Jamain S

References (4)

Title : The use of a gene expression signature and connectivity map to repurpose drugs for bipolar disorder - Kidnapillai_2018_World.J.Biol.Psychiatry__1
Author(s) : Kidnapillai S , Bortolasci CC , Udawela M , Panizzutti B , Spolding B , Connor T , Sanigorski A , Dean OM , Crowley T , Jamain S , Gray L , Scarr E , Leboyer M , Dean B , Berk M , Walder K
Ref : World J Biological Psychiatry , :1 , 2018
Abstract : OBJECTIVES: To create a gene expression signature (GES) to represent the biological effects of a combination of known drugs for bipolar disorder (BD) on cultured human neuronal cells (NT2-N) and rat brains, which also has evidence of differential expression in individuals with BD. To use the GES to identify new drugs for BD using Connectivity Map (CMap). METHODS: NT2-N (n = 20) cells and rats (n = 8) were treated with a BD drug combination (lithium, valproate, quetiapine and lamotrigine) or vehicle for 24 and 6 h, respectively. Following next-generation sequencing, the differential expression of genes was assessed using edgeR in R. The derived GES was compared to differentially expressed genes in post-mortem brains of individuals with BD. The GES was then used in CMap analysis to identify similarly acting drugs. RESULTS: A total of 88 genes showed evidence of differential expression in response to the drug combination in both models, and therefore comprised the GES. Six of these genes showed evidence of differential expression in post-mortem brains of individuals with BD. CMap analysis identified 10 compounds (camptothecin, chlorambucil, flupenthixol, valdecoxib, rescinnamine, GW-8510, cinnarizine, lomustine, mifepristone and nimesulide) acting similarly to the BD drug combination. CONCLUSIONS: This study shows that GES and CMap can be used as tools to repurpose drugs for BD.
ESTHER : Kidnapillai_2018_World.J.Biol.Psychiatry__1
PubMedSearch : Kidnapillai_2018_World.J.Biol.Psychiatry__1
PubMedID: 29956574

Title : Reduced social interaction and ultrasonic communication in a mouse model of monogenic heritable autism - Jamain_2008_Proc.Natl.Acad.Sci.U.S.A_105_1710
Author(s) : Jamain S , Radyushkin K , Hammerschmidt K , Granon S , Boretius S , Varoqueaux F , Ramanantsoa N , Gallego J , Ronnenberg A , Winter D , Frahm J , Fischer J , Bourgeron T , Ehrenreich H , Brose N
Ref : Proc Natl Acad Sci U S A , 105 :1710 , 2008
Abstract : Autism spectrum conditions (ASCs) are heritable conditions characterized by impaired reciprocal social interactions, deficits in language acquisition, and repetitive and restricted behaviors and interests. In addition to more complex genetic susceptibilities, even mutation of a single gene can lead to ASC. Several such monogenic heritable ASC forms are caused by loss-of-function mutations in genes encoding regulators of synapse function in neurons, including NLGN4. We report that mice with a loss-of-function mutation in the murine NLGN4 ortholog Nlgn4, which encodes the synaptic cell adhesion protein Neuroligin-4, exhibit highly selective deficits in reciprocal social interactions and communication that are reminiscent of ASCs in humans. Our findings indicate that a protein network that regulates the maturation and function of synapses in the brain is at the core of a major ASC susceptibility pathway, and establish Neuroligin-4-deficient mice as genetic models for the exploration of the complex neurobiological disorders in ASCs.
ESTHER : Jamain_2008_Proc.Natl.Acad.Sci.U.S.A_105_1710
PubMedSearch : Jamain_2008_Proc.Natl.Acad.Sci.U.S.A_105_1710
PubMedID: 18227507
Gene_locus related to this paper: mouse-4neur

Title : Neuroligin 2 is exclusively localized to inhibitory synapses - Varoqueaux_2004_Eur.J.Cell.Biol_83_449
Author(s) : Varoqueaux F , Jamain S , Brose N
Ref : European Journal of Cell Biology , 83 :449 , 2004
Abstract : Neuroligins are cell adhesion proteins that are thought to instruct the formation and alignment of synaptic specializations. The three known rodent neuroligin isoforms share homologous extracellular acetylcholinesterase-like domains that bridge the synaptic cleft and bind beta-neurexins. All neuroligins have identical intracellular C-terminal motifs that bind to PDZ domains of various target proteins. Neuroligin 1 is specifically localized to glutamatergic postsynaptic specializations. We show here that neuroligin 2 is exclusively localized to inhibitory synapses in rat brain and dissociated neurons. In immature neurons, neuroligin 2 is found at synapses and also at GABAA receptor aggregates that are not facing presynaptic termini, indicating that postsynaptic mechanisms lead to synaptic recruitment of neuroligin 2. Our findings identify neuroligin 2 as a new cell adhesion protein specific for inhibitory synapses and open new avenues for identifiying the constituents of this unique type of postsynaptic specialization.
ESTHER : Varoqueaux_2004_Eur.J.Cell.Biol_83_449
PubMedSearch : Varoqueaux_2004_Eur.J.Cell.Biol_83_449
PubMedID: 15540461

Title : Mutations of the X-linked genes encoding neuroligins NLGN3 and NLGN4 are associated with autism - Jamain_2003_Nat.Genet_34_27
Author(s) : Jamain S , Quach H , Betancur C , Rastam M , Colineaux C , Gillberg IC , Soderstrom H , Giros B , Leboyer M , Gillberg C , Bourgeron T
Ref : Nat Genet , 34 :27 , 2003
Abstract : Many studies have supported a genetic etiology for autism. Here we report mutations in two X-linked genes encoding neuroligins NLGN3 and NLGN4 in siblings with autism-spectrum disorders. These mutations affect cell-adhesion molecules localized at the synapse and suggest that a defect of synaptogenesis may predispose to autism.
ESTHER : Jamain_2003_Nat.Genet_34_27
PubMedSearch : Jamain_2003_Nat.Genet_34_27
PubMedID: 12669065
Gene_locus related to this paper: human-NLGN2 , human-NLGN4X , human-NLGN4Y , mouse-4neur , human-NLGN3