A postsynaptic signaling pathway that may account for the cognitive defect due to IL1RAPL1 mutation

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378050%3A_____%2F10%3A00346778" target="_blank" >RIV/68378050:_____/10:00346778 - isvavai.cz</a>

Result on the web

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DOI - Digital Object Identifier

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Result language

angličtina

Original language name

A postsynaptic signaling pathway that may account for the cognitive defect due to IL1RAPL1 mutation

Original language description

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 regionof the hippocampus. These structural abnormalities are associated with specific deficits in hippocampal long-term synaptic plasticity.

Czech name

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Czech description

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Type

J_x - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)

CEP classification

EB - Genetics and molecular biology

OECD FORD branch

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Project

<a href="/en/project/GA303%2F08%2F1591" target="_blank" >GA303/08/1591: Study of glutamate receptors conformational changes using novel fluorescent techniques</a><br>

Continuities

Z - Vyzkumny zamer (s odkazem do CEZ)

Publication year

2010

Confidentiality

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Name of the periodical

Current Biology

ISSN

0960-9822

e-ISSN

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Volume of the periodical

20

Issue of the periodical within the volume

2

Country of publishing house

GB - UNITED KINGDOM

Number of pages

13

Pages from-to

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UT code for WoS article

000274113900022

EID of the result in the Scopus database

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