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• W2905295282 abstract "Autism spectrum disorders (ASDs) include a variety of developmental brain disorders with clinical findings implicating the dysfunction of the left hemisphere. Here, we generate mice lacking one copy of Sh3rf2, which was detected in ASD patients, to determine whether Sh3rf2 is involved in brain development and whether mutation of SH3RF2 is causative for ASD and the mechanisms linking it to ASD traits. We find that mice with Sh3rf2 haploinsufficiency display significant deficits in social interaction and communication, as well as stereotyped or repetitive behaviors and hyperactivity and seizures. Disturbances in hippocampal dendritic spine development, aberrant composition of glutamatergic receptor subunits, and abnormal excitatory synaptic transmission were detected in heterozygous mutants. Remarkably, these defects are selectively unilateral. Our results support a notion that Sh3rf2 haploinsufficiency is a highly penetrant risk factor for ASD, with disease pathogenesis most likely resulting from deficits in synaptic function in the left hemisphere of the brain." @default.
• W2905295282 created "2018-12-22" @default.
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• W2905295282 date "2018-12-01" @default.
• W2905295282 modified "2023-10-17" @default.
• W2905295282 title "Sh3rf2 Haploinsufficiency Leads to Unilateral Neuronal Development Deficits and Autistic-Like Behaviors in Mice" @default.
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• W2905295282 doi "https://doi.org/10.1016/j.celrep.2018.11.044" @default.
• W2905295282 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30540932" @default.
• W2905295282 hasPublicationYear "2018" @default.
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