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Similarity
SHANK proteins: roles at the synapse and in autism spectrum disorder.
Patricia Monteiro, Guoping Feng. Nat Rev Neurosci 2017
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Shank3 mutant mice display autistic-like behaviours and striatal dysfunction.
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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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The 22q13.3 Deletion Syndrome (Phelan-McDermid Syndrome).
K Phelan, H E McDermid. Mol Syndromol 2012
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Loss of predominant Shank3 isoforms results in hippocampus-dependent impairments in behavior and synaptic transmission.
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Synaptic dysfunction and abnormal behaviors in mice lacking major isoforms of Shank3.
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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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Prospective investigation of autism and genotype-phenotype correlations in 22q13 deletion syndrome and SHANK3 deficiency.
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Mutations of the X-linked genes encoding neuroligins NLGN3 and NLGN4 are associated with autism.
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Molecular characterisation of the 22q13 deletion syndrome supports the role of haploinsufficiency of SHANK3/PROSAP2 in the major neurological symptoms.
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Adult restoration of Shank3 expression rescues selective autistic-like phenotypes.
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Prevalence of SHANK3 variants in patients with different subtypes of autism spectrum disorders.
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Mutations in the SHANK2 synaptic scaffolding gene in autism spectrum disorder and mental retardation.
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Disruption of the ProSAP2 gene in a t(12;22)(q24.1;q13.3) is associated with the 22q13.3 deletion syndrome.
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De novo mutations in the gene encoding the synaptic scaffolding protein SHANK3 in patients ascertained for schizophrenia.
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Autism-like Deficits in Shank3-Deficient Mice Are Rescued by Targeting Actin Regulators.
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Delineation of the genetic and clinical spectrum of Phelan-McDermid syndrome caused by SHANK3 point mutations.
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Molecular mechanisms generating and stabilizing terminal 22q13 deletions in 44 subjects with Phelan/McDermid syndrome.
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Mice with Shank3 Mutations Associated with ASD and Schizophrenia Display Both Shared and Distinct Defects.
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SHANK3 haploinsufficiency: a "common" but underdiagnosed highly penetrant monogenic cause of autism spectrum disorders.
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De novo mutations revealed by whole-exome sequencing are strongly associated with autism.
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Autistic-like social behaviour in Shank2-mutant mice improved by restoring NMDA receptor function.
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Shank3-mutant mice lacking exon 9 show altered excitation/inhibition balance, enhanced rearing, and spatial memory deficit.
Jiseok Lee, Changuk Chung, Seungmin Ha, Dongmin Lee, Do-Young Kim, Hyun Kim, Eunjoon Kim. Front Cell Neurosci 2015
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SHANK3 and IGF1 restore synaptic deficits in neurons from 22q13 deletion syndrome patients.
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Social deficits in Shank3-deficient mouse models of autism are rescued by histone deacetylase (HDAC) inhibition.
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SHANK3 gene mutations associated with autism facilitate ligand binding to the Shank3 ankyrin repeat region.
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Coupling of mGluR/Homer and PSD-95 complexes by the Shank family of postsynaptic density proteins.
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Brain region-specific disruption of Shank3 in mice reveals a dissociation for cortical and striatal circuits in autism-related behaviors.
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Pharmacological enhancement of mGlu5 receptors rescues behavioral deficits in SHANK3 knock-out mice.
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Autism-Associated Insertion Mutation (InsG) of Shank3 Exon 21 Causes Impaired Synaptic Transmission and Behavioral Deficits.
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Sporadic autism exomes reveal a highly interconnected protein network of de novo mutations.
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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.