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A postsynaptic signaling pathway that may account for the cognitive defect due to IL1RAPL1 mutation
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SYSNO ASEP 0346778 Document Type J - Journal Article R&D Document Type Journal Article Subsidiary J Článek ve WOS Title A postsynaptic signaling pathway that may account for the cognitive defect due to IL1RAPL1 mutation Author(s) Pavlowski, A. (FR)
Gianfelice, A. (IT)
Pallotto, M. (IT)
Zanchi, A. (IT)
Vara, H. (IT)
Khelfaoui, M. (FR)
Valnegri, P. (IT)
Rezai, X. (FR)
Bassani, S. (IT)
Brambilla, D. (IT)
Kumpošt, Jiří (UMG-J)
Blahoš, Jaroslav (UMG-J) RID
Roux, M.J. (FR)
Humeau, Y. (FR)
Chelly, J. (FR)
Passafaro, M. (IT)
Giustetto, M. (IT)
Billuart, P. (FR)
Sala, C. (IT)Source Title Current Biology. - : Cell Press - ISSN 0960-9822
Roč. 20, č. 2 (2010), s. 103-115Number of pages 13 s. Language eng - English Country GB - United Kingdom Keywords synaptic plasticity ; hippocampal neurons ; PSD-95 Subject RIV EB - Genetics ; Molecular Biology R&D Projects GA303/08/1591 GA ČR - Czech Science Foundation (CSF) CEZ AV0Z50520514 - UMG-J (2005-2011) UT WOS 000274113900022 DOI 10.1016/j.cub.2009.12.030 Annotation Here we show that IL1RAPL1 is present in dendritic spine where it interacts with PSD-95, a major component of excitatory postsynaptic compartment. Using gain- and loss-of-function experiments in neurons, we demonstrated that IL1RAPL1 regulates the synaptic localization of PSD-95 by controlling c-Jun terminal kinase (JNK) activity and PSD-95 phosphorylation. Mice carrying a null mutation of the mouse Il1rapl1 gene show a reduction of both dendritic spine density and excitatory synapses in the CA1 region of the hippocampus. These structural abnormalities are associated with specific deficits in hippocampal long-term synaptic plasticity. Workplace Institute of Molecular Genetics Contact Nikol Škňouřilová, nikol.sknourilova@img.cas.cz, Tel.: 241 063 217 Year of Publishing 2011
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