ArticleMolecular autism2018
Clustering the autisms using glutamate synapse protein interaction networks from cortical and hippocampal tissue of seven mouse models.
Article in Molecular autism, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- Transcriptomic metaanalyses of autistic brains reveals shared gene expression and biological pathway abnormalities with cancer.Molecular autism · 2019Pooled it
- Genetic Rescue of Disrupted Synaptic Protein Interaction Network Dynamics Following SYNGAP1 Reactivation.Molecular & cellular proteomics : MCP · 2026Article
- Prenatal valproic acid exposure alters striatal proteomic signatures associated with autism spectrum disorder in mice.Translational psychiatry · 2026Article
- Genetic rescue of disrupted synaptic protein interaction network dynamics followingbioRxiv : the preprint server for biology · 2025Article
- Gut microbiota diversity is altered in a sex-dependent manner in Shank3B heterozygote mice.Frontiers in microbiomes · 2025Article
- SRC family kinase inhibition rescues molecular and behavioral phenotypes, but not protein interaction network dynamics, in a mouse model of Fragile X syndrome.Molecular psychiatry · 2024Article
- Review
- Three Decades of Valproate: A Current Model for Studying Autism Spectrum Disorder.Current neuropharmacology · 2024Review
- A synaptic molecular dependency network in knockdown of autism- and schizophrenia-associated genes revealed by multiplexed imaging.Cell reports · 2023Article
- Comparing synaptic proteomes across five mouse models for autism reveals converging molecular similarities including deficits in oxidative phosphorylation and Rho GTPase signaling.Frontiers in aging neuroscience · 2023Article
- Article
- The Shank3Frontiers in neuroscience · 2022Article
- Synaptic protein interaction networks encode experience by assuming stimulus-specific and brain-region-specific states.Cell reports · 2021Article
- Altered network and rescue of human neurons derived from individuals with early-onset genetic epilepsy.Molecular psychiatry · 2021Article
- Effects of Mutations in TSC Genes on Neurodevelopment and Synaptic Transmission.International journal of molecular sciences · 2021Review
- Proteomic insights into synaptic signaling in the brain: the past, present and future.Molecular brain · 2021Review
- Emerging proteomic approaches to identify the underlying pathophysiology of neurodevelopmental and neurodegenerative disorders.Molecular autism · 2020Review
- Quantification of Protein Interaction Network Dynamics using Multiplexed Co-Immunoprecipitation.Journal of visualized experiments : JoVE · 2019Article
- Activity-dependent changes in synaptic protein complex composition are consistent in different detergents despite differential solubility.Scientific reports · 2019Article
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
Background: Autism spectrum disorders (ASDs) are a heterogeneous group of behaviorally defined disorders and are associated with hundreds of rare genetic mutations and several environmental risk factors. Mouse models of specific risk factors have been successful in identifying molecular mechanisms associated with a given factor. However, comparisons among different models to elucidate underlying common pathways or to define clusters of biologically relevant disease subtypes have been complicated by different methodological approaches or different brain regions examined by the labs that developed each model. Here, we use a novel proteomic technique, quantitative multiplex co-immunoprecipitation or QMI, to make a series of identical measurements of a synaptic protein interaction network in seven different animal models. We aim to identify molecular disruptions that are common to multiple models. Methods: QMI was performed on 92 hippocampal and cortical samples taken from seven mouse models of ASD: Shank3B, Shank3Δex4-9, Ube3a Results: Each model displayed a unique set of disrupted interactions, but some interactions were disrupted in multiple models. These tended to be interactions that are known to change with synaptic activity. Clustering revealed potential relationships among models and suggested deficits in AKT signaling in Ube3a Conclusions: These data highlight the great heterogeneity among models, but suggest that high-dimensional measures of a synaptic protein network may allow differentiation of subtypes of ASD with shared molecular pathology.
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