Autism Rat Models Consortium: Publications
From ARC
Results
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Adult restoration of SHANK3 expression rescues selective autistic-like phenotypes.
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Loss of UBE3A from TH-expressing neurons suppresses GABA co-release and enhances VTA-NAc optical self-stimulation.
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Reciprocal effects on neurocognitive and metabolic phenotypes in mouse models of 16p11.2 deletion and duplication syndromes.
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Layer specific and general requirements for ERK/MAPK signaling in the developing neocortex.
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A highly penetrant form of childhood apraxia of speech due to deletion of 16p11.2.
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Drosophila homolog of human KIF22 at the autism-linked 16p11.2 loci influences synaptic connectivity at larval neuromuscular junctions.
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Rett syndrome: Crossing the threshold to clinical translation.
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Developmental dynamics of Rett syndrome.
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The cellular and molecular landscapes of the developing human central nervous system.
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The role of mGluR copy number variation in genetic and environmental forms of syndromic autism spectrum disorder.
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Increased expression of the PI3K catalytic subunit p110-delta underlies elevated S6 phosphorylation and protein synthesis in an individual with autism from a multiplex family.
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A search for blood biomarkers for autism: Peptoids.
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Reduced GABAergic action in the autistic brain.
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Genome sequencing of autism-affected families reveals disruption of putative noncoding regulatory DNA.
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Mice with Shank3 mutations associated with ASD and schizophrenia display both shared and distinct defects.
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Human iPS cell-derived neurons uncover the impact of increased Ras signaling in Costello syndrome.
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Behavior and sensory interests questionnaire: Validation in a sample of children with autism spectrum disorder and other developmental disability.
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Maternal modifiers and parent-of-origin bias of the autism-associated 16p11.2 CNV.
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Defining the effect of the 16p11.2 duplication on cognition, behavior, and medical comorbidities.
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Disruptive de novo mutations of DYRK1A lead to a syndromic form of autism and ID.
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De novo missense variants in PPP2R5D are associated with intellectual disability, macrocephaly, hypotonia, and autism.
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Expression of CNTNAP2 (CASPR2) in multiple levels of sensory systems.
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BONLAC: A combinatorial proteomic technique to measure stimulus-induced translational profiles in brain slices.
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Mapping sub-second structure in mouse behavior.
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DUF1220 copy number is associated with schizophrenia risk and severity: Implications for understanding autism and schizophrenia as related diseases.
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De novo mutations in congenital heart disease with neurodevelopmental and other congenital anomalies.
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Compromising the phosphodependent regulation of the GABAAR β3 subunit reproduces the core phenotypes of autism spectrum disorders.
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Patterns of risk for multiple co-occurring medical conditions replicate across distinct cohorts of children with autism spectrum disorder.
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7q11.23 duplication syndrome: Physical characteristics and natural history.
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The influence of microdeletions and microduplications of 16p11.2 on global transcription profiles.
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An AKT3-FOXG1-reelin network underlies defective migration in human focal malformations of cortical development.
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7q11.23 duplication syndrome.
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miRNA-target chimeras reveal miRNA 3'-end pairing as a major determinant of Argonaute target specificity.
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Genes, circuits, and precision therapies for autism and related neurodevelopmental disorders.
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Correspondence between resting-state activity and brain gene expression.
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16p11.2 deletion mice display cognitive deficits in touchscreen learning and novelty recognition tasks.
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The autism inpatient collection: Methods and preliminary sample description.
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Atypical visual saliency in autism spectrum disorder quantified through model-based eye tracking.
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Dissociation of locomotor and cerebellar deficits in a murine Angelman syndrome model.
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Female autism phenotypes investigated at different levels of language and developmental abilities.
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Neurons in the human amygdala encode face identity, but not gaze direction.
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EIF4E/FMR1 double mutant mice display cognitive impairment in addition to ASD-like behaviors.
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Perceptual learning in autism: Over-specificity and possible remedies.
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Interactive analysis and assessment of single-cell copy-number variations.
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Thalamic control of sensory selection in divided attention.
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Low load for disruptive mutations in autism genes and their biased transmission.
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Regulatory domain or CpG site variation in SLC12A5, encoding the chloride transporter KCC2, in human autism and schizophrenia.
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Maternal UBE3A loss disrupts sleep homeostasis but leaves circadian rhythmicity largely intact.