http://www.cnr.it/ontology/cnr/individuo/prodotto/ID38763
A postsynaptic signaling pathway that may account for the cognitive defect due to IL1RAPL1 mutation. (Articolo in rivista)
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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
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- 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)
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- ISI Web of Science (WOS) (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
- 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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