The association of GPR85 with PSD-95-neuroligin complex and autism spectrum disorder: a molecular analysis / Eriko FUJITA-JIMBO in Molecular Autism, (March 2015)  

Public ISBD [article]  inMolecular Autism > (March 2015) . - p.1-10 Titre : The association of GPR85 with PSD-95-neuroligin complex and autism spectrum disorder: a molecular analysis Type de document : Texte imprimé et/ou numérique Auteurs : Eriko FUJITA-JIMBO, Auteur ; Yuko TANABE, Auteur ; Zhiling YU, Auteur ; Karin KOJIMA, Auteur ; Masato MORI, Auteur ; Hong LI, Auteur ; Sadahiko IWAMOTO, Auteur ; Takanori YAMAGATA, Auteur ; Mariko Y. MOMOI, Auteur ; Takashi MOMOI, Auteur Article en page(s) : p.1-10 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Autism spectrum disorder (ASD) has a complex genetic etiology. Some symptoms and mutated genes, including neuroligin (NLGN), neurexin (NRXN), and SH3 and multiple ankyrin repeat domains protein (SHANK), are shared by schizophrenia and ASD. Little is known about the molecular pathogenesis of ASD. One of the possible molecular pathogenesis is an imbalance of excitatory and inhibitory receptors linked with the NLGN-PSD-95-SHANK complex via postsynaptic density protein/Drosophila disc large tumor suppressor/zonula occludens-1 protein (PDZ) binding. In the present study, we focused on GPR85 as a candidate gene for ASD because the C-terminal amino acid sequence of GPR85 [Thr-Cys-Val-Ile (YCVI)] is classified as a type II PDZ-binding motif, and GPR85 is a risk factor for schizophrenia. GPR85 is an orphan receptor that regulates neural and synaptic plasticity and modulates diverse behaviors, including learning and memory. While searching for molecules that associate with GPR85, we found that GPR85 was associated with postsynaptic density protein (PSD)-95 linked with NLGN in the brain. En ligne : http://dx.doi.org/10.1186/s13229-015-0012-5 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=277 [article] The association of GPR85 with PSD-95-neuroligin complex and autism spectrum disorder: a molecular analysis [Texte imprimé et/ou numérique] / Eriko FUJITA-JIMBO, Auteur ; Yuko TANABE, Auteur ; Zhiling YU, Auteur ; Karin KOJIMA, Auteur ; Masato MORI, Auteur ; Hong LI, Auteur ; Sadahiko IWAMOTO, Auteur ; Takanori YAMAGATA, Auteur ; Mariko Y. MOMOI, Auteur ; Takashi MOMOI, Auteur . - p.1-10. Langues : Anglais (eng) in Molecular Autism > (March 2015) . - p.1-10 Index. décimale : PER Périodiques Résumé : Autism spectrum disorder (ASD) has a complex genetic etiology. Some symptoms and mutated genes, including neuroligin (NLGN), neurexin (NRXN), and SH3 and multiple ankyrin repeat domains protein (SHANK), are shared by schizophrenia and ASD. Little is known about the molecular pathogenesis of ASD. One of the possible molecular pathogenesis is an imbalance of excitatory and inhibitory receptors linked with the NLGN-PSD-95-SHANK complex via postsynaptic density protein/Drosophila disc large tumor suppressor/zonula occludens-1 protein (PDZ) binding. In the present study, we focused on GPR85 as a candidate gene for ASD because the C-terminal amino acid sequence of GPR85 [Thr-Cys-Val-Ile (YCVI)] is classified as a type II PDZ-binding motif, and GPR85 is a risk factor for schizophrenia. GPR85 is an orphan receptor that regulates neural and synaptic plasticity and modulates diverse behaviors, including learning and memory. While searching for molecules that associate with GPR85, we found that GPR85 was associated with postsynaptic density protein (PSD)-95 linked with NLGN in the brain. En ligne : http://dx.doi.org/10.1186/s13229-015-0012-5 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=277

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