ArticleHuman molecular genetics2011
Synaptic dysfunction and abnormal behaviors in mice lacking major isoforms of Shank3.
Article in Human molecular genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 336 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
336 citing papers in PubMed, 2 syntheses or guidelines pooled it, 543 citations in OpenAlex.
- Convergent blood-brain barrier breakdown in schizophrenia and autism spectrum disorders: a systematic review of preclinical animal models.Fluids and barriers of the CNS · 2026Pooled it
- Genetic variability in scaffolding proteins and risk for schizophrenia and autism-spectrum disorders: a systematic review.Journal of psychiatry & neuroscience : JPN · 2018Pooled it
- Preserved social development but impaired executive function in aResearch square · 2026Article
- Gut Microbiota-Elicited Aberrant Phosphorylation Induces Protein Structural Anomalies: A Non-Negligible Pathogenic Driver of Autism Spectrum Disorder.Microorganisms · 2026Article
- Sex- and experience-dependent regulation of synaptic protein turnover.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Genetic Rescue of Pathogenic O-GlcNAc Dyshomeostasis Associated with Microcephaly and Motor Deficits.eNeuro · 2026Article
- Potential glutamatergic and GABAergic false neurotransmitters in models of excitation-inhibition imbalance.Scientific reports · 2026Article
- Dynamic recruitment of CaMKII into SHANK3 phase-separated condensates tunes postsynaptic density remodeling during long-term potentiation.Nature communications · 2026Article
- Kv4.2The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Early-life sleep disruption in Shank3-deficient rats: A preclinical model for autism-related sleep mechanisms and interventions.Translational psychiatry · 2026Article
- Altered Structural Plasticity Mediated by mGlu and NMDA Receptors and Impaired Cognition in a Genetic ASD Model (Shank3The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Disrupted cortex-wide dynamics impair motor planning in Shank3-mutant mice.bioRxiv : the preprint server for biology · 2026Article
- Rubber tail illusion is not obvious in SH3 and multiple ankyrin repeat domains 3 (Oxford open neuroscience · 2026Article
- 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
- Autism-associatedProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Sex and experience dependent regulation of synaptic protein turnover.bioRxiv : the preprint server for biology · 2025Article
- Deficiency of Shank3 in the nucleus accumbens reveals a loss of social-specific motivation.Communications biology · 2025Article
- Heightened empathic responses led by imbalanced cortico-amygdala circuit inbioRxiv : the preprint server for biology · 2025Article
- A Frank Assessment of SHANK: Impacts of Pathogenic Variations in SHANK3 on Preclinical Models of Phelan McDermid Syndrome.Autism research : official journal of the International Society for Autism Research · 2025Review
- Learning-Associated Flexibility of Cortical Taste Coding Is Impaired in Shank3 Knockout Mice.bioRxiv : the preprint server for biology · 2025Article
276 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
18 authors at 7 institutions in 5 countries.
Funding
Abstract
SHANK3 is a synaptic scaffolding protein enriched in the postsynaptic density (PSD) of excitatory synapses. Small microdeletions and point mutations in SHANK3 have been identified in a small subgroup of individuals with autism spectrum disorder (ASD) and intellectual disability. SHANK3 also plays a key role in the chromosome 22q13.3 microdeletion syndrome (Phelan-McDermid syndrome), which includes ASD and cognitive dysfunction as major clinical features. To evaluate the role of Shank3 in vivo, we disrupted major isoforms of the gene in mice by deleting exons 4-9. Isoform-specific Shank3(e4-9) homozygous mutant mice display abnormal social behaviors, communication patterns, repetitive behaviors and learning and memory. Shank3(e4-9) male mice display more severe impairments than females in motor coordination. Shank3(e4-9) mice have reduced levels of Homer1b/c, GKAP and GluA1 at the PSD, and show attenuated activity-dependent redistribution of GluA1-containing AMPA receptors. Subtle morphological alterations in dendritic spines are also observed. Although synaptic transmission is normal in CA1 hippocampus, long-term potentiation is deficient in Shank3(e4-9) mice. We conclude that loss of major Shank3 species produces biochemical, cellular and morphological changes, leading to behavioral abnormalities in mice that bear similarities to human ASD patients with SHANK3 mutations.
Indexed as
Identifiers
What OpenQuestion holds
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.