Hyperphosphorylation of tau is mediated by ERK activation during anticancer drug-induced apoptosis in neuroblastoma cells

Guise, S.; Braguer, Diane; Carles, Gérard; Delacourte, André; Briand, Claudette

doi:10.1002/1097-4547(20010201)63:3<257::aid-jnr1019>3.0.co;2-t

Cited by 87 publications

(61 citation statements)

References 42 publications

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“…In contrast, our present results suggest that doxorubicin-induced MEK/ERK signaling is proapoptotic, which agrees with other investigations [14][15][16], and we found that the PI3-K/Akt pathway plays an important role in endothelial cell apoptosis caused by doxorubicin. Of particular interest, our results reveal a previously unreported inhibition of the PI3-K/Akt pathway by p38 MAPK.…”

Section: Doxorubicin-induced P38 Mapk Activation Negatively Regulatessupporting

confidence: 93%

“…3B). These results suggest that ERK signaling is proapoptotic in doxorubicin-treated cells, which agrees with findings reported by other investigators [14][15][16]. It seems that this proapoptotic role of ERK is partly independent of the p38 MAPK pathway.…”

Section: Participation Of Other Map Kinases and Akt In Doxorubicin-insupporting

confidence: 93%

“…The ERK pathway is initiated by mitogenic stimuli, such as growth factors, cytokines, and phorbol esters, and it plays a major role in regulating cell growth and differentiation [13]. However, ERK signaling has been suggested to be proapoptotic in cells undergoing doxorubicininduced apoptosis [14][15][16].…”

Section: Introductionmentioning

confidence: 99%

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p38 MAPK downregulates phosphorylation of Bad in doxorubicin-induced endothelial apoptosis

Grethe¹,

Coltella²,

Pörn-Ares³

2006

Biochemical and Biophysical Research Communications

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Doxorubicin is the anthracycline with the widest spectrum of antitumor activity, and it has been shown that the antitumor activity is mediated in vivo by selective triggering of apoptosis in proliferating endothelial cells. We studied cultured human endothelial cells and observed that doxorubicin-induced apoptosis was mediated by p38 mitogen-activated protein kinase (MAPK). Doxorubicin-provoked apoptosis was significantly inhibited by expression of dominant negative p38 MAPK or pharmacological inhibition with SB203580.Furthermore, blocking phosphatidylinositol-3-kinase/Akt signaling significantly increased doxorubicin-induced caspase-3 activity and cell death, indicating that Akt is a survival factor in this system. Notably, we also found that doxorubicin-provoked apoptosis included p38 MAPK-mediated inhibition of Akt and Bad phosphorylation. Furthermore, doxorubicinstimulated phosphorylation of Bad in cells expressing dominant negative p38 MAPK was impeded by the inhibition of PI3-K. In addition to the impact on Bad phosphorylation, doxorubicin-treatment caused p38 MAPK-dependent downregulation of Bcl-xL protein.

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Section: Doxorubicin-induced P38 Mapk Activation Negatively Regulatessupporting

confidence: 93%

Section: Participation Of Other Map Kinases and Akt In Doxorubicin-insupporting

confidence: 93%

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p38 MAPK downregulates phosphorylation of Bad in doxorubicin-induced endothelial apoptosis

Grethe¹,

Coltella²,

Pörn-Ares³

2006

Biochemical and Biophysical Research Communications

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“…Furthermore, oxidative stress has been shown to activate ERK as a protective mechanism (Guyton et al, 1996;Aikawa et al, 1997;Bhatt et al, 2002). However, a proapoptotic role has been demonstrated for ERK in several studies with different stimuli, including anticancer drugs (Stanciu et al, 2000;Wang et al, 2000;Guise et al, 2001;Xiao and Singh, 2002;Lee et al, 2003;Zhang et al, 2003;Nguyen et al, 2004).…”

Section: Hpr-induced Apoptosis In Hnscc Cellsmentioning

confidence: 99%

N-(4-Hydroxyphenyl)retinamide-induced apoptosis triggered by reactive oxygen species is mediated by activation of MAPKs in head and neck squamous carcinoma cells

et al. 2006

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“…Estos eventos de hiperfosforilación son previos a la formación de estructuras anómalas generadas por la autoagregación de las formas hiperfosforiladas de tau, que forman una red fi lamentosa y compacta. Se ha descrito la hiperfosforilación de tau por acción de diversos estímulos neurotóxicos que, además, inducen apoptosis, como por ejemplo lo que ocurre en animales sometidos a isquemia transciente 46 o por alteración del metabolismo de la glucosa 47 ; en cultivos neuronales tratados con radicales libres 48 , en neuroblastomas tratados con plaquitaxel y doxorubicina (compuestos anticancerígenos) 49 , en neuroblastomas sometidos a estrés hiperosmótico 50 e incluso tratados con inhibidores de la quinasa de supervivencia PI3K 51 . Todos estos hallazgos indican que los eventos de hiperfosforilación de tau, ocurren en la vía de activación del proceso apoptótico, quizás como requerimiento para todos los cambios que ocurren a nivel celular que fi nalizan con la generación de los cuerpos apoptóticos.…”

Section: Hsv-1 Como Factor De Riesgo Asociado Con La Enfermedad De Alunclassified

Herpes simplex virus tipo 1 como factor de riesgo asociado con la enfermedad de Alzheimer

et al. 2011

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Herpes simplex virus tipo 1 L a familia Herpesviridae, se encuentra ampliamente diseminada en la naturaleza. Existen más de 100 tipos diferentes de herpesvirus, los que presentan la misma estructura, ADN lineal de doble hebra dentro de una cápside icosaédrica, rodeada por un tegumento proteico y cubierto por una envoltura lipídica (Figura 1) 1,2 . Una característica que distingue a los herpesvirus, es su capacidad para establecer infecciones persistentes latentes en el hospedero infectado, estado en el cual el genoma viral se encuentra en forma episomal en el núcleo de la célula infectada, con una expresión limitada de genes específi cos para el mantenimiento del estado de latencia (transcritos LAT) y sin producir partículas virales infectivas 3,4 . Este tipo de infección se piensa que constituye una estrategia viral para evadir su detección por parte del sistema inmune. Bajo ciertas condiciones -incluyendo la exposición a radiación UV, estrés emocional, alteración del balance hormonal, depresión del sistema inmunológico, entre otros-se puede interrumpir el estado de latencia, induciendo una reactivación del genoma viral, con la consecuente producción de nuevas partículas virales infectivas que inician la recurrencia del cuadro clínico 1,4 . Sin embargo, los mecanismos celulares y moleculares de este proceso, aún se desconocen en detalle.En base al tipo de célula en que establecen latencia y otras características, los herpesvirus humanos han sido clasificados en distintas

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Hyperphosphorylation of tau is mediated by ERK activation during anticancer drug-induced apoptosis in neuroblastoma cells

Cited by 87 publications

References 42 publications

p38 MAPK downregulates phosphorylation of Bad in doxorubicin-induced endothelial apoptosis

p38 MAPK downregulates phosphorylation of Bad in doxorubicin-induced endothelial apoptosis

N-(4-Hydroxyphenyl)retinamide-induced apoptosis triggered by reactive oxygen species is mediated by activation of MAPKs in head and neck squamous carcinoma cells

Herpes simplex virus tipo 1 como factor de riesgo asociado con la enfermedad de Alzheimer

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