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Daniel Rueda
Researcher at Complutense University of Madrid
Publications - 67
Citations - 2836
Daniel Rueda is an academic researcher from Complutense University of Madrid. The author has contributed to research in topics: Lynch syndrome & Microsatellite instability. The author has an hindex of 19, co-authored 60 publications receiving 2493 citations. Previous affiliations of Daniel Rueda include Laboratory of Molecular Biology & University of Lausanne.
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Journal Article
Inhibition of Glioma Growth in Vivo by Selective Activation of the CB2 Cannabinoid Receptor
Cristina Sánchez,María L. de Ceballos,Teresa Gómez del Pulgar,Daniel Rueda,Cesar Corbacho,Guillermo Velasco,Ismael Galve-Roperh,John W. Huffman,Santiago Ramón y Cajal,Manuel Guzmán +9 more
TL;DR: It is shown that local administration of the selective CB(2) agonist JWH-133 at 50 microg/day to Rag-2(-/-) mice induced a considerable regression of malignant tumors generated by inoculation of C6 glioma cells, and showed that selective activation of the CB( 2) receptor signaled apoptosis via enhanced ceramide synthesis de novo.
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The proteolytic activity of the paracaspase MALT1 is key in T cell activation.
Fabien Rebeaud,Stephan Hailfinger,Anita Posevitz-Fejfar,Myriam Tapernoux,Roger Moser,Daniel Rueda,Olivier Gaide,Montserrat Guzzardi,Emanuela M. Iancu,Nathalie Rufer,Nicolas Fasel,Margot Thome +11 more
TL;DR: The proteolytic activity of MALT1 is central to T cell activation, which suggests a possible target for the development of immunomodulatory or anticancer drugs.
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The endocannabinoid anandamide inhibits neuronal progenitor cell differentiation through attenuation of the Rap1/B-Raf/ERK pathway.
TL;DR: The data indicate that endocannabinoids inhibit neuronal progenitor cell differentiation through attenuation of the ERK pathway and suggest that they constitute a new physiological system involved in the regulation of neurogenesis.
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Mechanism of Extracellular Signal-Regulated Kinase Activation by the CB1 Cannabinoid Receptor
TL;DR: In U373 MG human astrocytoma cells, CB(1) receptor activation with the cannabinoid agonist delta(8)-tetrahydrocannabinol dimethyl heptyl (HU-210) was coupled to ERK activation and protection from ceramide-induced apoptosis, and this effect may have important consequences in the control of cell death/survival decision.
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The CB(1) cannabinoid receptor is coupled to the activation of c-Jun N-terminal kinase.
TL;DR: It is shown that Δ9-tetrahydrocannabinol (THC), the major active component of marijuana, induces the activation of c-Jun N-terminal kinase (JNK), and data indicate that activation of JNK and p38 mitogen-activated protein kinase may be responsible for some of the cellular responses elicited by the CB1 cannabinoid receptor.