ReviewNeuron2013
Modeling autism by SHANK gene mutations in mice.
Review in Neuron, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 303 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
303 citing papers in PubMed, 1 synthesis or guideline pooled it, 500 citations in OpenAlex.
- Optimal dosage of group-based organized physical activity for enhancing social abilities in autistic children: insights from a multilevel meta-analysis.The international journal of behavioral nutrition and physical activity · 2025Pooled it
- HPSC-derived mesenchymal stromal cells ameliorate murine autistic-like phenotypes through activating oxytocinergic neurons.Science advances · 2026Article
- Graph theory identifies altered prefrontal microcircuit organization in Shank3 mice, a mouse Model of autism.Cell reports · 2026Article
- Spatiotemporal dynamics of β-arrestin-mediated Src activation in 5-HT7 receptor signaling pathway.The FEBS journal · 2026Article
- Social Novelty Recruits a Dysfunctional Nucleus Accumbens Ensemble That Drives Social Avoidance in abioRxiv : the preprint server for biology · 2026Article
- Serum MAP1A as a Potential Biomarker for Autism Spectrum Disorder.Brain sciences · 2026Article
- Shank3B deficiency disrupts GABAergic synaptic transmission in pyramidal neurons of the medial prefrontal cortex region in autism spectrum disorder.Molecular brain · 2026Article
- Acute stress induces changes in epigenome-wide DNA methylation.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Graph Theory Identifies Autistic Patterns in the Prefrontal Circuit of a Mouse Model of Autism.Research square · 2026Article
- SHANK3 Deficiency in AgRP Neurons Inhibits Diet-Induced Obesity by Activating p38α.Neuroscience bulletin · 2026Article
- Article
- Shank3 establishes AMPA receptor subunit composition at cerebellar mossy fiber-granule cell synapses and is associated with altered regional microglial morphology.Neurobiology of disease · 2025Article
- Multiplexed smFISH Reveals the Spatial Organization of Neuropil Localized mRNAs Is Linked to Abundance.eNeuro · 2025Article
- Deficiency of Shank3 in the nucleus accumbens reveals a loss of social-specific motivation.Communications biology · 2025Article
- Activity Deprivation Modulates the Shank3/Homer1/mGluR5 Signaling Pathway to Enable Synaptic Upscaling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Early postnatal dysfunction of ACC PV interneurons in Shank3BMolecular psychiatry · 2025Article
- Neurometabolic profiles of autism spectrum disorder patients with genetic variants in specific neurotransmission and synaptic genes.Scientific reports · 2025Article
- Impairment of Group I Metabotropic Glutamate Receptors in the Dorsal Striatum of the R451C-Neuroligin 3 Mouse Model of Autism Spectrum Disorder.Journal of neurochemistry · 2025Article
- Association between anesthetics and autism spectrum disorder: from bench to bedside.Journal of anesthesia · 2025Review
- Article
243 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Shank family proteins (Shank1, Shank2, and Shank3) are synaptic scaffolding proteins that organize an extensive protein complex at the postsynaptic density (PSD) of excitatory glutamatergic synapses. Recent human genetic studies indicate that SHANK family genes (SHANK1, SHANK2, and SHANK3) are causative genes for idiopathic autism spectrum disorders (ASD). Neurobiological studies of Shank mutations in mice support a general hypothesis of synaptic dysfunction in the pathophysiology of ASD. However, the molecular diversity of SHANK family gene products, as well as the heterogeneity in human and mouse phenotypes, pose challenges to modeling human SHANK mutations. Here, we review the molecular genetics of SHANK mutations in human ASD and discuss recent findings where such mutations have been modeled in mice. Conserved features of synaptic dysfunction and corresponding behaviors in Shank mouse mutants may help dissect the pathophysiology of ASD, but also highlight divergent phenotypes that arise from different mutations in the same gene.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.