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Times Cited: 437
Times Cited
Times Co-cited
Similarity
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Shank3 mutant mice display autistic-like behaviours and striatal dysfunction.
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SHANK proteins: roles at the synapse and in autism spectrum disorder.
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Mutations in the SHANK2 synaptic scaffolding gene in autism spectrum disorder and mental retardation.
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Meta-analysis of SHANK Mutations in Autism Spectrum Disorders: a gradient of severity in cognitive impairments.
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Altered mGluR5-Homer scaffolds and corticostriatal connectivity in a Shank3 complete knockout model of autism.
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Autism-like Deficits in Shank3-Deficient Mice Are Rescued by Targeting Actin Regulators.
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Social deficits in Shank3-deficient mouse models of autism are rescued by histone deacetylase (HDAC) inhibition.
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Adult restoration of Shank3 expression rescues selective autistic-like phenotypes.
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Haploinsufficiency of the autism-associated Shank3 gene leads to deficits in synaptic function, social interaction, and social communication.
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Mutations in the gene encoding the synaptic scaffolding protein SHANK3 are associated with autism spectrum disorders.
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Shank, a novel family of postsynaptic density proteins that binds to the NMDA receptor/PSD-95/GKAP complex and cortactin.
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Genetic and functional analyses of SHANK2 mutations suggest a multiple hit model of autism spectrum disorders.
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From the genetic architecture to synaptic plasticity in autism spectrum disorder.
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Smaller dendritic spines, weaker synaptic transmission, but enhanced spatial learning in mice lacking Shank1.
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NMDA receptor dysfunction in autism spectrum disorders.
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Large-Scale Exome Sequencing Study Implicates Both Developmental and Functional Changes in the Neurobiology of Autism.
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The contribution of de novo coding mutations to autism spectrum disorder.
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Advancing the understanding of autism disease mechanisms through genetics.
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A neuroligin-3 mutation implicated in autism increases inhibitory synaptic transmission in mice.
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Loss of predominant Shank3 isoforms results in hippocampus-dependent impairments in behavior and synaptic transmission.
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Cell-Type-Specific Shank2 Deletion in Mice Leads to Differential Synaptic and Behavioral Phenotypes.
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Mutations of the X-linked genes encoding neuroligins NLGN3 and NLGN4 are associated with autism.
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Mice with Shank3 Mutations Associated with ASD and Schizophrenia Display Both Shared and Distinct Defects.
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Identification and functional characterization of rare SHANK2 variants in schizophrenia.
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The emerging role of SHANK genes in neuropsychiatric disorders.
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Postsynaptic ProSAP/Shank scaffolds in the cross-hair of synaptopathies.
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Coupling of mGluR/Homer and PSD-95 complexes by the Shank family of postsynaptic density proteins.
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SHANK3 overexpression causes manic-like behaviour with unique pharmacogenetic properties.
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Shank synaptic scaffold proteins: keys to understanding the pathogenesis of autism and other synaptic disorders.
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Functional impact of global rare copy number variation in autism spectrum disorders.
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Amelioration of autism-like social deficits by targeting histone methyltransferases EHMT1/2 in Shank3-deficient mice.
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SHANK2 mutations associated with autism spectrum disorder cause hyperconnectivity of human neurons.
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Dysfunctional cerebellar Purkinje cells contribute to autism-like behaviour in Shank2-deficient mice.
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Sociability and preference for social novelty in five inbred strains: an approach to assess autistic-like behavior in mice.
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Co-cited is the co-citation frequency, indicating how many articles cite the article together with the query article. Similarity is the co-citation as percentage of the times cited of the query article or the article in the search results, whichever is the lowest. These numbers are calculated for the last 100 citations when articles are cited more than 100 times.