neurodegenerative Diseases
description Genetic screening in Alzheimer's disease (AD) has identified only a handful of genes that are mutated in the disorder. Thus, for a very large proportion of patients, the biology of their disease is poorly understood. Epigenetic alterations may provide an explanation in these cases. Using DNA methylation profiles of human hippocampus from controls and patients, we have identified the presence of promoter hypermethylation of the dual-specificity phosphatase 22 (DUSP22) gene in AD. DUSP22 is a likely candidate gene for involvement in the pathogenesis of the disorder since, as we demonstrate here, it inhibits PKA activity and thereby determines TAU phosphorylation status and CREB signaling.
publishDate 2014
dc.date.none.fl_str_mv 2014
2017
2017
2017
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv https://hdl.handle.net/2445/111024
url https://hdl.handle.net/2445/111024
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv Reproducció del document publicat a: https://doi.org/10.1002/hipo.22245
Hippocampus, 2014, vol. 24, num. 4, p. 363-368
https://doi.org/10.1002/hipo.22245
dc.rights.none.fl_str_mv cc by-nc-nd (c) Sánchez-Mut et al., 2014
http://creativecommons.org/licenses/by-nc-nd/3.0/
info:eu-repo/semantics/openAccess
rights_invalid_str_mv cc by-nc-nd (c) Sánchez-Mut et al., 2014
http://creativecommons.org/licenses/by-nc-nd/3.0/
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 6 p.
application/pdf
dc.publisher.none.fl_str_mv Wiley
publisher.none.fl_str_mv Wiley
dc.source.none.fl_str_mv Articles publicats en revistes (Ciències Fisiològiques)
reponame:Recercat. Dipósit de la Recerca de Catalunya
instname:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
instname_str Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
reponame_str Recercat. Dipósit de la Recerca de Catalunya
collection Recercat. Dipósit de la Recerca de Catalunya
repository.name.fl_str_mv
repository.mail.fl_str_mv
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