Autistic-like behaviours and hyperactivity in mice lacking ProSAP1/Shank2

[1]  Elodie Ey,et al.  Genetic and Functional Analyses of SHANK2 Mutations Suggest a Multiple Hit Model of Autism Spectrum Disorders , 2012, PLoS genetics.

[2]  S. Scherer,et al.  Inherited and de novo SHANK2 variants associated with autism spectrum disorder impair neuronal morphogenesis and physiology , 2011, Human molecular genetics.

[3]  T. Boeckers,et al.  Postsynaptic ProSAP/Shank scaffolds in the cross-hair of synaptopathies. , 2011, Trends in cell biology.

[4]  A. Beaudet,et al.  Synaptic dysfunction and abnormal behaviors in mice lacking major isoforms of Shank3. , 2011, Human molecular genetics.

[5]  T. Südhof,et al.  An autism‐associated point mutation in the neuroligin cytoplasmic tail selectively impairs AMPA receptor‐mediated synaptic transmission in hippocampus , 2011, The EMBO journal.

[6]  Jacqueline N. Crawley,et al.  Communication Impairments in Mice Lacking Shank1: Reduced Levels of Ultrasonic Vocalizations and Scent Marking Behavior , 2011, PloS one.

[7]  Jacqueline N. Crawley,et al.  Sociability and motor functions in Shank1 mutant mice , 2011, Brain Research.

[8]  R. Huganir,et al.  Excess of de novo deleterious mutations in genes associated with glutamatergic systems in nonsyndromic intellectual disability. , 2011, American journal of human genetics.

[9]  G. Feng,et al.  Shank3 mutant mice display autistic-like behaviours and striatal dysfunction , 2011, Nature.

[10]  D C Blanchard,et al.  Motor and cognitive stereotypies in the BTBR T+tf/J mouse model of autism , 2011, Genes, brain, and behavior.

[11]  T. Bourgeron,et al.  Behavioral profiles of mouse models for autism spectrum disorders , 2011, Autism research : official journal of the International Society for Autism Research.

[12]  J. N. Crawley,et al.  Unusual repertoire of vocalizations in adult BTBR T+tf/J mice during three types of social encounters , 2011, Genes, brain, and behavior.

[13]  Michael R Kreutz,et al.  Concerted action of zinc and ProSAP/Shank in synaptogenesis and synapse maturation , 2011, The EMBO journal.

[14]  Mark J. Harris,et al.  Haploinsufficiency of the autism-associated Shank3 gene leads to deficits in synaptic function, social interaction, and social communication , 2010, Molecular autism.

[15]  Thomas Bourgeron,et al.  Key role for gene dosage and synaptic homeostasis in autism spectrum disorders. , 2010, Trends in genetics : TIG.

[16]  Gary D Bader,et al.  Functional impact of global rare copy number variation in autism spectrum disorders , 2010, Nature.

[17]  Ute Moog,et al.  Mutations in the SHANK2 synaptic scaffolding gene in autism spectrum disorder and mental retardation , 2010, Nature Genetics.

[18]  T. Boeckers,et al.  Synaptic Cross-talk between N-Methyl-d-aspartate Receptors and LAPSER1-β-Catenin at Excitatory Synapses* , 2009, The Journal of Biological Chemistry.

[19]  Laurent Mottron,et al.  Novel de novo SHANK3 mutation in autistic patients , 2009, American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics.

[20]  D. Geschwind,et al.  Advances in autism genetics: on the threshold of a new neurobiology , 2008, Nature Reviews Genetics.

[21]  K. Stevens Transgenic and Knockout Models of Neuropsychiatric Disorders. , 2008, The American journal of psychiatry.

[22]  Mark F Bear,et al.  Smaller Dendritic Spines, Weaker Synaptic Transmission, but Enhanced Spatial Learning in Mice Lacking Shank1 , 2008, The Journal of Neuroscience.

[23]  Yiping Shen,et al.  Disruption of neurexin 1 associated with autism spectrum disorder. , 2008, American journal of human genetics.

[24]  Christian R Marshall,et al.  Contribution of SHANK3 mutations to autism spectrum disorder. , 2007, American journal of human genetics.

[25]  Jacqueline Blundell,et al.  A Neuroligin-3 Mutation Implicated in Autism Increases Inhibitory Synaptic Transmission in Mice , 2007, Science.

[26]  R. Jaenisch,et al.  Postnatal Loss of Methyl-CpG Binding Protein 2 in the Forebrain is Sufficient to Mediate Behavioral Aspects of Rett Syndrome in Mice , 2006, Biological Psychiatry.

[27]  Eckart D Gundelfinger,et al.  An Architectural Framework That May Lie at the Core of the Postsynaptic Density , 2006, Science.

[28]  J. Piven,et al.  Automated apparatus for quantitation of social approach behaviors in mice , 2004, Genes, brain, and behavior.

[29]  Dietmar Schmitz,et al.  Presynaptic kainate receptors impart an associative property to hippocampal mossy fiber long-term potentiation , 2003, Nature Neuroscience.

[30]  Thomas Bourgeron,et al.  Mutations of the X-linked genes encoding neuroligins NLGN3 and NLGN4 are associated with autism , 2003, Nature Genetics.

[31]  M. Schachner,et al.  Misguided Axonal Projections, Neural Cell Adhesion Molecule 180 mRNA Upregulation, and Altered Behavior in Mice Deficient for the Close Homolog of L1 , 2002, Molecular and Cellular Biology.

[32]  D. Richter,et al.  Somatostatin Receptor Interacting Protein Defines a Novel Family of Multidomain Proteins Present in Human and Rodent Brain* , 1999, The Journal of Biological Chemistry.

[33]  T. Boeckers,et al.  Proline-Rich Synapse-Associated Protein-1/Cortactin Binding Protein 1 (ProSAP1/CortBP1) Is a PDZ-Domain Protein Highly Enriched in the Postsynaptic Density , 1999, The Journal of Neuroscience.

[34]  E. Fisher,et al.  Behavioral and functional analysis of mouse phenotype: SHIRPA, a proposed protocol for comprehensive phenotype assessment , 1997, Mammalian Genome.

[35]  Thomas Bourgeron,et al.  Mutations in the gene encoding the synaptic scaffolding protein SHANK3 are associated with autism spectrum disorders , 2007, Nature Genetics.

[36]  T. Bourgeron,et al.  Animal Models of Autism , 2006 .

[37]  Bryan Kolb,et al.  Analysis of Behavior in Laboratory Rodents , 1999 .