A postsynaptic signaling pathway that may account for the cognitive defect due to IL1RAPL1 mutation. (Articolo in rivista)

Type
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  • A postsynaptic signaling pathway that may account for the cognitive defect due to IL1RAPL1 mutation. (Articolo in rivista) (literal)
Anno
  • 2010-01-01T00:00:00+01:00 (literal)
Alternative label
  • Pavlowsky A, Gianfelice A, Pallotto M, Zanchi A, Vara H, Khelfaoui M, Valnegri P, Rezai X, Bassani S, Brambilla D, Kumpost J, Blahos J, Roux MJ, Humeau Y, Chelly J, Passafaro M, Giustetto M, Billuart P and Sala C (2010)
    A postsynaptic signaling pathway that may account for the cognitive defect due to IL1RAPL1 mutation.
    in Current biology
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Pavlowsky A, Gianfelice A, Pallotto M, Zanchi A, Vara H, Khelfaoui M, Valnegri P, Rezai X, Bassani S, Brambilla D, Kumpost J, Blahos J, Roux MJ, Humeau Y, Chelly J, Passafaro M, Giustetto M, Billuart P and Sala C (literal)
Pagina inizio
  • 103 (literal)
Pagina fine
  • 115 (literal)
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  • 20 (literal)
Rivista
Note
  • ISI Web of Science (WOS) (literal)
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  • 1Department of Genetics and Development, Institut Cochin, Universite´ Paris Descartes, Centre National de la Recherche Scientifique (CNRS) Unite´ Mixte de Recherche (UMR) 8104, 75014 Paris, France 2Inserm U567, 75014 Paris, France 3CNR Neuroscience Institute and Department of Pharmacology, University of Milan, 20129 Milan, Italy 4National Institute of Neuroscience-Italy and Department of Anatomy, Pharmacology and Forensic Medicine, University of Turin, 10126 Turin, Italy 5Institut des Neurosciences Cellulaires et Inte´ gratives, UPR3212, CNRS, 67084 Strasbourg, France 6Dulbecco Telethon Institute, 20129 Milano, Italy 7Institut de Ge´ ne´ tique et de Biologie Mole´ culaire et Cellulaire-Institut de la Souris (IGBMC-ICS), 1 rue Laurent Fries BP10142, 67404 Illkirch cedex, France 8Department of Human Physiology, University of Milan, 20133 Milan, Italy 9Department of Molecular Pharmacology, Institute of Molecular Genetics AS CR, 142 20 Prague 4, Czech Republic 10Neuromuscular Diseases and Neuroimmunology, Neurological Institute Foundation ''Carlo Besta,'' 20133 Milan, Italy (literal)
Titolo
  • A postsynaptic signaling pathway that may account for the cognitive defect due to IL1RAPL1 mutation. (literal)
Abstract
  • Interleukin-1 receptor accessory protein-like 1 (IL1RAPL1) gene mutations are associated with cognitive impairment ranging from nonsyndromic X-linked mental retardation to autism. IL1RAPL1 belongs to a novel family of Toll/IL- 1 receptors, whose expression in the brain is upregulated by neuronal activity. Currently, very little is known about the function of this protein. We previously showed that IL1RAPL1 interacts with the neuronal calcium sensor NCS-1 and that it regulates voltage-gated calcium channel activity in PC12 cells. Results: 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. (literal)
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